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<title>Clinical Journal of the American Society of Nephrology</title>
<url>http://cjasn.asnjournals.org/icons/banner/title.gif</url>
<link>http://cjasn.asnjournals.org</link>
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<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1693?rss=1">
<title><![CDATA[Caveats for Scientific Publication in the Modern Marketplace]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1693?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Will, E. J.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06460909</dc:identifier>
<dc:title><![CDATA[Caveats for Scientific Publication in the Modern Marketplace]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1695</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1693</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1696?rss=1">
<title><![CDATA[Dystroglycan in the Molecular Diagnosis of the Podocytopathies]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1696?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kopp, J. B.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06910909</dc:identifier>
<dc:title><![CDATA[Dystroglycan in the Molecular Diagnosis of the Podocytopathies]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1698</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1696</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1699?rss=1">
<title><![CDATA[More Mixed Messages in Terms of Salt]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1699?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Luft, F. C.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06200909</dc:identifier>
<dc:title><![CDATA[More Mixed Messages in Terms of Salt]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1700</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1699</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1701?rss=1">
<title><![CDATA[Rare but Relevant Kidney Disorders]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1701?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Grunfeld, J.-P., Scholl, U., Choi, M, Liu, T, Ramaekers, V., Hausler, M., Grimmer, J, Tobe, S., Farhi, A, Nelson-Williams, C, Lifton, R., Bockenhauer, D, Feather, S, Stanescu, H., Bandulik, S, Zdebik, A., Reichold, M, Tobin, J, Lieberer, E, Sterner, C, Landoure, G, Arora, R, Sirimanna, T, Thompson, D, Cross, J., van't Hoff, W, Al Masri, O, Tullus, K, Yeung, S, Anikster, Y, Klootwijk, E, Hubank, M, Dillon, M., Heitzmann, D, Arcos-Burgos, M, Knepper, M., Dobbie, A, Gahl, W., Warth, R, Sheridan, E, Kleta, R, Glaudemans, B, van der Wijst, J, Scola, R, Lorenzoni, P., Heister, A, van der Kemp, A, Knoers, N., Hoenderop, J., Bindels, R., van Bommel, E., Jansen, I, Hendriksz, T., Aarnoudse, A., Scheel, P., Feeley, N, Delvaeye, M, Noris, M, De Vriese, A, Esmon, C., Esmon, N., Ferrell, G, Del-Favero, J, Plaisance, S, Claes, B, Lambrechts, D, Remuzzi, G, Conway, E.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06710909</dc:identifier>
<dc:title><![CDATA[Rare but Relevant Kidney Disorders]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1704</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1701</prism:startingPage>
<prism:section>Presse R&amp;eacute;nale</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1705?rss=1">
<title><![CDATA[Evaluation of Trial Outcomes in Acute Kidney Injury by Creatinine Modeling]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1705?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Clinical trials of acute kidney injury (AKI) use changes in creatinine as outcome metrics. This study investigated how outcome metrics and baseline creatinine affect trial outcome.</p>
<p>Design, setting, participants, &amp; measurements: A one-compartment pharmacokinetic model of creatinine change resulting from a decrease in GFR was applied to a population of 10,000 simulated virtual inpatients. Treatment was simulated as an amelioration of GFR decrease by a specified percentage, the treatment efficacy, in 50%. Three categorical and two continuous outcome metrics were calculated and compared. Outcomes were compared for measured and estimated baseline creatinine levels that were back-calculated assuming a GFR of 100 or 75 ml/min.</p>
<p>Results: The continuous metrics, the average value of creatinine and the average value of creatinine relative to baseline decreased approximately linearly with increase in treatment efficacy. The categorical metrics displayed a sigmoidal decrease and erroneously suggested perfect treatment when GFR decrease was ameliorated by only 60 to 80%. Using an estimate of baseline creatinine increased the number of patients who were classified as having AKI.</p>
<p>Conclusions: When used to determine clinical trial outcome, continuous metrics correctly detected the extent of intervention. At low treatment efficacy, categorical metrics underestimated and at high treatment efficacy overestimated the effect of treatment. These effects were exaggerated when the population contained a high proportion of patients with more severe AKI. An estimated baseline creatinine level will overestimate AKI prevalence compared with a measured baseline value. Clinical trials of AKI should use a continuous outcome metric and a measured baseline and report baseline median and interquartile range.</p>
]]></description>
<dc:creator><![CDATA[Pickering, J. W., Frampton, C. M., Endre, Z. H.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00820209</dc:identifier>
<dc:title><![CDATA[Evaluation of Trial Outcomes in Acute Kidney Injury by Creatinine Modeling]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1715</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1705</prism:startingPage>
<prism:section>Acute Renal Failure</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1716?rss=1">
<title><![CDATA[Soluble TWEAK Plasma Levels as a Novel Biomarker of Endothelial Function in Patients with Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1716?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Recently, we showed that soluble TNF-like weak inducer of apoptosis (sTWEAK) plasma levels are diminished in hemodialysis patients and had additive effects with IL-6 on survival. Because sTWEAK plasma level has been associated with the presence of chronic kidney disease (CKD) and cardiovascular disease, we hypothesized that in patients with CKD, sTWEAK levels may relate to the increased prevalence of endothelial dysfunction that usually accompanies the decline of estimated GFR (eGFR).</p>
<p>Design, setting, participants, &amp; measurements: We studied 295 patients with different stages of nondiabetic CKD (52% male; age 47 &plusmn; 12 yr), testing the association between sTWEAK plasma levels and CKD stage and the relationship between flow-mediated dilation (FMD) and sTWEAK concentrations. Fifty-five healthy volunteers (51% male; age 47 &plusmn; 11 yr) served as matched control subjects.</p>
<p>Results: A gradual decrease in FMD was observed as eGFR decreased. Compared with healthy control subjects, sTWEAK plasma levels were diminished in all stages of CKD and correlated strongly with eGFR. FMD levels were associated with sTWEAK concentrations in univariate analysis. This association persisted after multivariate adjustment for eGFR levels, high-sensitivity C-reactive protein, diastolic BP, and sTWEAK, all of which were found to be significant and independent contributors to FMD.</p>
<p>Conclusions: A decline in eGFR is accompanied by gradual reductions in sTWEAK plasma levels. Because sTWEAK strongly and independently correlated with FMD, our study suggests novel links between sTWEAK and endothelial dysfunction in patients with CKD.</p>
]]></description>
<dc:creator><![CDATA[Yilmaz, M. I., Carrero, J. J., Ortiz, A., Martin-Ventura, J. L., Sonmez, A., Saglam, M., Yaman, H., Yenicesu, M., Egido, J., Blanco-Colio, L. M.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02760409</dc:identifier>
<dc:title><![CDATA[Soluble TWEAK Plasma Levels as a Novel Biomarker of Endothelial Function in Patients with Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1723</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1716</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1724?rss=1">
<title><![CDATA[Longitudinal Formulas to Estimate GFR in Children with CKD]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1724?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Whereas current GFR estimating equations approximate direct GFR measurement at a single time point, formulas that capitalize on changes in easily measured biologic parameters could improve the accuracy and precision of GFR estimation.</p>
<p>Design, setting, participants, &amp; measurements: In the Chronic Kidney Disease in Children Cohort (aged 1 to 16 yr), we measured GFR by plasma disappearance of iohexol (iGFR) and biomarkers in the first two annual visits. Models took the form GFR<SUB>2</SUB> = a[GFR<SUB>1</SUB>/40]<sup>b</sup>[X<SUB>2</SUB>/X<SUB>1</SUB>]<sup>c</sup>, where GFR<SUB>2</SUB> and GFR<SUB>1</SUB> represented the current and previous years' iGFR, 40 ml/min per 1.73 m<sup>2</sup> was the cohort mean, and X<SUB>2</SUB>/X<SUB>1</SUB> was the change in predictors over time. Using data from 360 participants with a median age of 12.1 yr, we evaluated the predictive performance of a past GFR measurement and 20 other variables using a two-thirds random sample of the data. A one-third sample was reserved for validation.</p>
<p>Results: Previous iGFR measurements were strongly predictive of subsequent iGFR and adding change in height/serum creatinine significantly improved the explanatory power to 78%. In the validation set, the correlation between estimated and measured GFR was 0.88, and 48 and 88% of estimated GFRs were within 10 and 30% of observed iGFRs. When the past GFR measurement was not used, addition of change in markers to a cross-sectional model did not improve prediction.</p>
<p>Conclusions: Longitudinal formulas to estimate iGFR capitalize on the high predictive power of previous iGFR measurements and in this study yielded a parsimonious prediction model with the potential for assessing progression in the clinical setting.</p>
]]></description>
<dc:creator><![CDATA[Abraham, A. G., Schwartz, G. J., Furth, S., Warady, B. A., Munoz, A.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01860309</dc:identifier>
<dc:title><![CDATA[Longitudinal Formulas to Estimate GFR in Children with CKD]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1730</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1724</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1731?rss=1">
<title><![CDATA[A Randomized Controlled Study of Weekly and Biweekly Dosing of Epoetin Alfa in CKD Patients With Anemia]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1731?rss=1</link>
<description><![CDATA[
<p>Background and objectives: In clinical practice, physicians often use once-weekly (QW) and biweekly (Q2W) dosing of epoetin alfa to treat anemia in patients with chronic kidney disease (CKD). Although the literature supports this practice, previous studies were limited by short treatment duration, lack of randomization, or absence of the approved three times per week (TIW) dosing arm. This randomized trial evaluated extended dosing regimens of epoetin alfa, comparing QW and Q2W to TIW dosing in anemic CKD subjects. The primary objective was to show that treatment with epoetin alfa at QW and Q2W intervals was not inferior to TIW dosing.</p>
<p>Design, setting, participants, &amp; measurements: 375 subjects with stage 3 to 4 CKD were randomized equally to the three groups and treated for 44 wk; to explore the impact of changing from TIW to QW administration on hemoglobin (Hb) control and adverse events, subjects on TIW switched to QW after 22 wk. The Hb was measured weekly, and the dose of epoetin alfa was adjusted to achieve and maintain an Hb level of 11.0 to 11.9 g/dl.</p>
<p>Results: Both the QW and Q2W regimens met the primary efficacy endpoint. More subjects in the TIW group than in the QW and Q2W groups exceeded the Hb ceiling. Adverse events were similar across treatment groups and consistent with the morbidities of CKD patients.</p>
<p>Conclusions: Administration of epoetin alfa at QW and Q2W intervals are potential alternatives to TIW dosing for the treatment of anemia in stage 3 to 4 CKD subjects.</p>
]]></description>
<dc:creator><![CDATA[Pergola, P. E., Gartenberg, G., Fu, M., Wolfson, M., Rao, S., Bowers, P.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03470509</dc:identifier>
<dc:title><![CDATA[A Randomized Controlled Study of Weekly and Biweekly Dosing of Epoetin Alfa in CKD Patients With Anemia]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1740</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1731</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1741?rss=1">
<title><![CDATA[Renal Function in Glycogen Storage Disease Type I, Natural Course, and Renopreservative Effects of ACE Inhibition]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1741?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Renal failure is a major complication in glycogen storage disease type I (GSD I). We studied the natural course of renal function in GSD I patients. We studied differences between patients in optimal and nonoptimal metabolic control and possible renoprotective effects of angiotensin converting enzyme inhibition.</p>
<p>Design, setting, participants, &amp; measurements: Thirty-nine GSD I patients that visited our clinic were studied. GFR and effective renal plasma flow (ERPF) were measured by means of I<sup>125</sup> iothalamate and I<sup>131</sup> hippuran clearance and corrected for body surface area. Microalbuminuria was defined as &gt;2.5 mg albumin/mmol creatinine and proteinuria as &gt;0.2 g protein per liter. Optimal metabolic control was present when blood glucoses were &gt;3.5 mmol/L, urine lactate/creatinine ratios &lt;0.06 mmol/mmol, triglycerides &lt;6.0 mmol/L, and uric acid concentrations &lt;450 &micro;mol/L.</p>
<p>Results: Quadratic regression analysis showed a biphasic pattern in the course of GFR and ERPF related to age. Microalbuminuria was observed significantly less frequently in the patients with optimal metabolic control compared with the patients with nonoptimal metabolic control. A significant decrease in GFR was observed after starting ACE inhibition.</p>
<p>Conclusions: This study describes a biphasic pattern of the natural course of GFR and ERPF in GSD I patients, followed by the development of microalbuminuria and proteinuria. Optimal metabolic control has a renoprotective effect on the development of microalbuminuria and proteinuria in GSD I patients. Treatment with ACE inhibitors significantly decreases the GFR, especially in GSD I patients with glomerular hyperfiltration.</p>
]]></description>
<dc:creator><![CDATA[Martens, D. H. J., Rake, J. P., Navis, G., Fidler, V., van Dael, C. M. L., Smit, G. P. A.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00050109</dc:identifier>
<dc:title><![CDATA[Renal Function in Glycogen Storage Disease Type I, Natural Course, and Renopreservative Effects of ACE Inhibition]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1746</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1741</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1747?rss=1">
<title><![CDATA[Dystroglycan in the Diagnosis of FSGS]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1747?rss=1</link>
<description><![CDATA[
<p>Background and objectives: - and &beta;-dystroglycan (DG), which link the actin cytoskeleton of the podocyte to the glomerular basement membrane, are maintained in FSGS but decreased in minimal change disease (MCD). Fibrosis has been linked to increased fibroblast-specific protein-1 (FSP1) and epithelial&ndash;mesenchymal transition. We studied DG, FSP1, and podocyte differentiation in FSGS variants and cases of suspected FSGS.</p>
<p>Design, setting, participants, &amp; measurements: We studied renal biopsies with FSGS, not otherwise specified (NOS), tip lesion, or collapsing variants (COLL), <I>versus</I> secondary FSGS or cases without segmental sclerotic lesions where a diagnosis of MCD <I>versus</I> FSGS could not be established (undefined [UNDEF]) and compared the expression of DG, FSP1, and podocyte Wilms' tumor antigen (WT1).</p>
<p>Results: WT1 is markedly decreased in NOS <I>versus</I> normal and correlates with the extent of sclerosis. - and &beta;-DG are maintained in most primary and secondary FSGS cases. In contrast, -DG is significantly decreased in UNDEF, supporting a diagnosis of MCD. Furthermore, follow-up shows remission or decreased proteinuria in four of six of these UNDEF cases in response to therapy. Interstitial FSP1 is numerically highest in COLL but is only rarely found in tubules or podocytes in any other forms of FSGS.</p>
<p>Conclusions: We conclude that increased FSP1 may be a marker of the aggressive course of collapsing FSGS. Furthermore, DG staining is a useful adjunct to assist in distinction of FSGS <I>versus</I> MCD in biopsies without defining lesions.</p>
]]></description>
<dc:creator><![CDATA[Giannico, G., Yang, H., Neilson, E. G., Fogo, A. B.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01510209</dc:identifier>
<dc:title><![CDATA[Dystroglycan in the Diagnosis of FSGS]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1753</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1747</prism:startingPage>
<prism:section>Clinical Immunology and Pathology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1754?rss=1">
<title><![CDATA[Oral Cyclophosphamide for Lupus Glomerulonephritis: An Underused Therapeutic Option]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1754?rss=1</link>
<description><![CDATA[
<p>Background and objectives: In our center, systemic lupus erythematosus nephritis is routinely treated with an oral cyclophosphamide (POCY) regimen. POCY is easy to administer and less expensive than intravenous cyclophosphamide (IVCY) as it is currently used in the United States; however, the use of POCY has declined in favor of IVCY. Our experience with POCY suggests that it is well tolerated and consistently associated with good long-term outcomes. Here we report this experience to build a case for maintaining POCY as a therapeutic option in lupus nephritis.</p>
<p>Design, setting, participants, &amp; measurements: This is a single-center, retrospective analysis of the outcome of 46 patients who had systemic lupus erythematosus with nephritis and were treated with POCY between 1995 and 2006. POCY was given for 2 to 4 mo at a dosage of 1.0 to 1.5 mg/kg ideal body weight. After completing POCY, the patients received either azathioprine or mycophenolate mofetil.</p>
<p>Results: Median follow-up was 23.5 mo, and median duration of POCY was 4 mo (range 1 to 16 mo). Durable complete or partial remission of proteinuria was achieved in 32 (70%) patients, whereas 5 (11%) progressed to ESRD. Outcomes were comparable in black and white individuals. Adverse effects occurred in fewer than 10% of the cohort, and only four patients discontinued POCY.</p>
<p>Conclusions: These results suggest that sequential therapy of POCY followed by azathioprine or mycophenolate mofetil is comparable to IVCY regimens but that efficacy may not be affected by race.</p>
]]></description>
<dc:creator><![CDATA[McKinley, A., Park, E., Spetie, D., Hackshaw, K. V., Nagaraja, S., Hebert, L. A., Rovin, B. H.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02670409</dc:identifier>
<dc:title><![CDATA[Oral Cyclophosphamide for Lupus Glomerulonephritis: An Underused Therapeutic Option]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1760</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1754</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1761?rss=1">
<title><![CDATA[Eosinophil Count Is Positively Correlated with Albumin Excretion Rate in Men with Type 2 Diabetes]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1761?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Patients with allergic disorders such as allergic rhinitis or asthma have been reported to be at increased risk for atherosclerosis. In this study, we evaluated the relationships between peripheral eosinophil count and degree of albumin excretion rate, which is a useful marker of cardiovascular mortality as well as diabetic nephropathy in patients with type 2 diabetes.</p>
<p>Design, setting, participants, &amp; measurements: We evaluated relationships of peripheral eosinophil count to degree of albumin excretion rate as well as to major cardiovascular risk factors, including age, BP, serum lipid concentration, and glycemic control (glycosylated hemoglobin); body mass index; current treatment for diabetes; smoking status; and presence of cardiovascular disease in 783 patients (416 men and 367 women) with type 2 diabetes.</p>
<p>Results: Log(eosinophil count) was positively associated with systolic BP (<I>r</I> = 0.124, <I>P</I> = 0.0108), serum triglyceride concentration (<I>r</I> = 0.108, <I>P</I> = 0.0284), and log(albumin excretion rate) (<I>r</I> = 0.301, <I>P</I> &lt; 0.0001) in men; however, no association was found between log(eosinophil count) and log(albumin excretion rate) (<I>r</I> = 0.085, <I>P</I> = 0.1050) in women. Multivariate linear regression analysis demonstrated that log(eosinophil count) (&beta; = 0.260, <I>P</I> &lt; 0.0001), duration of diabetes (&beta; = 0.203, <I>P</I> = 0.0003), glycosylated hemoglobin (&beta; = 0.117, <I>P</I> = 0.0238), systolic BP (&beta; = 0.205, <I>P</I> = 0.0001), and serum triglyceride concentration (&beta; = 0.162, <I>P</I> = 0.0038) were independent determinants of log(albumin excretion rate) in men.</p>
<p>Conclusions: Allergic disorders may be associated with microalbuminuria in men with type 2 diabetes.</p>
]]></description>
<dc:creator><![CDATA[Fukui, M., Tanaka, M., Hamaguchi, M., Senmaru, T., Sakabe, K., Shiraishi, E., Harusato, I., Yamazaki, M., Hasegawa, G., Nakamura, N.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:22 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03330509</dc:identifier>
<dc:title><![CDATA[Eosinophil Count Is Positively Correlated with Albumin Excretion Rate in Men with Type 2 Diabetes]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1765</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1761</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1766?rss=1">
<title><![CDATA[Predictors of Complication after Percutaneous Ultrasound-Guided Kidney Biopsy in HIV-Infected Individuals: Possible Role of Hepatitis C and HIV Co-infection]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1766?rss=1</link>
<description><![CDATA[
<p>Background and objectives: HIV-infected patients often undergo kidney biopsy. The risks of percutaneous ultrasound-guided kidney biopsy in this population are not well established.</p>
<p>Design, setting, participants, &amp; measurements: This was a case-control, single-center study of 1116 (243 with HIV infection and 873 without) consecutive ultrasound-guided biopsies from 1024 patients. The primary outcome was any major or minor complication. Major complications included biopsy-associated bleeding that required transfusion, angiography, or surgery; hypotension that required intervention; and death. Minor complications included development of a hematoma or gross hematuria. The odds of complication was assessed with logistic regression.</p>
<p>Results: Overall complication rates (8.6 <I>versus</I> 7.2%) did not significantly differ between HIV-infected and noninfected individuals. HIV-positive status did not predict complication. In the entire cohort, hepatitis C infection was associated with a 2.08 (95% confidence interval [CI] 1.47 to 2.93) increased odds of complication, and each 10,000-cells/mm<sup>3</sup> decrease in prebiopsy platelet count a 1.05 (95% CI 1.02 to 1.08) increased odds of complication. In addition, prebiopsy hematocrit &lt;30% and estimated GFR &lt;30 ml/min per 1.73 m<sup>2</sup> were associated with major complication. Whereas the association of prebiopsy platelet count was not modified by HIV infection, hepatitis C/HIV co-infection was associated with a 5.71 (95% CI 1.89 to 17.2) increased odds of complication as compared with 1.27 (95% CI 0.73 to 2.19) in hepatitis C&ndash;positive/HIV-negative individuals.</p>
<p>Conclusions: Ultrasound-guided percutaneous kidney biopsy is a relatively safe, well-tolerated procedure in the HIV-infected population. HIV-infected individuals who are co-infected with hepatitis C seem to be at greatest risk.</p>
]]></description>
<dc:creator><![CDATA[Tabatabai, S., Sperati, C. J., Atta, M. G., Janjua, K., Roxbury, C., Lucas, G. M., Fine, D. M.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03880609</dc:identifier>
<dc:title><![CDATA[Predictors of Complication after Percutaneous Ultrasound-Guided Kidney Biopsy in HIV-Infected Individuals: Possible Role of Hepatitis C and HIV Co-infection]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1773</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1766</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1774?rss=1">
<title><![CDATA[Impact of Gestational Age and Birth Weight on Amikacin Clearance on Day 1 of Life]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1774?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Intrauterine growth restriction (IUGR) and prematurity are associated with a low nephron endowment. It can therefore be expected that neonates who are born premature and/or after IUGR have a lower GFR. Measurement of GFR in neonates is difficult, but the clearance of amikacin has been proven to be a reliable marker. We hypothesized that amikacin clearance is lower after IUGR or premature birth as a marker of low nephron endowment.</p>
<p>Design, setting, participants, &amp; measurements: Amikacin clearance was retrospectively analyzed in 161 neonates who received amikacin within the first 24 h of life. Using the MW/Pharm computer program, a population one-compartment model was calculated. The mean population pharmacokinetic parameters were individualized for each patient according to the maximum <I>a posteriori</I> Bayesian fitting method and provided the amikacin clearance.</p>
<p>Results: Our results show that birth weight <I>z</I> score and gestational age are correlated with the clearance of amikacin (partial correlation coefficient 0.159, <I>P</I> = 0.046, and 0.396, <I>P</I> &lt; 0.001, respectively), after correction for other factors.</p>
<p>Conclusions: We conclude that renal clearance on the first day of life is lower in neonates with a lower gestational age and/or birth weight <I>z</I> score. This indicates that both prematurity and IUGR impair GFR on the first day of life.</p>
]]></description>
<dc:creator><![CDATA[Schreuder, M. F., Wilhelm, A. J., Bokenkamp, A., Timmermans, S. M.H., Delemarre-van de Waal, H. A., van Wijk, J. A.E.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02230409</dc:identifier>
<dc:title><![CDATA[Impact of Gestational Age and Birth Weight on Amikacin Clearance on Day 1 of Life]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1778</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1774</prism:startingPage>
<prism:section>Clinical Pharmacology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1779?rss=1">
<title><![CDATA[Correlates and Outcomes of Fatigue among Incident Dialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1779?rss=1</link>
<description><![CDATA[
<p>Background &amp; objectives: Fatigue is a debilitating symptom experienced by patients undergoing dialysis, but there is only limited information on its prevalence and its association with patient outcomes. This study examines the correlates of self-reported fatigue at initiation of dialysis and after 1 yr and assesses the extent to which fatigue was associated with health-related quality of life and survival.</p>
<p>Design, setting, participants, &amp; measurements: A longitudinal cohort of 917 incident hemodialysis and peritoneal dialysis patients who completed the CHOICE Health Experience Questionnaire (CHEQ) participated in the study. Fatigue was assessed using the SF-36 vitality scale. Known predictors of fatigue including sociodemographic and psychosocial factors, dialysis-related factors, biochemical variables including inflammatory markers, comorbidities, and medications were used as covariates.</p>
<p>Results: A low vitality score was independently associated with white race, higher Index of Coexistent Disease score, higher body mass index, lack of physical exercise, antidepressant use, and higher C-reactive protein levels (CRP). A lower vitality score was strongly associated with lower SF-36 physical functioning, mental health, bodily pain scores, and decreased sleep quality (all <I>P</I> &lt; 0.001) at baseline. Among surviving participants, higher serum creatinine at baseline was associated with preserved vitality at 1 yr. Patients with the highest baseline vitality scores were associated with longer survival (hazard ratio 0.75; 95% CI 0.58 to 0.96, <I>P</I> = 0.03).</p>
<p>Conclusions: The findings of this study demonstrate that ESRD patients experience profound levels of fatigue and elucidate its correlates. Also, the association of fatigue with survival may have significant implications for this population.</p>
]]></description>
<dc:creator><![CDATA[Jhamb, M., Argyropoulos, C., Steel, J. L., Plantinga, L., Wu, A. W., Fink, N. E., Powe, N. R., Meyer, K. B., Unruh, M. L., for the Choices for Healthy Outcomes in Caring for End-Stage Renal Disease (CHOICE) Study]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00190109</dc:identifier>
<dc:title><![CDATA[Correlates and Outcomes of Fatigue among Incident Dialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1786</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1779</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1787?rss=1">
<title><![CDATA[Does Heparin Coating Improve Patency or Reduce Infection of Tunneled Dialysis Catheters?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1787?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Tunneled dialysis catheters are prone to frequent malfunction and infection. Catheter thrombosis occurs despite prophylactic anticoagulant locks. Catheter thrombi may also serve as a nidus for catheter infection, thereby increasing the risk of bacteremia. Thus, heparin coating of catheters may reduce thrombosis and infection. This study evaluated whether heparin-coated hemodialysis catheters have fewer infections or greater cumulative survival than noncoated catheters.</p>
<p>Design, setting, participants, &amp; measurements: We retrospectively queried a prospective access database to analyze the outcomes of 175 tunneled dialysis catheters placed in the internal jugular vein, including 89 heparin-coated catheters and 86 noncoated catheters. The primary outcome was cumulative catheter survival, and the secondary outcome was infection-free catheter survival.</p>
<p>Results: The two patient groups were similar in demographics and clinical and catheter features. Catheter-related bacteremia occurred less frequently with heparin-coated catheters than with noncoated catheters (34 <I>versus</I> 60%, <I>P</I> &lt; 0.001). Cumulative catheter survival was similar in heparin-coated and noncoated catheters (hazard ratio, 0.87; 95% confidence interval, 0.55 to 1.36; <I>P</I> = 0.53). On multiple variable survival analysis including catheter type, age, sex, diabetes, coronary artery disease, peripheral vascular disease, cerebrovascular disease, catheter location, and previous catheter, only catheter location predicted cumulative catheter survival (hazard ratio, 2.03; 95% CI, 1.27 to 3.25, with the right internal jugular location being the reference group, <I>P</I> = 0.003). The frequency of thrombolytic instillation was 1.8 per 1000 catheter-days in both groups.</p>
<p>Conclusions: Heparin coating decreases the frequency of catheter-related bacteremia but does not reduce the frequency of catheter malfunction.</p>
]]></description>
<dc:creator><![CDATA[Jain, G., Allon, M., Saddekni, S., Barker, J.-F., Maya, I. D.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03920609</dc:identifier>
<dc:title><![CDATA[Does Heparin Coating Improve Patency or Reduce Infection of Tunneled Dialysis Catheters?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1790</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1787</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1791?rss=1">
<title><![CDATA[Combining Near-Subject Absolute and Relative Measures of Longitudinal Hydration in Hemodialysis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1791?rss=1</link>
<description><![CDATA[
<p>Background and objectives: The feasibility and additional value of combining bioimpedance analysis (BIA) with near-subject absolute measurement of total body water using deuterium dilution (TBW<SUB>D</SUB>) in determining longitudinal fluid status was investigated.</p>
<p>Design, setting, participants, &amp; measurements: Fifty-nine hemodialysis patients (17 female; age 58.4 &plusmn; 16.1 yr; body mass index 27.0 &plusmn; 5.4) were enrolled into a 12-mo, two-center, prospective cohort study. Deuterium concentration was measured in breath by flowing-afterglow mass spectrometry using a validated protocol ensuring full equilibration with the TBW; BIA was measured using a multifrequency, multisegmental device. Comorbidity was quantified by the Stoke score. Clinicians were blinded to body composition data.</p>
<p>Results: At baseline and 12 mo, there was an incremental discrepancy between TBW<SUB>BIA</SUB> and TBW<SUB>D</SUB> volumes such that greater comorbidity was associated with increasing overhydration. Forty-three patients who completed the study had no longitudinal differences in the prescribed or achieved postdialysis weights. In contrast, TBW<SUB>D</SUB> increased without a change in TBW<SUB>BIA</SUB> (mean difference &ndash;0.10 L). Changes in TBW and lean body mass differed according to baseline comorbidity; without comorbidity, BIA also identified an increase in TBW and lean body mass, whereas with increasing comorbid burden, BIA failed to demonstrate increases in tissue hydration identified by TBW<SUB>D</SUB>.</p>
<p>Conclusions: Combined near-patient measurements of absolute and BIA-estimated TBW are achievable in a dialysis facility by identifying changes in body composition not fully appreciated by routine assessment. BIA underestimates tissue overhydration that is associated with comorbidity, resulting in reduced sensitivity to longitudinal increases during a 12-mo period.</p>
]]></description>
<dc:creator><![CDATA[Chan, C., McIntyre, C., Smith, D., Spanel, P., Davies, S. J.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02510409</dc:identifier>
<dc:title><![CDATA[Combining Near-Subject Absolute and Relative Measures of Longitudinal Hydration in Hemodialysis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1798</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1791</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1799?rss=1">
<title><![CDATA[Randomized Controlled Trial of Icodextrin versus Glucose Containing Peritoneal Dialysis Fluid]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1799?rss=1</link>
<description><![CDATA[
<p>Background and objectives: While peritoneal dialysis with icodextrin is commonly used in patients with poor peritoneal membrane characteristics, the data on the usefulness of this solution in patients with lower transport characteristics are limited. The study was designed to compare icodextrin to glucose in Chinese prevalent peritoneal dialysis patients of different peritoneal transport characteristics (PET) categories.</p>
<p>Design, setting, participants, &amp; measurements: This was a randomized, double-blind, perspective control study. Stable prevalent continuous ambulatory peritoneal dialysis (CAPD) patients were randomized to either 7.5% icodextrin (ICO) or 2.5% glucose (GLU) solution for 4 wk. Peritoneal membrane function was measured to define PET category in baseline. Creatinine clearance (Ccr), urea nitrogen clearance (C<SUB>BUN</SUB>), ultrafiltration (UF) during the long night dwell, dialysate, and metabolic biomarkers were measured at baseline, 2, and 4 wk. UF, Ccr, and C<SUB>BUN</SUB> were compared among different PET categories.</p>
<p>Results: A total of 201 CAPD patients were enrolled in the study. There were no baseline differences between the groups. Following 2 and 4 wk of therapy, Ccr, C<SUB>BUN,</SUB> and UF were all significantly higher in the ICO <I>versus</I> the GLU group. Additionally, switching to ICO resulted in a significant increase in UF in high, high-average, and low-average transporters as compared with baseline. The extent of increased UF was more obvious in higher transporters. Blood cholesterol level in the ICO group decreased significantly than that in the GLU group.</p>
<p>Conclusion: Compared with glucose-based solution, 7.5% icodextrin significantly improved UF and small solute clearance, even in patients with low-average peritoneal transport.</p>
]]></description>
<dc:creator><![CDATA[Lin, A., Qian, J., Li, X., Yu, X., Liu, W., Sun, Y., Chen, N., Mei, C., for the Icodextrin National Multi-center Cooperation Group]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02950509</dc:identifier>
<dc:title><![CDATA[Randomized Controlled Trial of Icodextrin versus Glucose Containing Peritoneal Dialysis Fluid]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1804</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1799</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1805?rss=1">
<title><![CDATA[Serum Alkaline Phosphatase and Mortality in African Americans with Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1805?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Serum alkaline phosphatase has been associated with increased mortality in hemodialysis patients but its associations with mortality in chronic kidney disease (CKD) stages III and IV are unknown.</p>
<p>Design, settings, participants &amp; measurements: In 1094 participants in the African-American Study of Kidney Disease and Hypertension (AASK) database, the associations of serum alkaline phosphatase with mortality and cardiovascular events were examined in Cox models.</p>
<p>Results: The mean (&plusmn;SD) age was 54 &plusmn; 11 yr, and 61% were men. The median alkaline phosphatase was 80 IU/L, and interquartile range was 66 to 97 IU/L. The mean follow-up was 4.6 yr. There were 105 (9.6%) all-cause deaths and 149 (13.6%) cardiovascular events. Each doubling of serum alkaline phosphatase was significantly associated with increased hazard [hazard ratio (HR) 1.60, 95% confidence interval (CI) 1.08 &ndash;2.36] of all-cause mortality adjusted for demographics, drug and blood pressure groups, and comorbidity. With further adjustment for liver function tests as well as serum calcium and phosphorus, each doubling of serum alkaline phosphatase remained significantly associated with increased mortality (HR 1.55, 95% CI 1.03 to 2.33). Serum alkaline phosphatase was not significantly associated with increased risk of cardiovascular events.</p>
<p>Conclusions: Independent of liver function tests and serum calcium and phosphorus, higher levels of serum alkaline phosphatase are associated with increased mortality in the CKD population. Further studies are warranted to identify the potential mechanisms for this association.</p>
]]></description>
<dc:creator><![CDATA[Beddhu, S., Ma, X., Baird, B., Cheung, A. K., Greene, T.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01560309</dc:identifier>
<dc:title><![CDATA[Serum Alkaline Phosphatase and Mortality in African Americans with Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1810</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1805</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1811?rss=1">
<title><![CDATA[Acute Decline in Renal Function, Inflammation, and Cardiovascular Risk after an Acute Coronary Syndrome]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1811?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Chronic kidney disease is associated with a higher risk of cardiovascular outcomes. The prognostic significance of worsening renal function has also been shown in various cohorts of cardiac disease; however, the predictors of worsening renal function and the contribution of inflammation remains to be established.</p>
<p>Design, setting, participants, &amp; measurements: Worsening renal function was defined as a 25% or more decrease in estimated GFR (eGFR) over a 1-mo period in patients after a non-ST or ST elevation acute coronary syndromes participating in the Aggrastat-to-Zocor Trial; this occurred in 5% of the 3795 participants.</p>
<p>Results: A baseline C-reactive protein (CRP) in the fourth quartile was a significant predictor of developing worsening renal function (odds ratio, 2.48; 95% confidence interval, 1.49, 4.14). After adjusting for baseline CRP and eGFR, worsening renal function remained a strong multivariate predictor for the combined cardiovascular composite of CV death, recurrent myocardial infarction (MI), heart failure or stroke (hazard ratio, 1.6; 95% confidence interval, 1.1, 2.3).</p>
<p>Conclusions: Patients with an early decline in renal function after an acute coronary syndrome are at a significant increased risk for recurrent cardiovascular events. CRP is an independent predictor for subsequent decline in renal function and reinforces the idea that inflammation may be related to the pathophysiology of progressive renal disease.</p>
]]></description>
<dc:creator><![CDATA[Mielniczuk, L. M., Pfeffer, M. A., Lewis, E. F., Blazing, M. A., de Lemos, J. A., Mohanavelu, S., Rouleau, J., Fox, K., Pedersen, T. R., Califf, R. M.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03510509</dc:identifier>
<dc:title><![CDATA[Acute Decline in Renal Function, Inflammation, and Cardiovascular Risk after an Acute Coronary Syndrome]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1817</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1811</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1818?rss=1">
<title><![CDATA[Key Comorbid Conditions that Are Predictive of Survival among Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1818?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Abstracting information about comorbid illnesses from the medical record can be time-consuming, particularly when a large number of conditions are under consideration. We sought to determine which conditions are most prognostic and whether comorbidity continues to contribute to a survival model once laboratory and clinical parameters have been accounted for.</p>
<p>Design, setting, participants, &amp; measurements: Comorbidity data were abstracted from the medical records of Dialysis Outcomes and Practice Pattern Study (DOPPS) I, II, and III participants using a standardized questionnaire. Models that were composed of different combinations of comorbid conditions and case-mix factors were compared for explained variance (<I>R</I><sup>2</sup>) and discrimination (c statistic).</p>
<p>Results: Seventeen comorbid conditions account for 96% of the total explained variance that would result if 45 comorbidities that were expected to be predictive of survival were added to a demographics-adjusted survival model. These conditions together had more discriminatory power (c statistic 0.67) than age alone (0.63) or serum albumin (0.60) and were equivalent to a combination of routine laboratory and clinical parameters (0.67). The strength of association of the individual comorbidities lessened when laboratory/clinical parameters were added, but all remained significant. The total <I>R</I><sup>2</sup> of a model adjusted for demographics and laboratory/clinical parameters increased from 0.13 to 0.17 upon addition of comorbidity.</p>
<p>Conclusions: A relatively small list of comorbid conditions provides equivalent discrimination and explained variance for survival as a more extensive characterization of comorbidity. Comorbidity adds to the survival model a modest amount of independent prognostic information that cannot be substituted by clinical/laboratory parameters.</p>
]]></description>
<dc:creator><![CDATA[Miskulin, D., Bragg-Gresham, J., Gillespie, B. W., Tentori, F., Pisoni, R. L., Tighiouart, H., Levey, A. S., Port, F. K.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00640109</dc:identifier>
<dc:title><![CDATA[Key Comorbid Conditions that Are Predictive of Survival among Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1826</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1818</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1827?rss=1">
<title><![CDATA[The Alphabet Soup of Kidney Transplantation: SCD, DCD, ECD--Fundamentals for the Practicing Nephrologist]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1827?rss=1</link>
<description><![CDATA[
<p>There is significant variability in the quality of deceased-donor kidneys that are used for transplantation. The quality of the donor kidney has a direct effect on important clinical outcomes such as acute rejection, delayed graft function, and patient and allograft survival. Expanded-criteria donors (ECDs) refer to older kidney donors (&ge;60 yr) or donors who are aged 50 to 59 yr and have two of the following three features: Hypertension, terminal serum creatinine &gt;1.5 mg/dl, or death from cerebrovascular accident. By definition, ECD kidneys have a 70% greater likelihood of failure compared with one from a 35-yr-old male donor who died from a motor vehicle accident. Donation after cardiac death (DCD) is a small but rapidly growing fraction of donors. An ECD kidney transplant recipient has a projected average added-life-years of 5.1 yr compared with 10 yr for a kidney recipient from a standard-criteria donor. Kidney transplantation from DCD seems to have similar allograft and patient survival compared with kidney from donation after brain death; however DCD transplantation has a 42 to 51% risk for delayed graft function (need for at least one dialysis treatment during the first week after transplantation) compared with 24% in an standard-criteria donor kidney transplant. Familiarity with the comprehensive allocation rules governing different categories of deceased-donor kidneys by the nephrologists and dialysis team providers is essential to maximizing patient autonomy and to improve the outcomes of kidney transplantation.</p>
]]></description>
<dc:creator><![CDATA[Rao, P. S., Ojo, A.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02270409</dc:identifier>
<dc:title><![CDATA[The Alphabet Soup of Kidney Transplantation: SCD, DCD, ECD--Fundamentals for the Practicing Nephrologist]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1831</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1827</prism:startingPage>
<prism:section>Mini-Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1832?rss=1">
<title><![CDATA[Measurement and Estimation of GFR in Children and Adolescents]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1832?rss=1</link>
<description><![CDATA[
<p>GFR is the best indicator of renal function in children and adolescents and is critical for diagnosing acute and chronic kidney impairment, intervening early to prevent end-stage renal failure, prescribing nephrotoxic drugs and drugs cleared by a failing kidney, and monitoring for side effects of medications. Renal inulin clearance was the gold standard for GFR but is compromised by lack of availability, difficult assays, and problems of collecting timed urine samples, especially in children with vesicoureteral reflux or bladder dysfunction. Creatinine clearance-based estimates of GFR are often used in pediatrics. The addition of cimetidine to eliminate creatinine secretion permits accurate measurement of GFR in those who can completely empty their bladders to provide timed urine collections. Radioisotopes are used in plasma disappearance GFR determinations; however, these are not ideal for use in children, especially for repeated studies. The plasma disappearance of iohexol serves as a promising alternative GFR marker, because it is safe and not radioactive, easily measured, not metabolized or transported by the kidney, and excreted primarily by glomerular filtration. GFR estimating equations, based on serum concentrations of creatinine or cystatin C, are popular clinically and in research studies. Efforts are ongoing to improve these estimating equations for children and make the results readily available to clinicians obtaining standard chemistry profiles, as is being done for adults. However, at this time, there is no dependable substitute for an accurately determined GFR, and iohexol plasma disappearance offers the best combination of safety, accuracy, and reproducible precision.</p>
]]></description>
<dc:creator><![CDATA[Schwartz, G. J., Work, D. F.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01640309</dc:identifier>
<dc:title><![CDATA[Measurement and Estimation of GFR in Children and Adolescents]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1843</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1832</prism:startingPage>
<prism:section>Mini-Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1844?rss=1">
<title><![CDATA[Interstitial Cystitis: An Unsolved Enigma]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1844?rss=1</link>
<description><![CDATA[
<p>Painful bladder syndrome/interstitial cystitis (PBS/IC) is a chronic disease of unknown etiology characterized by vague bladder pain and nonspecific urinary symptoms, such as urgency and frequency. Although it was initially considered to be a rare condition, its prevalence has significantly increased, possibly because of different definitions used and greater physician awareness. Because of the multiple diagnostic criteria used, there is significant variation in its prevalence. In addition, there is often a delay in the diagnosis of PBS/IC. It affects predominantly women of middle age, and it significantly decreases quality of life. Diagnosis of PBS/IC is mainly a diagnosis of exclusion; there are no characteristic symptoms or pathognomonic findings. Therefore, it is important to rule out diseases that have a similar clinical picture (<I>i.e.</I>, urinary infections, bladder carcinoma) but definite therapies and worse prognosis if left untreated. PBS/IC management suffers from lack of evidence; many therapies are empiric or based on small studies and case series. Treatment includes supportive therapies (psychosocial, behavioral, physical), oral treatments, and intravesical treatments, whereas other more invasive treatments such as electric neuromodulation and reconstructive surgery are reserved for refractory cases. Physicians should always keep in mind the diagnosis of PBS/IC in patients presenting with chronic urinary symptoms after excluding other more common diseases.</p>
]]></description>
<dc:creator><![CDATA[Moutzouris, D.-A., Falagas, M. E.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02000309</dc:identifier>
<dc:title><![CDATA[Interstitial Cystitis: An Unsolved Enigma]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1857</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1844</prism:startingPage>
<prism:section>Mini-Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1858?rss=1">
<title><![CDATA[Biomarkers for Lupus Nephritis: The Quest Continues]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1858?rss=1</link>
<description><![CDATA[
<p>Current treatment of severe lupus nephritis is unsatisfactory in terms of both outcome and toxicity. To improve the efficacy and decrease the adverse effects of immunosuppression, it would be ideal to be able to predict the course and pathology of lupus nephritis and adjust therapy appropriately. This will require biomarkers that reflect disease activity. Recently, significant effort has been put into identifying biomarkers that can anticipate impending lupus renal flare, forecast development of chronic kidney disease, or reflect kidney histology at the time of flare. Although these biomarkers are potentially useful, to date none has been clinically validated in a large, prospective cohort of patients with SLE. This article reviews the current status of lupus nephritis biomarker investigation and articulates a perspective of how future efforts should be focused.</p>
]]></description>
<dc:creator><![CDATA[Rovin, B. H., Zhang, X.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03530509</dc:identifier>
<dc:title><![CDATA[Biomarkers for Lupus Nephritis: The Quest Continues]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1865</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1858</prism:startingPage>
<prism:section>Mini-Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1866?rss=1">
<title><![CDATA[The Journey From Vitamin D-Resistant Rickets to the Regulation of Renal Phosphate Transport]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1866?rss=1</link>
<description><![CDATA[
<p>In 1937, Fuller Albright first described two rare genetic disorders: Vitamin D resistant rickets and polyostotic fibrous dysplasia, now respectively known as X-linked hypophosphatemic rickets (XLH) and the McCune-Albright syndrome. Albright carefully characterized and meticulously analyzed one patient, W.M., with vitamin D&ndash;resistant rickets. Albright subsequently reported additional carefully performed balance studies on W.M. In this review, which evaluates the journey from the initial description of vitamin D&ndash;resistant rickets (XLH) to the regulation of renal phosphate transport, we (<I>1</I>) trace the timeline of important discoveries in unraveling the pathophysiology of XLH, (<I>2</I>) cite the recognized abnormalities in mineral metabolism in XLH, (<I>3</I>) evaluate factors that may affect parathyroid hormone values in XLH, (<I>4</I>) assess the potential interactions between the phosphate-regulating gene with homology to endopeptidase on the X chromosome and fibroblast growth factor 23 (FGF23) and their resultant effects on renal phosphate transport and vitamin D metabolism, (<I>5</I>) analyze the complex interplay between FGF23 and the factors that regulate FGF23, and (<I>6</I>) discuss the genetic and acquired disorders of hypophosphatemia and hyperphosphatemia in which FGF23 plays a role. Although Albright could not measure parathyroid hormone, he concluded on the basis of his studies that showed calcemic resistance to parathyroid extract in W.M. that hyperparathyroidism was present. Using a conceptual approach, we suggest that a defect in the skeletal response to parathyroid hormone contributes to hyperparathyroidism in XLH. Finally, at the end of the review, abnormalities in renal phosphate transport that are sometimes found in patients with polyostotic fibrous dysplasia are discussed.</p>
]]></description>
<dc:creator><![CDATA[Levine, B. S., Kleeman, C. R., Felsenfeld, A. J.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03000509</dc:identifier>
<dc:title><![CDATA[The Journey From Vitamin D-Resistant Rickets to the Regulation of Renal Phosphate Transport]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1877</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1866</prism:startingPage>
<prism:section>In-Depth Review</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/11/1878?rss=1">
<title><![CDATA[Can Dietary Sodium Intake Be Modified by Public Policy?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/11/1878?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[McCarron, D. A., Geerling, J. C., Kazaks, A. G., Stern, J. S.]]></dc:creator>
<dc:date>Tue, 03 Nov 2009 10:02:23 PST</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04660709</dc:identifier>
<dc:title><![CDATA[Can Dietary Sodium Intake Be Modified by Public Policy?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>11</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1882</prism:endingPage>
<prism:publicationDate>2009-11-01</prism:publicationDate>
<prism:startingPage>1878</prism:startingPage>
<prism:section>Special Feature</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1541?rss=1">
<title><![CDATA[Fuller Albright: The Consummate Clinical Investigator]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1541?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kleeman, C. R., Levine, B. S., Felsenfeld, A. J.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:27 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03030509</dc:identifier>
<dc:title><![CDATA[Fuller Albright: The Consummate Clinical Investigator]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1546</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1541</prism:startingPage>
<prism:section>Nephrology Hall of Fame</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1547?rss=1">
<title><![CDATA[Long-Term Outcome of Children with Steroid-Sensitive Idiopathic Nephrotic Syndrome]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1547?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Niaudet, P.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:27 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05950809</dc:identifier>
<dc:title><![CDATA[Long-Term Outcome of Children with Steroid-Sensitive Idiopathic Nephrotic Syndrome]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1548</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1547</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1549?rss=1">
<title><![CDATA[The Need for a Children's Oncology Group-Oriented Approach to Advance the Care of Children with Idiopathic Nephrotic Syndrome]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1549?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mahan, J. D., Smoyer, W. E.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06060809</dc:identifier>
<dc:title><![CDATA[The Need for a Children's Oncology Group-Oriented Approach to Advance the Care of Children with Idiopathic Nephrotic Syndrome]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1550</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1549</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1551?rss=1">
<title><![CDATA[Serum Indoxyl Sulfate Is Associated with Vascular Disease and Mortality in Chronic Kidney Disease Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1551?rss=1</link>
<description><![CDATA[
<p>Background and objectives: As a major component of uremic syndrome, cardiovascular disease is largely responsible for the high mortality observed in chronic kidney disease (CKD). Preclinical studies have evidenced an association between serum levels of indoxyl sulfate (IS, a protein-bound uremic toxin) and vascular alterations. The aim of this study is to investigate the association between serum IS, vascular calcification, vascular stiffness, and mortality in a cohort of CKD patients.</p>
<p>Design, setting, participants, &amp; measurements: One-hundred and thirty-nine patients (mean &plusmn; SD age: 67 &plusmn; 12; 60% male) at different stages of CKD (8% at stage 2, 26.5% at stage 3, 26.5% at stage 4, 7% at stage 5, and 32% at stage 5D) were enrolled.</p>
<p>Results: Baseline IS levels presented an inverse relationship with renal function and a direct relationship with aortic calcification and pulse wave velocity. During the follow-up period (605 &plusmn; 217 d), 25 patients died, mostly because of cardiovascular events (<I>n</I> = 18). In crude survival analyses, the highest IS tertile was a powerful predictor of overall and cardiovascular mortality (<I>P</I> = 0.001 and 0.012, respectively). The predictive power of IS for death was maintained after adjustment for age, gender, diabetes, albumin, hemoglobin, phosphate, and aortic calcification.</p>
<p>Conclusions: The study presented here indicates that IS may have a significant role in the vascular disease and higher mortality observed in CKD patients.</p>
]]></description>
<dc:creator><![CDATA[Barreto, F. C., Barreto, D. V., Liabeuf, S., Meert, N., Glorieux, G., Temmar, M., Choukroun, G., Vanholder, R., Massy, Z. A., on behalf of the European Uremic Toxin Work Group (EUTox)]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03980609</dc:identifier>
<dc:title><![CDATA[Serum Indoxyl Sulfate Is Associated with Vascular Disease and Mortality in Chronic Kidney Disease Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1558</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1551</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1559?rss=1">
<title><![CDATA[Rapid Curbing of a Vancomycin-Resistant Enterococcus faecium Outbreak in a Nephrology Department]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1559?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Vancomycin-resistant enterococci (VRE) are recovered with increasing frequency among patients with chronic renal failure, making VRE a major concern in nephrology departments, especially for patients who are treated by hemodialysis. We report herein the successful aggressive management of a VRE outbreak in a nephrology department.</p>
<p>Design, setting, participants, &amp; measurements: An <I>Enterococcus faecium</I> vanB strain was isolated from a peritoneal dialysis solution from an inpatient. Immediately, infection control measures were enforced and active screening was performed for all contact patients. Carriers were isolated, and patients were divided into three cohorts: Positive, contact, and noncontact patients. We then performed a case-control study to understand risk factors for VRE carriage comparing VRE carriers with contact patients who were negative for VRE.</p>
<p>Results: A total of 14 VRE-positive and 125 VRE-negative contact patients were identified. VRE-positive patients were more likely to receive hemodialysis and have longer hospital stays in nephrology. VRE-positive patients more often had a central venous catheter for a longer period of time and received more antibiotics than VRE-negative patients. Treatment with large-spectrum &beta;-lactams and number of days in the nephrology ward were significantly associated with a higher risk for VRE carriage by using multivariate analysis.</p>
<p>Conclusions: These findings suggest that case mix, longer hospital stays, and antibiotic use are major risk factors for VRE acquisition. In addition, it demonstrates that strict enforcement of isolation precautions and cohorting associated with active screening are successful to curb the transmission of VRE in renal units despite continuous colonization pressure.</p>
]]></description>
<dc:creator><![CDATA[Servais, A., Mercadal, L., Brossier, F., Venditto, M., Issad, B., Isnard-Bagnis, C., Deray, G., Robert, J.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03310509</dc:identifier>
<dc:title><![CDATA[Rapid Curbing of a Vancomycin-Resistant Enterococcus faecium Outbreak in a Nephrology Department]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1564</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1559</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1565?rss=1">
<title><![CDATA[Weight Loss Interventions in Chronic Kidney Disease: A Systematic Review and Meta-analysis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1565?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Obesity is an independent risk factor for development and progression of chronic kidney disease (CKD). We conducted a systematic review to assess the benefits of intentional weight loss in patients with non&ndash;dialysis-dependent CKD and glomerular hyperfiltration.</p>
<p>Design, setting, participants, &amp; measurements: We searched MEDLINE, SCOPUS, and conference proceedings for randomized, controlled trials and observational studies that examined various surgical and nonsurgical interventions (diet, exercise, and/or antiobesity agents) in adult patients with CKD. Results were summarized using random-effects model.</p>
<p>Results: Thirteen studies were included. In patients with CKD, body mass index (BMI) decreased significantly (weighted mean difference [WMD] &ndash;3.67 kg/m<sup>2</sup>; 95% confidence interval [CI] &ndash;6.56 to &ndash;0.78) at the end of the study period with nonsurgical interventions. This was associated with a significant decrease in proteinuria (WMD &ndash;1.31 g/24 h; 95% CI &ndash;2.11 to &ndash;0.51) and systolic BP with no further decrease in GFR during a mean follow-up of 7.4 mo. In morbidly obese individuals (BMI &gt;40 kg/m<sup>2</sup>) with glomerular hyperfiltration (GFR &gt;125 ml/min), surgical interventions decreased BMI, which resulted in a decrease in GFR (WMD &ndash;25.56 ml/min; 95% CI &ndash;36.23 to &ndash;14.89), albuminuria, and systolic BP.</p>
<p>Conclusions: In smaller, short-duration studies in patients with CKD, nonsurgical weight loss interventions reduce proteinuria and BP and seem to prevent further decline in renal function. In morbidly obese individuals with glomerular hyperfiltration, surgical interventions normalize GFR and reduce BP and microalbuminuria. Larger, long-term studies to analyze renal outcomes such as development of ESRD are needed.</p>
]]></description>
<dc:creator><![CDATA[Navaneethan, S. D., Yehnert, H., Moustarah, F., Schreiber, M. J., Schauer, P. R., Beddhu, S.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02250409</dc:identifier>
<dc:title><![CDATA[Weight Loss Interventions in Chronic Kidney Disease: A Systematic Review and Meta-analysis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1574</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1565</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1575?rss=1">
<title><![CDATA[Scaling of Measured Glomerular Filtration Rate in Kidney Donor Candidates by Anthropometric Estimates of Body Surface Area, Body Water, Metabolic Rate, or Liver Size]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1575?rss=1</link>
<description><![CDATA[
<p>Background and objectives: GFR is scaled to body surface area (S), whereas hemodialysis dosage is scaled to total body water (V). Scaling to metabolic rate (M) or liver size (L) has also been proposed.</p>
<p>Design, setting, participants, &amp; measurements: In 1551 potential kidney donors (662 men and 889 women) for whom GFR had been estimated from <sup>125</sup>I-iothalamate clearance (iGFR) between the years 1973 and 2005, iGFR scaling was examined. Scaling was to estimates of S, V, M, or L. The study looked at the variation of iGFR by gender, age, S, V, M, and L within the study population.</p>
<p>Results: In multiple regression analysis, neither gender nor race was significantly associated with iGFR after controlling for height, weight, and age. Raw iGFR averaged 122 &plusmn; 23 ml/min in men and 106 &plusmn; 21 ml/min in women (<I>P</I> &lt; 0.001). In an adjusted analysis, iGFR scaled to S or L was similar for men and women (NS), whereas iGFR scaled to either V or M was substantially different between the genders (<I>P</I> &lt; 0.001). When the patients by gender were divided into five quintiles of V or S, the iGFR-V ratio varied more with body size than iGFR scaled to the other measures.</p>
<p>Conclusions: iGFR scaled to S or L was similar in men and women. Scaling to either M or V resulted in a sizeable gender difference, whereas scaling to V led to markedly different values of iGFR across body size.</p>
]]></description>
<dc:creator><![CDATA[Daugirdas, J. T., Meyer, K., Greene, T., Butler, R. S., Poggio, E. D.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05581008</dc:identifier>
<dc:title><![CDATA[Scaling of Measured Glomerular Filtration Rate in Kidney Donor Candidates by Anthropometric Estimates of Body Surface Area, Body Water, Metabolic Rate, or Liver Size]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1583</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1575</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1584?rss=1">
<title><![CDATA[Sodium Bicarbonate for the Prevention of Contrast Induced-Acute Kidney Injury: A Systematic Review and Meta-analysis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1584?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Infusion of sodium bicarbonate has been suggested as a preventative strategy but reports are conflicting on its efficacy. The aim of this study was to assess the effectiveness of hydration with sodium bicarbonate for the prevention of contrast-induced acute kidney injury (CI-AKI).</p>
<p>Design, setting, participants, &amp; measurements: Medline, EMBASE, Cochrane library, and the Internet were searched for randomized controlled trials comparing hydration between sodium bicarbonate and chloride for the prevention of CI-AKI between 1966 and November 2008. Fourteen trials that included 2290 patients were identified. There was significant heterogeneity between studies (<I>P</I> heterogeneity = 0.02; <I>I</I><sup>2</sup> = 47.8%), which was largely accounted for by trial size (<I>P</I> = 0.016). Trials were therefore classified by size.</p>
<p>Results: Three trials were categorized as large (<I>n</I> = 1145) and 12 as small (<I>n</I> = 1145). Among the large trials, the incidence of CI-AKI for sodium bicarbonate and sodium chloride was 10.7 and 12.5%, respectively; the relative risk (RR) [95% confidence interval (CI)] was 0.85 (0.63 to 1.16) without evidence of heterogeneity (<I>P</I> = 0.89, <I>I</I><sup>2</sup> = 0%). The pooled RR (95% CI) among the 12 small trials was 0.50 (0.27 to 0.93) with significant between-trial heterogeneity (<I>P</I> = 0.01; <I>I</I><sup>2</sup> = 56%). The small trials were more likely to be of lower methodological quality.</p>
<p>Conclusions: A significant clinical and statistical heterogeneity was observed that was largely explained by trial size and published status. Among the large randomized trials there was no evidence of benefit for hydration with sodium bicarbonate compared with sodium chloride for the prevention of CI-AKI. The benefit of sodium bicarbonate was limited to small trials of lower methodological quality.</p>
]]></description>
<dc:creator><![CDATA[Brar, S. S., Hiremath, S., Dangas, G., Mehran, R., Brar, S. K., Leon, M. B.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03120509</dc:identifier>
<dc:title><![CDATA[Sodium Bicarbonate for the Prevention of Contrast Induced-Acute Kidney Injury: A Systematic Review and Meta-analysis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1592</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1584</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1593?rss=1">
<title><![CDATA[Long-Term Outcome of Biopsy-Proven, Frequently Relapsing Minimal-Change Nephrotic Syndrome in Children]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1593?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Frequently relapsing and steroid-dependent minimal-change nephrotic syndrome (MCNS) that originates in childhood can persist after puberty in &gt;20% of patients. These patients require immunosuppressive treatment during several decades of their life. We examined long-term adverse effects of persistent nephrotic syndrome and immunosuppressive medications, focusing on renal function, growth, obesity, osteoporosis, hypertension, ocular complications, and fertility in adult patients with biopsy-proven childhood-onset MCNS. Molecular analysis was performed to evaluate a possible association of a complicated course of MCNS with podocyte gene mutations.</p>
<p>Design, setting, participants, &amp; measurements: We performed a prospective clinical examination of 15 adult patients that included serum and urine analysis; dual-energy x-ray absorptiometry; ophthalmologic examination; semen examination; and molecular analysis of <I>NPHS1</I>, <I>NPHS2</I>, <I>CD2AP</I>, and <I>ACTN4</I> genes.</p>
<p>Results: All patients had normal GFR. Most frequent long-term complications were hypertension (in seven of 15 patients) and osteoporosis in one third of patients. Oligozoospermia was found in one patient, reduced sperm motility in four of eight patients, and teratozoospermia in six of eight patients. Ophthalmologic examination revealed myopia in 10 of 15 patients and cataract in three of 15 patients.</p>
<p>Conclusions: Children with MCNS that persists after puberty are at risk for complications such as osteoporosis, hypertension, cataract, and sperm abnormalities. Our study underscores a need for more effective and less toxic therapies for relapsing MCNS.</p>
]]></description>
<dc:creator><![CDATA[Kyrieleis, H. A.C., Lowik, M. M., Pronk, I., Cruysberg, H. R.M., Kremer, J. A.M., Oyen, W. J.G., van den Heuvel, B. L.P., Wetzels, J. F.M., Levtchenko, E. N.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05691108</dc:identifier>
<dc:title><![CDATA[Long-Term Outcome of Biopsy-Proven, Frequently Relapsing Minimal-Change Nephrotic Syndrome in Children]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1600</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1593</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1601?rss=1">
<title><![CDATA[Bacteremia Associated with Tunneled Hemodialysis Catheters: Outcome after Attempted Salvage]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1601?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Treatment without catheter replacement (catheter salvage) has been described for bacteremia associated with tunneled venous catheters in hemodialysis patients, but few data are available on which to base an estimation of the likelihood of treatment success.</p>
<p>Design, setting, participants, &amp; measurements: In a prospective cohort study, all cases of catheter-associated bacteremia that occurred in a large dialysis center were identified during a 12-mo period. Catheter salvage was attempted according to a standard protocol in all cases in which a favorable early response to antibiotic therapy was seen, and patients were followed for at least 6 mo. Bacteremias, catheter changes, and all major clinical events were recorded.</p>
<p>Results: During a period covering 252,986 catheter days, 208 episodes were identified involving 133 patients, 74% of which were selected for attempted salvage. Salvage was successful in 66.1% of incident bacteremias with a very low complication risk (0.9%). Some bacteremias, however, recurred as late as 6 mo after the initial infection; salvage was less likely to be successful in treating recurrences.</p>
<p>Conclusions: Appropriately used catheter salvage can be successful in approximately two thirds of cases; however, recurrences continue to occur up to 6 mo later and are unlikely to be cured without catheter replacement.</p>
]]></description>
<dc:creator><![CDATA[Ashby, D. R., Power, A., Singh, S., Choi, P., Taube, D. H., Duncan, N. D., Cairns, T. D.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01840309</dc:identifier>
<dc:title><![CDATA[Bacteremia Associated with Tunneled Hemodialysis Catheters: Outcome after Attempted Salvage]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1605</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1601</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1606?rss=1">
<title><![CDATA[Cystatin C Levels in Functionally Anephric Patients Undergoing Dialysis: The Effect of Different Methods and Intensities]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1606?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Cystatin C, a low molecular weight protein, is produced by nucleated cells, filtered by glomeruli, and degraded by tubules at a constant rate. Its serum concentration has been proposed as a marker of GFR. Its size should make it dialyzable. It is hypothesized that serum cystatin C levels are influenced by the method and intensity of dialysis received.</p>
<p>Design: This is a cross-sectional pilot study of cystatin C in functionally anephric dialysis patients. It was measured predialysis in 14 patients on conventional (3 to 5 h, 3 <FONT FACE="arial,helvetica">x</FONT> wk) hemodialysis; eight on nocturnal hemodialysis (three to seven nights, 6 to 8 h); three on daily hemodialysis (6 d, 11/2 to 21/2 h); and 10 on automated peritoneal dialysis. All had urea kinetic studies and values for single pool Kt/V (Sp Kt/V), standard weekly Kt/V (Std Kt/V), and protein equivalent of nitrogen appearance (nPNA; g/kg/d). C reactive protein (CRP; mg/L) and thyroid stimulating hormone (TSH; mIU/L) were measured as factors known to influence cystatin C.</p>
<p>Results: There was no correlation between cystatin C and Sp Kt/V, but there was a significant inverse linear correlation with Std Kt/V and there were significant differences between treatment modalities in cystatin C levels and in Std Kt/V. The estimation of cystatin C was reliable and stable over 3 to 6 wk and its levels uninfluenced by nPNA, CRP, or TSH.</p>
<p>Conclusion: Serum cystatin C levels are influenced by the method and intensity of dialysis and may have a role in treatment adequacy monitoring.</p>
]]></description>
<dc:creator><![CDATA[Al-Malki, N., Heidenheim, P. A., Filler, G., Yasin, A., Lindsay, R. M.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02910509</dc:identifier>
<dc:title><![CDATA[Cystatin C Levels in Functionally Anephric Patients Undergoing Dialysis: The Effect of Different Methods and Intensities]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1610</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1606</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1611?rss=1">
<title><![CDATA[Is Maximum Conservative Management an Equivalent Treatment Option to Dialysis for Elderly Patients with Significant Comorbid Disease?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1611?rss=1</link>
<description><![CDATA[
<p>Background and objectives: There is ongoing growth of elderly populations with ESRD in Western Europe and North America. In our center, we offer an alternative care pathway of &lsquo;maximum conservative management&rsquo; (MCM) to patients who elect not to start dialysis, often because of a heavy burden of comorbid illness and advanced age. The objective of our study was to compare clinical outcomes for patients who had ESRD and chose either MCM or renal replacement therapy (RRT).</p>
<p>Design, setting, participants, &amp; measurements: This is an observational study of a single-center cohort in the United Kingdom that evaluating 202 elderly (&ge;70 yr) patients who had ESRD and had chosen either MCM (<I>n</I> = 29) or RRT (<I>n</I> = 173). We report survival, hospitalization rates, and location of death for this cohort. Survival was measured from a standardized &lsquo;threshold&rsquo; estimated GFR of 10.8 ml/min per 1.73 m<sup>2</sup>.</p>
<p>Results: Median survival, including the first 90 d, was 37.8 mo (range 0 to 106 mo) for RRT patients and 13.9 mo (range 2 to 44) for MCM patients (<I>P</I> &lt; 0.01). RRT patients had higher rates of hospitalization (0.069 [95% confidence interval (CI) 0.068 to 0.070]) <I>versus</I> 0.043 [95% CI 0.040 to 0.047] hospital days/patient-days survived) compared with MCM patients. MCM patients were significantly more likely to die at home or in a hospice (odds ratio 4.15; 95% CI 1.67 to 10.25). A survey of the literature describing elderly ESRD outcomes is also presented.</p>
<p>Conclusions: Dialysis prolongs survival for elderly patients who have ESRD with significant comorbidity by approximately 2 yr; however, patients who choose MCM can survive a substantial length of time, achieving similar numbers of hospital-free days to patients who choose hemodialysis.</p>
]]></description>
<dc:creator><![CDATA[Carson, R. C., Juszczak, M., Davenport, A., Burns, A.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00510109</dc:identifier>
<dc:title><![CDATA[Is Maximum Conservative Management an Equivalent Treatment Option to Dialysis for Elderly Patients with Significant Comorbid Disease?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1619</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1611</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1620?rss=1">
<title><![CDATA[Association of Dialysis Modality and Cardiovascular Mortality in Incident Dialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1620?rss=1</link>
<description><![CDATA[
<p>Background and objectives: The aim of the investigation presented here was to compare the rates, causes, and timing of cardiovascular (CV) death in incident peritoneal dialysis (PD) and hemodialysis (HD) patients.</p>
<p>Design, setting, participants, &amp; measurements: The study included all adult Australian and New Zealand patients commencing dialysis between January 1, 1997 and December 31, 2007. Rates of and times to CV death were compared by incident rate ratios, cumulative incidence, and multivariable Cox proportional hazards model analyses. Dialysis modality was included in the model as a time-varying covariate, and a competing risks approach was used to obtain cause-specific hazard ratios.</p>
<p>Results: Of the 24,587 patients who commenced dialysis (first treatment PD <I>n</I> = 6521; HD <I>n</I> = 18,066) during the study, 5669 (21%) died from CV causes [PD 2044 (28%) <I>versus</I> HD 3625 (21%)]. The incidence rates of CV mortality in PD and HD patients were 9.99 and 7.96 per 100 patient-years, respectively (incidence rate ratio PD <I>versus</I> HD, 1.25; 95% confidence interval 1.12 to 1.32). PD was consistently associated with an increased hazard of CV death compared with HD after 1 yr of treatment. This increased risk in PD patients was largely accounted for by an increased risk of death due to myocardial infarction.</p>
<p>Conclusions: Dialysis modality is significantly associated with the risk, causes, and timing of CV death experienced by ESRD patients in Australia and New Zealand.</p>
]]></description>
<dc:creator><![CDATA[Johnson, D. W., Dent, H., Hawley, C. M., McDonald, S. P., Rosman, J. B., Brown, F. G., Bannister, K., Wiggins, K. J.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01750309</dc:identifier>
<dc:title><![CDATA[Association of Dialysis Modality and Cardiovascular Mortality in Incident Dialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1628</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1620</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1629?rss=1">
<title><![CDATA[Is Valvular Calcification a Part of the Missing Link between Residual Kidney Function and Cardiac Hypertrophy in Peritoneal Dialysis Patients?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1629?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Residual renal function (RRF) predicts survival and shows an important inverse relation with cardiac hypertrophy in peritoneal dialysis (PD) patients. We hypothesized that valvular calcification and the calcification milieu may be part of the process linking loss of RRF and cardiac hypertrophy.</p>
<p>Design, setting, participants, &amp; measurements: A cross-sectional study was conducted by performing two-dimensional echocardiography on 230 PD patients to assess valvular calcification and left ventricular (LV) mass and collecting 24-h urine for estimation of RRF.</p>
<p>Results: Patients having valvular calcification had lower RRF than those without. Patients with no RRF showed higher calcium-phosphorus product (Ca <FONT FACE="arial,helvetica">x</FONT> P) and C-reactive protein (CRP). Using multiple logistic regression analysis, every 1-ml/min per 1.73 m<sup>2</sup> increase in residual GFR was associated with a 28% reduction in the risk for valvular calcification. The association was lost after additional adjustment for Ca <FONT FACE="arial,helvetica">x</FONT> P and CRP. Using multiple linear regression analysis, loss of RRF showed significant association with increased LV mass index, but this association was lost after additional adjustment for CRP, Ca <FONT FACE="arial,helvetica">x</FONT> P, and valvular calcification. Patients with all three calcification risk factors, namely inflammation, high Ca<FONT FACE="arial,helvetica">x</FONT>P, and no RRF, showed the highest prevalence of valvular calcification and had the most severe cardiac hypertrophy.</p>
<p>Conclusions: The association among loss of RRF, valvular calcification, and cardiac hypertrophy was closely linked to increased inflammation and high Ca <FONT FACE="arial,helvetica">x</FONT> P in PD patients. These data suggest that valvular calcification and the calcification milieu are part of the processes linking loss of RRF and worsening cardiac hypertrophy in PD.</p>
]]></description>
<dc:creator><![CDATA[Wang, A. Y.-M., Lam, C. W.-K., Wang, M., Chan, I. H.-S., Lui, S.-F., Sanderson, J. E.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03100509</dc:identifier>
<dc:title><![CDATA[Is Valvular Calcification a Part of the Missing Link between Residual Kidney Function and Cardiac Hypertrophy in Peritoneal Dialysis Patients?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1636</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1629</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1637?rss=1">
<title><![CDATA[Peripheral Vascular Disease-Related Procedures in Dialysis Patients: Predictors and Prognosis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1637?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Peripheral vascular disease (PVD) is prevalent among dialysis patients, and many dialysis patients undergo PVD-related procedures. We aimed to examine the risk factors for and prognosis after such procedures in the dialysis setting.</p>
<p>Design, setting, participants, &amp; measurements: In a national prospective cohort study of 1041 incident dialysis patients, we examined the factors that are associated with PVD procedures (lower extremity amputations and bypasses) after the start of dialysis. Adjusted risk for PVD procedures of various factors was estimated using multivariable Cox proportional hazards models. Incidence rates of subsequent cardiovascular events, infectious hospitalizations, PVD- and cardiovascular disease&ndash;related mortality, and all-cause mortality were compared for those with and without a PVD procedure.</p>
<p>Results: Overall, 217 (21%) patients underwent a PVD procedure after the start of dialysis. For those without diabetes, only PVD history (relative hazard [RH] 2.9; 95% confidence interval [CI] 1.3 to 6.6) and increased fibrinogen (RH 1.2; 95% CI 1.0 to 1.5) predicted PVD procedures. For those with diabetes, increased serum phosphate (RH 1.2; 95% CI 1.1 to 1.4), along with decreased albumin, increased C-reactive protein and fibrinogen, and lower SBP, was associated with risk for PVD procedures. Of those who had a procedure compared with those who did not, 68 <I>versus</I> 30% experienced a subsequent cardiovascular event, 85 <I>versus</I> 66% an infectious hospitalization, 11 <I>versus</I> 2% a PVD-related death, and 81 <I>versus</I> 59% all-cause death (mean follow-up 3.0 yr).</p>
<p>Conclusions: Prognosis after PVD procedures is poor, and providers should be aware that risk factors for PVD procedures may differ by diabetes status.</p>
]]></description>
<dc:creator><![CDATA[Plantinga, L. C., Fink, N. E., Coresh, J., Sozio, S. M., Parekh, R. S., Melamed, M. L., Powe, N. R., Jaar, B. G.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02220409</dc:identifier>
<dc:title><![CDATA[Peripheral Vascular Disease-Related Procedures in Dialysis Patients: Predictors and Prognosis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1645</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1637</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1646?rss=1">
<title><![CDATA[Mineral Metabolism and Inflammation in Chronic Kidney Disease Patients: A Cross-Sectional Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1646?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Mineral metabolism abnormalities and inflammation are concerns in chronic kidney disease (CKD). Interrelationships among these parameters have not been analyzed.</p>
<p>Design, setting, participants, &amp; measurements: The study included 133 patients with CKD not on dialysis and not receiving calcium (Ca) supplements, phosphate binders, or vitamin D. Estimated GFR (eGFR) was 34.1 &plusmn; 6.8 ml/min/1.73 m<sup>2</sup>; 107 participants had stage 3 CKD, and 26 had stage 4.</p>
<p>Results: Patients were classified by tertiles of Ca, phosphorus (P), Ca-P product (Ca x P), and parathyroid hormone (PTH). After adjustment for age, gender, and eGFR, the levels of C-reactive protein (CRP) and IL-6 (IL-6) of the third tertile of P, Ca x P, and PTH were significantly higher than those of the first and second tertiles. Serum P and Ca x P directly correlated with CRP and IL-6, whereas HDL-cholesterol and eGFR inversely correlated with the levels of the inflammatory parameters. After partial correlation analysis, the previous associations between CRP and eGFR, and serum P, as well as the relationship between IL-6 and eGFR, and serum P, remained significant. Multiple regression analysis demonstrated that eGFR and serum P were independently associated with CRP and IL-6. Finally, logistic regression analysis using the presence/absence of an inflammatory state as the dependent variable showed that eGFR was a protective factor, whereas serum P was an independent risk factor for the presence of an inflammatory state.</p>
<p>Conclusions: Elevated serum P might play a role in the development of inflammation in CKD.</p>
]]></description>
<dc:creator><![CDATA[Navarro-Gonzalez, J. F., Mora-Fernandez, C., Muros, M., Herrera, H., Garcia, J.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02420409</dc:identifier>
<dc:title><![CDATA[Mineral Metabolism and Inflammation in Chronic Kidney Disease Patients: A Cross-Sectional Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1654</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1646</prism:startingPage>
<prism:section>Mineral Metabolism and Bone Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1655?rss=1">
<title><![CDATA[Uric Acid Levels Have No Significant Effect on Renal Function in Adult Renal Transplant Recipients: Evidence from the Symphony Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1655?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Uric acid (UA) has been linked to renal damage in experimental models of kidney failure. In humans, no definitive link between UA and renal function has been established, but several epidemiologic studies have suggested that higher UA levels are associated with accelerated loss of renal function, higher incidence of dialysis, and death. Many of the associations have been limited by the colinearity between UA levels and renal function. Renal transplantation is no exception, and limited information is available concerning the independent role of UA on progression of renal function in transplant recipients.</p>
<p>Design, setting, participants, &amp; measurements: We investigated the association between UA and renal function progression during the first 3 yr after transplantation, adjusted for baseline renal function, in 1645 patients who were enrolled in the Symphony study.</p>
<p>Results: When corrected for baseline renal function, UA levels 1 mo after transplantation were not associated with 3-yr renal function (<I>P</I> = 0.62). There was a strong colinearity between calculated renal function and UA levels 1 mo after transplantation. In fact, when not corrected for baseline renal function, there was a significant association between UA and renal function at 3 yr (<I>P</I> = 0.005).</p>
<p>Conclusions: Low renal function is associated with higher UA levels, but higher UA levels are not independently associated with progression of renal dysfunction after kidney transplantation.</p>
]]></description>
<dc:creator><![CDATA[Meier-Kriesche, H.-U., Schold, J. D., Vanrenterghem, Y., Halloran, P. F., Ekberg, H.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02700409</dc:identifier>
<dc:title><![CDATA[Uric Acid Levels Have No Significant Effect on Renal Function in Adult Renal Transplant Recipients: Evidence from the Symphony Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1660</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1655</prism:startingPage>
<prism:section>Renal Transplantation</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1661?rss=1">
<title><![CDATA[Immunosuppressive Drugs and Tregs: A Critical Evaluation!]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1661?rss=1</link>
<description><![CDATA[
<p>To define therapeutic strategies that promote tolerance, it is of critical importance to determine the effects of immunosuppressive drugs on regulatory T cells (Tregs). This review discusses the current knowledge about the physiology of Tregs in humans, the role or Tregs in transplantation, and the impact of the different types of immunosuppressive agents on the frequency and functionality of Tregs in <I>in vitro</I> and <I>in vivo</I> systems.</p>
]]></description>
<dc:creator><![CDATA[De Serres, S. A., Sayegh, M. H., Najafian, N.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03180509</dc:identifier>
<dc:title><![CDATA[Immunosuppressive Drugs and Tregs: A Critical Evaluation!]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1669</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1661</prism:startingPage>
<prism:section>Mini-Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1670?rss=1">
<title><![CDATA[Can We Personalize Treatment for Kidney Diseases?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1670?rss=1</link>
<description><![CDATA[
<p>The idea of individualizing therapies to obtain optimal clinical results is not new but has only recently been applied to kidney diseases. Nonetheless, kidney disorders present a variety of opportunities to personalize medicine. Here, the heterogeneity of kidney disorders is reviewed to provide a rationale for pursuing personalized medicine. Data on adjusting therapy on the basis of pharmacogenetics/genomics and pharmacodynamics are summarized to demonstrate where the field is, and biomarker studies that reflect the future of personalized medicine are discussed. The goal of this review is to demonstrate that we can personalize therapy for kidney diseases but that considerable investment in new research will be required for personalized medicine to be routinely used in nephrology clinics.</p>
]]></description>
<dc:creator><![CDATA[Rovin, B. H., McKinley, A. M., Birmingham, D. J.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:28 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04140609</dc:identifier>
<dc:title><![CDATA[Can We Personalize Treatment for Kidney Diseases?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1676</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1670</prism:startingPage>
<prism:section>Mini-Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1677?rss=1">
<title><![CDATA[The Science of Stewardship: Due Diligence for Kidney Donors and Kidney Function in Living Kidney Donation--Evaluation, Determinants, and Implications for Outcomes]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1677?rss=1</link>
<description><![CDATA[
<p>Living kidney donor transplantation is now a common treatment for ESRD because it provides excellent outcomes to transplant recipients and is considered a safe procedure for prospective donors. The short- and long-term safety of prospective donors is paramount to the continued success of this procedure. Whereas the initial experiences with living kidney donors mostly included the healthiest, the increase in the need for organs and the changing demographic characteristics of the general population have subtly reshaped the suitability for donation. Kidney function assessment is a critical component of the evaluation of prospective donors; therefore, special emphasis is usually placed on this aspect of the evaluation. At the same time, consideration of kidney function after donation is important because it assists with the determination of renal health in donors. This review summarizes the process of predonation kidney function assessment, determinants of pre- and postdonation renal function, and, importantly, the potential implications of kidney function to the long-term outcomes of kidney donors.</p>
]]></description>
<dc:creator><![CDATA[Poggio, E. D., Braun, W. E., Davis, C.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:29 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02740409</dc:identifier>
<dc:title><![CDATA[The Science of Stewardship: Due Diligence for Kidney Donors and Kidney Function in Living Kidney Donation--Evaluation, Determinants, and Implications for Outcomes]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1684</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1677</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/10/1685?rss=1">
<title><![CDATA[Mineralocorticoid Receptor Blockers and Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/10/1685?rss=1</link>
<description><![CDATA[
<p>The increasing prevalence of chronic kidney disease (CKD) and the public health initiatives for detection and slowing its progression have placed special emphasis on controlling proteinuria and the renin-angiotensin-aldosterone system (RAAS). In addition to the traditional blockers of angiotensin-converting enzyme and angiotensin receptors, mineralocorticoid receptor blockers (MRBs) have come into focus as anti-proteinuric agents with moderate anti-hypertensive effects. The beneficial effects of MRBs on mortality in patients with cardiac disease have been well described. We review the role of aldosterone in end-organ damage, the rationales for using MRBs as adjuncts to angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) in treating CKD, and the adverse effects that may occur when these agents are used in combination. Suggestions are included for avoiding serious adverse events in CKD patients treated with MRBs. There is a clearly defined need for prospective outcome studies focused on cardiovascular mortality as well as progression of CKD in patients treated with MRBS and other inhibitors of the RAAS.</p>
]]></description>
<dc:creator><![CDATA[Jain, G., Campbell, R. C., Warnock, D. G.]]></dc:creator>
<dc:date>Mon, 05 Oct 2009 10:02:29 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01340209</dc:identifier>
<dc:title><![CDATA[Mineralocorticoid Receptor Blockers and Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>10</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1691</prism:endingPage>
<prism:publicationDate>2009-10-01</prism:publicationDate>
<prism:startingPage>1685</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1401?rss=1">
<title><![CDATA[Will Nephrologists Use a Wearable Artificial Kidney?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1401?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Friedman, E. A.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:30 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04600709</dc:identifier>
<dc:title><![CDATA[Will Nephrologists Use a Wearable Artificial Kidney?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1402</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1401</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1403?rss=1">
<title><![CDATA[Dialysate ... Ho-Hum!]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1403?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Golper, T. A., Ward, R. A.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:30 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04940709</dc:identifier>
<dc:title><![CDATA[Dialysate ... Ho-Hum!]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1404</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1403</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1405?rss=1">
<title><![CDATA[Cinacalcet Hydrochloride in Chronic Kidney Disease-Mineral Bone Disorder]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1405?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Yokoyama, K.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:30 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05030709</dc:identifier>
<dc:title><![CDATA[Cinacalcet Hydrochloride in Chronic Kidney Disease-Mineral Bone Disorder]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1408</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1405</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1409?rss=1">
<title><![CDATA[Risk Factors for Cyclosporin A Nephrotoxicity in Children with Steroid-Dependant Nephrotic Syndrome]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1409?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Cyclosporin A (CsA) is a well-established treatment for steroid-dependent nephrotic syndrome (SDNS) that may, however, cause chronic ischemic renal lesions. The objective of the study was to assess the prevalence of CsA nephrotoxicity (CsAN) in protocol biopsies of children with SDNS.</p>
<p>Design, settings, participants, &amp; measurements: From 1990 through 2008, we performed 71 renal biopsies in 53 patients with SDNS. The mean CsA C2 levels were 466 &plusmn; 134 ng/ml, and the mean duration of treatment was 4.7 &plusmn; 2.0 yr before biopsy (range 2.9 to 12.7 yr).</p>
<p>Results: CsAN was observed in 22 (31%) of 71 renal biopsies. Of these, 11 corresponded to isolated vascular or tubular lesions, and 11 corresponded to combined vascular and tubular lesions. The majority of CsAN lesions were mild (17 of 22). In no cases were lesions graded as severe. By regression analysis, CsAN was positively associated with the use of angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin II receptor blockers (ARBs) and with hyperuricemia and negatively associated with minimal-change lesions. By multivariate analysis, only association with the use of ACEIs or ARBs retained significance. Stratification of the population according to CsA C2 levels showed increased risk for CsAN for C2 levels &gt;600 ng/ml.</p>
<p>Conclusions: Mild to moderate CsAN occurs in approximately one third of patients who have SDNS and are treated with CsA for &gt;3 yr. Our data suggest that patients who require high dosages of CsA or treatment for hypertension, in particular when ACEIs/ARBs are used, are at higher risk for CsAN.</p>
]]></description>
<dc:creator><![CDATA[Kengne, S.-W., Massella, L., Diomedi, F.-C., Gianviti, A., Vivarelli, M., Greco, M., Rita, G. S., Emma, F.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:30 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01520209</dc:identifier>
<dc:title><![CDATA[Risk Factors for Cyclosporin A Nephrotoxicity in Children with Steroid-Dependant Nephrotic Syndrome]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1416</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1409</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1417?rss=1">
<title><![CDATA[The Natural History of the Non-Nephrotic Membranous Nephropathy Patient]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1417?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Although early studies suggest that patients with idiopathic membranous nephropathy (MGN) and subnephrotic range proteinuria overall do well, these studies were small and follow-up was short or difficult to discern.</p>
<p>Design, setting, participants, &amp; measurements: Three hundred ninety-five cases of idiopathic MGN with at least 12 mo of follow-up from the Toronto Glomerulonephritis Registry were reviewed to determine the outcome of the subgroup of patients that presented with subnephrotic range proteinuria. Onset and follow-up data included mean arterial pressure (MAP) and creatinine clearance (CrCl) as determined by the Cockcroft-Gault equation. Outcome variables included the rate of progression (slope of CrCl), 50% reduction in initial CrCl, and end-stage renal disease (ESRD).</p>
<p>Results: One hundred eight (27% of the total) patients presented with subnephrotic proteinuria and almost 40% (42 of 108) of this subgroup remained subnephrotic. Their long-term slope was &ndash;0.93 ml/min/yr. In contrast, those who subsequently developed nephrotic range proteinuria had a progression rate almost four times faster (&ndash;3.52 ml/min/yr). The majority who developed nephrotic syndrome did so within the first year of follow-up. The only distinguishing baseline feature between the two groups was a higher level of urine protein in the group that subsequently developed nephrotic syndrome (1.98 [0.3 to 3.4] <I>versus</I> 2.43 [0.5 to 3.4] g/d).</p>
<p>Conclusions: Patients with MGN and sustained subnephrotic range proteinuria have an excellent prognosis. Conservative management with close monitoring is recommended given the difficulty predicting which patients will develop nephrotic range proteinuria and then progress more rapidly.</p>
]]></description>
<dc:creator><![CDATA[Hladunewich, M. A., Troyanov, S., Calafati, J., for the Metropolitan Toronto Glomerulonephritis Registry, Cattran, D. C.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:30 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01330209</dc:identifier>
<dc:title><![CDATA[The Natural History of the Non-Nephrotic Membranous Nephropathy Patient]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1422</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1417</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1423?rss=1">
<title><![CDATA[Renal Involvement in Primary Sjogren's Syndrome: A Clinicopathologic Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1423?rss=1</link>
<description><![CDATA[
<p>Background &amp; objectives: Renal pathology and clinical outcomes in patients with primary Sj&ouml;gren's syndrome (pSS) who underwent kidney biopsy (KB) because of renal impairment are reported.</p>
<p>Design, setting, participants, &amp; measurements: Twenty-four of 7276 patients with pSS underwent KB over 40 years. Patient cases were reviewed by a renal pathologist, nephrologist, and rheumatologist. Presentation, laboratory findings, renal pathology, initial treatment, and therapeutic response were noted.</p>
<p>Results: Seventeen patients (17 of 24; 71%) had acute or chronic tubulointerstitial nephritis (TIN) as the primary lesion, with chronic TIN (11 of 17; 65%) the most common presentation. Two had cryoglobulinemic GN. Two had focal segmental glomerulosclerosis. Twenty patients (83%) were initially treated with corticosteroids. In addition, three received rituximab during follow-up. Sixteen were followed after biopsy for more than 12 mo (median 76 mo; range 17 to 192), and 14 of 16 maintained or improved renal function through follow-up. Of the seven patients presenting in stage IV chronic kidney disease, none progressed to stage V with treatment.</p>
<p>Conclusions: This case series supports chronic TIN as the predominant KB finding in patients with renal involvement from pSS and illustrates diverse glomerular lesions. KB should be considered in the clinical evaluation of kidney dysfunction in pSS. Treatment with glucocorticoids or other immunosuppressive agents appears to slow progression of renal disease. Screening for renal involvement in pSS should include urinalysis, serum creatinine, and KB where indicated. KB with characteristic findings (TIN) should be considered as an additional supportive criterion to the classification criteria for pSS because it may affect management and renal outcome.</p>
]]></description>
<dc:creator><![CDATA[Maripuri, S., Grande, J. P., Osborn, T. G., Fervenza, F. C., Matteson, E. L., Donadio, J. V., Hogan, M. C.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00980209</dc:identifier>
<dc:title><![CDATA[Renal Involvement in Primary Sjogren's Syndrome: A Clinicopathologic Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1431</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1423</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1432?rss=1">
<title><![CDATA[Determinants of Decline in Glomerular Filtration Rate in Nonproteinuric Subjects with or without Diabetes and Hypertension]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1432?rss=1</link>
<description><![CDATA[
<p>Background and objectives: This study investigated whether the slope of estimated GFR is different between nonproteinuric subjects with and without diabetes, and what clinical factors are associated with the GFR slope.</p>
<p>Design, setting, participants, &amp; measurements: An observational cohort study was performed in 923 subjects, and the predictive value of baseline variables on the GFR slope was investigated.</p>
<p>Results: On the basis of the median 3-yr follow-up and 7 measurements of GFR, GFR slope (%/yr, median and interquartile range) was significantly larger in subjects with diabetes (&ndash;2.39 (&ndash;4.86 to 0.15), <I>n</I> = 729) than in those without diabetes (&ndash;1.02 (&ndash;4.28 to 1.37), <I>n</I> = 194), and this difference remained significant with or without presence of hypertension. After adjustments for confounding factors, predictors of GFR decline were found to be baseline high values of glycosylated hemoglobin A<SUB>1C</SUB> (HbA<SUB>1C</SUB>), GFR, systolic blood pressure, and low plasma total protein in subjects with diabetes, whereas only the latter two were significant in subjects without diabetes. In subjects with diabetes, the high GFR was accounted for by high HbA<SUB>1C</SUB> at baseline, and the predictors of GFR decline differed between those with and without hypertension, or with high and low baseline GFR. Any combination of the predictors showed increased risk for GFR decline.</p>
<p>Conclusions: GFR slope is substantially affected by multiple factors at various stages. The degree of chronic hyperglycemia is likely to play a crucial role in elevating GFR and accelerating the decline in patients with type 2 diabetes even from the normoalbuminuric stage.</p>
]]></description>
<dc:creator><![CDATA[Yokoyama, H., Kanno, S., Takahashi, S., Yamada, D., Itoh, H., Saito, K., Sone, H., Haneda, M.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06511208</dc:identifier>
<dc:title><![CDATA[Determinants of Decline in Glomerular Filtration Rate in Nonproteinuric Subjects with or without Diabetes and Hypertension]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1440</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1432</prism:startingPage>
<prism:section>Diabetes and the Kidney</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1441?rss=1">
<title><![CDATA[Technical Breakthroughs in the Wearable Artificial Kidney (WAK)]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1441?rss=1</link>
<description><![CDATA[
<p>Background: The wearable artificial kidney (WAK) has been a holy grail in kidney failure for decades. Described herein are the breakthroughs that made possible the creation of the WAK V1.0 and its advanced versions V 1.1 and 1.2.</p>
<p>Design: The battery-powered WAK pump has a double channel pulsatile counter phase flow. This study clarifies the role of pulsatile blood and dialysate flow, a high-flux membrane with a larger surface area, and the optimization of the dialysate pH. Flows and clearances from the WAK pump were compared with conventional pumps and with gravity steady flow.</p>
<p>Results: Raising dialysate pH to 7.4 increased adsorption of ammonia. Clearances were higher with pulsatile flow as compared with steady flow. The light WAK pump, geometrically suitable for wearability, delivered the same clearances as larger and heavier pumps that cannot be battery operated. Beta<SUB>2</SUB> microglobulin (&beta;<SUB>2</SUB>M) was removed from human blood <I>in vitro</I>. Activated charcoal adsorbed most &beta;<SUB>2</SUB>M in the dialysate. The WAK V1.0 delivered an effective creatinine clearance of 18.5 &plusmn; 3.2 ml/min and the WAK V1.1 27.0 &plusmn; 4.0 ml/min in uremic pigs.</p>
<p>Conclusions: Half-cycle differences between blood and dialysate, alternating transmembrane pressures (TMP), higher amplitude pulsations, and a push-pull flow increased convective transport. This creates a yet undescribed type of hemodiafiltration. Further improvements were achieved with a larger surface area high-flux dialyzer and a higher dialysate pH. The data suggest that the WAK might be an efficient way of providing daily dialysis and optimizing end stage renal disease (ESRD) treatment.</p>
]]></description>
<dc:creator><![CDATA[Gura, V., Macy, A. S., Beizai, M., Ezon, C., Golper, T. A.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02790409</dc:identifier>
<dc:title><![CDATA[Technical Breakthroughs in the Wearable Artificial Kidney (WAK)]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1448</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1441</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1449?rss=1">
<title><![CDATA[Interferon for Hepatitis C Virus in Hemodialysis--an Individual Patient Meta-analysis of Factors Associated with Sustained Virological Response]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1449?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Hepatitis C virus (HCV) infection is prevalent in hemodialysis patients and causes excess mortality. Interferon (IFN) treatment of chronic HCV infection in hemodialysis patients results in high sustained virological response (SVR) rates 6 mo after treatment. The authors aimed to identify factors associated with SVR in hemodialysis patients through analysis of individual patient data obtained from systematic review of published literature.</p>
<p>Design, setting, participants &amp; measurements: Medline was searched from 1966 through February 2009, and prospective studies describing IFN treatment of hemodialysis patients with chronic HCV infection with published individual patient data were included. To identify factors associated with SVR, logistic regression was applied with adjustment for study.</p>
<p>Results: Twenty studies of IFN treatment provided data on 428 patients. Overall SVR was 45% and in univariate analyses was higher with: 1) three million units or higher three times weekly of IFN; 2) treatment for at least 6 mo; 3) treatment completion; 4) lower baseline HCV RNA; 5) female gender; and 6) early virological negativity. Although limited by missing data, these relationships persisted in multivariate regression.</p>
<p>Conclusions: SVR is more likely with larger IFN dose, longer treatment duration, treatment completion, female gender, lower HCV RNA and early virological negativity. For appropriate treatment candidates, regimens should consist of three million units of IFN three times weekly for at least 6 mo, with patients encouraged to complete the full course.</p>
]]></description>
<dc:creator><![CDATA[Gordon, C. E., Uhlig, K., Lau, J., Schmid, C. H., Levey, A. S., Wong, J. B.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01850309</dc:identifier>
<dc:title><![CDATA[Interferon for Hepatitis C Virus in Hemodialysis--an Individual Patient Meta-analysis of Factors Associated with Sustained Virological Response]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1458</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1449</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1459?rss=1">
<title><![CDATA[Increased Efficiency of Hemodialysis with Citrate Dialysate: A Prospective Controlled Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1459?rss=1</link>
<description><![CDATA[
<p>Background and objectives: A bicarbonate dialysate acidified with citrate (CD) has been reported to have local anticoagulant effect. This study examines the effect of CD on dialysis efficiency, measured as eKt/Vurea, and predialysis concentrations of BUN, creatinine, phosphate, and &beta;-2 microglobulin in chronic dialysis units.</p>
<p>Design, settings, participants, &amp; measurements: Three outpatient chronic hemodialysis units with 142 patients were switched to CD for 6 mo. Using each patient's prior 6 mo on regular bicarbonate dialysate acidified by acetate (AD) as control, eKt/Vurea was compared with that of CD. Follow-up data for 7 mo after the study were collected from about one-half of the participants remaining on CD and the others returned to AD.</p>
<p>Results: eKt/Vurea, increased (<I>P</I> &lt; 0.0001) from pre-CD value of 1.51 &plusmn; 0.01 to 1.57 &plusmn; 0.01 with CD. During CD use &beta;-2 microglobulin levels declined (<I>P</I> = 0.0001) from 28.1 &plusmn; 10.0 to 25.9 &plusmn; 10.0. Similarly, the concentrations of BUN, creatinine, and phosphate also decreased on CD (<I>P</I> &lt; 0.008). In the poststudy period, eKt/Vurea for the patients staying on CD remained unchanged at 1.60 &plusmn; 0.17 <I>versus</I> 1.59 &plusmn; 0.18 (<I>P</I> = NS), whereas in those returning to AD the eKt/Vurea decreased from 1.55 &plusmn; 0.20 to 1.52 &plusmn; 0.17 (<I>P</I> &lt; 0.0001).</p>
<p>Conclusions: Data suggest that CD use is associated with increased solute removal.</p>
]]></description>
<dc:creator><![CDATA[Kossmann, R. J., Gonzales, A., Callan, R., Ahmad, S.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02590409</dc:identifier>
<dc:title><![CDATA[Increased Efficiency of Hemodialysis with Citrate Dialysate: A Prospective Controlled Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1464</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1459</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1465?rss=1">
<title><![CDATA[Simultaneous Control of PTH and CaxP Is Sustained over Three Years of Treatment with Cinacalcet HCl]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1465?rss=1</link>
<description><![CDATA[
<p>Background &amp; objectives: Chronic kidney disease (CKD) is commonly complicated by secondary hyperparathyroidism (SHPT), leading to increased risk of morbidity and mortality. SHPT is a progressive disease often requiring long-term therapy to control parathyroid hormone (PTH) and mineral imbalances. Vitamin D sterols and phosphate binders, used as traditional therapies to lower PTH and phosphorus, may provide inadequate long-term control for many dialysis patients. Cinacalcet, by simultaneously lowering PTH, calcium, phosphorus, and calcium-phosphorus levels, may maintain PTH and mineral balance in these individuals. However, as with traditional therapies, long-term data are limited.</p>
<p>Design, setting, participants, &amp; measurement: Dialysis subjects from at least one of five lead-in studies (double-blind placebo-controlled, including one extension trial) completing up to 52 wk of either cinacalcet or placebo were eligible for this open-label extension study, including an 8-wk dose titration (initiated at 30 mg/d), followed by 24-wk maintenance and up to 132 wk of follow-up. Final efficacy analysis was at week 180.</p>
<p>Results: Three hundred thirty-four of 589 enrolled subjects received cinacalcet from the beginning of the lead-in study. Weekly median PTH values were &le;300 pg/ml (weeks 16 through 180) and median Ca<FONT FACE="arial,helvetica">x</FONT>P values were &le;55 mg<sup>2</sup>/dl<sup>2</sup> (weeks 4 through 180). Similar results were exhibited in the 255 subjects who initially received placebo. Among the patients exposed to cinacalcet from the beginning of the lead-in study, 3% of subjects exhibited treatment-related serious adverse events.</p>
<p>Conclusions: Cinacalcet effectively maintained PTH, Ca and P reductions in dialysis subjects for up to 180 wk.</p>
]]></description>
<dc:creator><![CDATA[Sprague, S. M., Evenepoel, P., Curzi, M. P., Gonzalez, M. T., Husserl, F. E., Kopyt, N., Sterling, L. R., Mix, C., Wong, G.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06141108</dc:identifier>
<dc:title><![CDATA[Simultaneous Control of PTH and CaxP Is Sustained over Three Years of Treatment with Cinacalcet HCl]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1476</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1465</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1477?rss=1">
<title><![CDATA[Determinants of Left Ventricular Mass and Hypertrophy in Hemodialysis Patients Assessed by Cardiac Magnetic Resonance Imaging]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1477?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Left ventricular hypertrophy (LVH) is an independent risk factor for premature cardiovascular death in hemodialysis (HD) patients and one of the three forms of uremic cardiomyopathy. Cardiovascular magnetic resonance (CMR) is a volume-independent technique to assess cardiac structure. We used CMR to assess the determinants of left ventricular mass (LVM) and LVH in HD patients.</p>
<p>Design, setting, participants, &amp; measurements: A total of 246 HD patients (63.8% male; mean age 51.5 &plusmn; 12.1 yr) underwent CMR on a postdialysis day. LVM was measured from a stack of cine loops and indexed for body surface area (LVM index [LVMI]). Demographic, past biochemical, hematologic, and dialysis data were collected by patient record review. Results up to 180 d before CMR were collected. LVH was defined as LVMI &gt;84.1 g/m<sup>2</sup> (male) or &gt;76.4 g/m<sup>2</sup> (female).</p>
<p>Results: A total of 157 (63.8%) patients had LVH. LVH was more common in patients with higher predialysis systolic BP, predialysis pulse pressure, and calcium-phosphate product (Ca <FONT FACE="arial,helvetica">x</FONT> PO<SUB>4</SUB>). Furthermore, LVH was significantly associated with higher end-diastolic and systolic volumes and lower ejection fraction. There were positive correlations with LVMI and end-diastolic and systolic volumes. There were weak positive correlations among LVMI, mean volume of ultrafiltration, and Ca <FONT FACE="arial,helvetica">x</FONT> PO<SUB>4</SUB>. Using multivariate linear and logistic regression (entering one BP and cardiac variable), the independent predictors of LVMI and LVH were end-diastolic volume, predialysis systolic BP, and Ca <FONT FACE="arial,helvetica">x</FONT> PO<SUB>4</SUB>.</p>
<p>Conclusions: The principal determinants of LVM and LVH in HD patients are end-diastolic LV volume, predialysis BP, and Ca <FONT FACE="arial,helvetica">x</FONT> PO<SUB>4</SUB>.</p>
]]></description>
<dc:creator><![CDATA[Patel, R. K., Oliver, S., Mark, P. B., Powell, J. R., McQuarrie, E. P., Traynor, J. P., Dargie, H. J., Jardine, A. G.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03350509</dc:identifier>
<dc:title><![CDATA[Determinants of Left Ventricular Mass and Hypertrophy in Hemodialysis Patients Assessed by Cardiac Magnetic Resonance Imaging]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1483</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1477</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1484?rss=1">
<title><![CDATA[Relationship between Bone Histology and Markers of Bone and Mineral Metabolism in African-American Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1484?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Racial differences in mineral metabolism exist in the chronic kidney disease population, especially as it relates to intact parathyroid hormone (iPTH) levels. Few data exist on the relationship of these markers to bone biopsy findings in African-American (AA) hemodialysis patients across the spectrum of renal osteodystrophy (ROD).</p>
<p>Design, setting, participants, &amp; measurements: In prevalent AA hemodialysis subjects, we prospectively evaluated subjects by performing transiliac bone biopsy and correlating biochemical and clinical data to bone histology.</p>
<p>Results: Study patients (<I>n</I> = 43) had an average age of 53.7 (&plusmn;11.6) yr, with dialysis vintage of 40.4 (&plusmn;24.5) mo, 30% with diabetes, and 51% male. Bone histology revealed adynamic bone disease (ABD) (16%), mild to moderate hyperparathyroidism (HPT) (72%), severe (12%) HPT, and no osteomalacia or mixed uremic osteodystrophy. At the time of biopsy, mean corrected calcium was 9.1, 8.9, and 9.4 mg/dl (<I>P</I> = 0.344); calcium-phosphorus (Ca <FONT FACE="arial,helvetica">x</FONT> PO<SUB>4</SUB>) product was 42, 55, and 62 mg<sup>2</sup>/dl<sup>2</sup> (<I>P</I> = 0.002); phosphorus was 4.6, 6.2, and 6.7 mg/dl (<I>P</I> = 0.005); and iPTH was 225, 566, and 975 pg/ml (<I>P</I> = 0.006), respectively. Median values for bone-specific alkaline phosphatase (BS-AP) were 16, 34, and 64 ng/ml (<I>P</I> &lt; 0.0001) among the three groups.</p>
<p>Conclusions: These data demonstrate that across the spectrum of ROD, iPTH levels are higher than expected in AA hemodialysis subjects. iPTH, PTH peptides, and bone-specific alkaline phosphatase correlated directly with histomorphometric measurements of bone turnover and when subjects were grouped by histologic diagnosis. Only 9.5% of subjects were simultaneously within suggested Kidney Disease Outcomes Quality Initiative (K/DOQI) ranges for Ca <FONT FACE="arial,helvetica">x</FONT> PO<SUB>4</SUB>, phosphorus, and iPTH, of which 75% demonstrated ABD on biopsy.</p>
]]></description>
<dc:creator><![CDATA[Moore, C., Yee, J., Malluche, H., Rao, D. S., Monier-Faugere, M.-C., Adams, E., Daramola-Ogunwuyi, O., Fehmi, H., Bhat, S., Osman-Malik, Y.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01770408</dc:identifier>
<dc:title><![CDATA[Relationship between Bone Histology and Markers of Bone and Mineral Metabolism in African-American Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1493</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1484</prism:startingPage>
<prism:section>Mineral Metabolism and Bone Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1494?rss=1">
<title><![CDATA[Arteriovenous Fistula Affects Bone Mineral Density Measurements in End-Stage Renal Failure Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1494?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Hemodialysis needs an arteriovenous fistula (AVF) that may influence the structure and growth of nearby bone and affect bone mass measurement. The study analyzed the effect of AVF in the assessment of forearm bone mineral density (BMD) measured by dual energy x-ray absorptiometry (DXA) and examined its influence on the final diagnosis of osteoporosis.</p>
<p>Design, setting, participants, &amp; measurements: Forty patients (52 &plusmn; 18 yr) in hemodialysis program (12 &plusmn; 8 yr) with permeable AVF in forearm were included. Patients were divided in two groups (over and under 50 yr). BMD of both forearms (three areas), lumbar spine, and femur was measured by DXA. Forearm measurements in each arm were compared. Patients were diagnosed as normal only if all territories were considered nonpathologic and osteoporosis/osteopenia was determined by the lowest score found.</p>
<p>Results: Ten patients were excluded and 30 patients were analyzed. BMD in the forearm with AVF was significantly lower than that observed in the contralateral forearm in both groups of patients and in all forearm areas analyzed. When only lumbar spine and femur measurements were considered, 70% of patients were nonpathologic and 30% were osteoporotic. However, inclusion of AVF forearm classified 63% as osteoporotic and a further 27% as osteopenic, leaving only 10% as nonpathologic.</p>
<p>Conclusions: Forearm AVF affects BMD measurements by decreasing their values in patients with end-stage renal failure. This may produce an overdiagnosis of osteoporosis, which should be taken into account when evaluating patients of this type.</p>
]]></description>
<dc:creator><![CDATA[Muxi, A., Torregrosa, J.-V., Fuster, D., Peris, P., Vidal-Sicart, S., Sola, O., Domenech, B., Martin, G., Casellas, J., Pons, F.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01470209</dc:identifier>
<dc:title><![CDATA[Arteriovenous Fistula Affects Bone Mineral Density Measurements in End-Stage Renal Failure Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1499</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1494</prism:startingPage>
<prism:section>Mineral Metabolism and Bone Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1500?rss=1">
<title><![CDATA[Long-Term Outcome of Adults Who Undergo Transplantation with Single Pediatric Kidneys: How Young Is too Young?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1500?rss=1</link>
<description><![CDATA[
<p>Background and objectives: The optimal donor age for transplanting a single pediatric kidney in an adult recipient remains unknown. <I>En block</I> kidney transplantation is usually performed when the donor age is &lt;5 yr.</p>
<p>Design, setting, participants, &amp; measurements: We compared the outcomes of adult patients who underwent transplantation with single pediatric kidneys from donors who were younger than 5 yr (group 1, <I>n</I> = 40) and from donors who were aged 5 to 10 yr of age (group 2, <I>n</I> = 39) in our center.</p>
<p>Results: The donor kidney sizes were significantly smaller in group 1 than in group 2 (<I>P</I> &lt; 0.001), and group 1 required more ureteral stents than group 2 (73 <I>versus</I> 38%). The surgical complications, delayed graft function, and development of proteinuria were similar in both groups. Group 1 had slightly higher rejection episodes than group 2 (25 <I>versus</I> 18%; <I>P</I> = 0.67), and graft function was comparable in both groups. There were no statistical differences between the two groups in patient (<I>P</I> = 0.73) or death-censored graft (<I>P</I> = 0.68) survivals over 5 yr.</p>
<p>Conclusions: Single pediatric kidney transplants from donors who are younger than 5 yr can be used with acceptable complications and long-term outcomes as those from older donors.</p>
]]></description>
<dc:creator><![CDATA[Zhang, R., Paramesh, A., Florman, S., Yau, C. L., Balamuthusamy, S., Krane, N. K., Slakey, D.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04610908</dc:identifier>
<dc:title><![CDATA[Long-Term Outcome of Adults Who Undergo Transplantation with Single Pediatric Kidneys: How Young Is too Young?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1506</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1500</prism:startingPage>
<prism:section>Renal Transplantation</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1507?rss=1">
<title><![CDATA[Introduction to the Second Annual Rostand Vitamin D Symposium]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1507?rss=1</link>
<description><![CDATA[
<p>The role of vitamin D in multiple organ systems is coming into sharp focus with recent advances in the understanding of its mechanisms of actions and interplay with multiple organ systems. Important distinctions between the role of 25-hydroxy metabolites that serve as substrates for subsequent hydroxylase reactions and the class of vitamin D receptor stimulating agents are important in understanding the clinical use of vitamin D in various clinical conditions.</p>
]]></description>
<dc:creator><![CDATA[Warnock, D. G., Rostand, S. G.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02580409</dc:identifier>
<dc:title><![CDATA[Introduction to the Second Annual Rostand Vitamin D Symposium]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1507</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1507</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1508?rss=1">
<title><![CDATA[Vitamin D and Parathyroid Hormone in General Populations: Understandings in 2009 and Applications to Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1508?rss=1</link>
<description><![CDATA[
<p>Vitamin D is now recognized as an important prohormone in health and disease. Its role in immunoregulation and cardiovascular and bone health has become topical in the lay press and the medical press in the past 5 yr. The target audience for this review includes the interested clinician and researchers. The prevalence of chronic kidney disease in the general population has further increased the interest and perhaps the applicability of findings of population studies. The basic physiology of vitamin D and receptor activation and biologic importance is reviewed, as well as various vitamin D analogues and nomenclature. Issues related to measurement of vitamin D and parathyroid hormone have the potential to complicate the clinical use of these tests and should be understood by all clinicians so as to ensure informed decision making and stimulate interest in participation in clinical trials. The epidemiology of vitamin D deficiency and supplementation in association with health status and disease status is reviewed, and issues related to association <I>versus</I> causation are highlighted. Some recommendations for pragmatic approaches and study design are suggested.</p>
]]></description>
<dc:creator><![CDATA[Johal, M., Levin, A.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02160309</dc:identifier>
<dc:title><![CDATA[Vitamin D and Parathyroid Hormone in General Populations: Understandings in 2009 and Applications to Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1514</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1508</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1515?rss=1">
<title><![CDATA[Vitamin D and the Cardiovascular System]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1515?rss=1</link>
<description><![CDATA[
<p>Several epidemiologic and clinical studies have suggested that there is a strong association between hypovitaminosis D and cardiovascular disease (CVD). Hypovitaminosis D was reported as a risk factor for increased cardiovascular events among 1739 adult participants in the Framingham Offspring Study. Analysis of more than 13,000 adults in the Third National Health and Nutrition Examination Survey (NHANES III) showed that even though hypovitaminosis D is associated with an increased prevalence of CVD risk factors, its association with all-cause mortality is independent of these risk factors. Importantly, epidemiologic studies suggested that patients who had chronic kidney disease and were treated with activated vitamin D had a survival advantage when compared with those who did not receive treatment with these agents. Mechanistically, emerging data have linked vitamin D administration with improved cardiac function and reduced proteinuria, and hypovitaminosis D is associated with obesity, insulin resistance, and systemic inflammation. Preliminary studies suggested that activated vitamin D inhibits the proliferation of cardiomyoblasts by promoting cell-cycle arrest and enhances the formation of cardiomyotubes without inducing apoptosis. Activated vitamin D has also been shown to attenuate left ventricular dysfunction in animal models and humans. In summary, emerging studies suggest that hypovitaminosis D has emerged as an independent risk factor for all-cause and cardiovascular mortality, reinforcing its importance as a public health problem. There is a need to advance our understanding of the biologic pathways through which vitamin D affects cardiovascular health and to conduct prospective clinical interventions to define precisely the cardioprotective effects of nutritional vitamin D repletion.</p>
]]></description>
<dc:creator><![CDATA[Artaza, J. N., Mehrotra, R., Norris, K. C.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02260409</dc:identifier>
<dc:title><![CDATA[Vitamin D and the Cardiovascular System]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1522</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1515</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1523?rss=1">
<title><![CDATA[Vitamin D, Proteinuria, Diabetic Nephropathy, and Progression of CKD]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1523?rss=1</link>
<description><![CDATA[
<p>Although the endocrine effects of vitamin D are widely recognized, somewhat less appreciated is that vitamin D may serve paracrine functions through local activation by 1--hydroxylase and thus maintain immunity, vascular function, cardiomyocyte health, and abrogate inflammation and insulin resistance. In the kidney, vitamin D may be important for maintaining podocyte health, preventing epithelial-to-mesenchymal transformation, and suppressing renin gene expression and inflammation. Replacement with pharmacologic dosages of vitamin D receptor agonists (VDRA) in animal models of kidney disease consistently show reduction in albuminuria, abrogation of glomerulosclerosis, glomerulomegaly, and glomerular inflammation, effects that may be independent of BP and parathyroid hormone, but the effects of VDRA in preventing tubulointerstitial fibrosis and preventing the progression of kidney failure in these animal models are less clear. Emerging evidence in patients with chronic kidney disease (CKD) show that vitamin D can reduce proteinuria or albuminuria even in the presence of angiotensin-converting enzyme inhibition. In addition to reducing proteinuria, VDRA may reduce insulin resistance, BP, and inflammation and preserve podocyte loss providing biologic plausibility to the notion that the use of VDRA may be associated with salubrious outcomes in patients with diabetic nephropathy. Patients with CKD have a very high prevalence of deficiency of 25-hydroxyvitamin D. Whether pharmacologic dosages of vitamin D instead of VDRA in patients with CKD can overcome the paracrine and endocrine functions of this vitamin remains unknown. To demonstrate the putative benefits of native vitamin D and VDRA among patients with CKD, randomized, controlled trials are needed.</p>
]]></description>
<dc:creator><![CDATA[Agarwal, R.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02010309</dc:identifier>
<dc:title><![CDATA[Vitamin D, Proteinuria, Diabetic Nephropathy, and Progression of CKD]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1528</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1523</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/9/1529?rss=1">
<title><![CDATA[Clinical Outcomes with Active versus Nutritional Vitamin D Compounds in Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/9/1529?rss=1</link>
<description><![CDATA[
<p>Increasing confusion exists as to which vitamin D compounds are more appropriate for persons with chronic kidney disease (CKD). Some opinion-based guidelines recommend administration of such nutritional vitamin D agents as ergocalciferol or cholecalciferol as the first therapy in hyperparathyroidism associated with low circulating levels of 25-hydroxy vitamin D (&lt;30 ng/ml) in nondialysis dependent CKD patients. Insufficient to deficient levels of 25-hydroxy vitamin D have been reported in the majority of individuals with CKD, including both nondialysis dependent and maintenance dialysis patients. Epidemiologic studies have almost consistently indicated the survival benefit of active vitamin D agents across all stages of CKD, including among dialysis patients with 25-hydroxy vitamin D deficiency. To date, no large observational or interventional studies have shown any survival advantage of nutritional vitamin D in CKD patients. Several recent (postguideline) small studies have yielded mixed results regarding the potential benefits of ergocalciferol in CKD, including satisfactory to inadequate lowering of PTH level to target ranges, improving response to erythropoietin stimulating agents, and salutary effects on glycemic controls. Compared with nutritional vitamin D agents, active vitamin D compounds appear to more effectively lower the circulating levels of alkaline phosphatase, a conveniently available biomarker associated with increased mortality and coronary artery calcification in CKD patients. The ideal vitamin D therapy for CKD patients should be the one that improves survival irrespective of suggested or imposed target ranges for arbitrary or opinion-based surrogate end points. Randomized controlled trials are needed to verify which agents offer superior survival advantages.</p>
]]></description>
<dc:creator><![CDATA[Kalantar-Zadeh, K., Kovesdy, C. P.]]></dc:creator>
<dc:date>Thu, 03 Sep 2009 14:47:31 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02140309</dc:identifier>
<dc:title><![CDATA[Clinical Outcomes with Active versus Nutritional Vitamin D Compounds in Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>9</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1539</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>1529</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1285?rss=1">
<title><![CDATA[Franklin H. Epstein--Researcher, Teacher, Clinician, and Humanist]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1285?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Brown, R. S., Karumanchi, S. A., Sukhatme, V. P., Zeidel, M. L.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03070509</dc:identifier>
<dc:title><![CDATA[Franklin H. Epstein--Researcher, Teacher, Clinician, and Humanist]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1289</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1285</prism:startingPage>
<prism:section>Nephrology Hall of Fame</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1290?rss=1">
<title><![CDATA[Phosphorus Additives in Food and their Effect in Dialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1290?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Uribarri, J.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03950609</dc:identifier>
<dc:title><![CDATA[Phosphorus Additives in Food and their Effect in Dialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1292</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1290</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1293?rss=1">
<title><![CDATA[Health-related Quality of Life in CKD Patients: Correlates and Evolution over Time]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1293?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Very few large-scale studies have investigated the determinants of health-related quality of life (HRQOL) in chronic kidney disease (CKD) patients not on dialysis or the evolution of HRQOL over time.</p>
<p>Design and setting: A prospective evaluation was undertaken of HRQOL in a cohort of 1186 CKD patients cared for in nephrology clinics in North America. Baseline and follow-up HRQOL were evaluated using the validated Kidney Disease Quality Of Life instrument.</p>
<p>Results: Baseline measures of HRQOL were reduced in CKD patients in proportion to the severity grade of CKD. Physical functioning score declined progressively with more advanced stages of CKD and so did the score for role-physical. Female gender and the presence of diabetes and a history of cardiovascular co-morbidities were also associated with reduced HRQOL (physical composite score: male: 41.0 &plusmn; 10.2; female: 37.7 &plusmn; 10.8; <I>P</I> &lt; 0.0001; diabetic: 37.3 &plusmn; 10.6; nondiabetic: 41.6 &plusmn; 10.2; <I>P</I> &lt; 0.0001; history of congestive heart failure, yes: 35.4 &plusmn; 9.7; no: 40.3 &plusmn; 10.6; <I>P</I> &lt; 0.0001; history of myocardial infarction, yes: 36.1 &plusmn; 10.0; no: 40.2 &plusmn; 10.6; <I>P</I> &lt; 0.0001). Anemia and beta blocker usage were also associated with lower HRQOL scores. HRQOL measures declined over time in this population. The main correlates of change over time were age, albumin level and co-existent co-morbidities.</p>
<p>Conclusions: These observations highlight the profound impact CKD has on HRQOL and suggest potential areas that can be targeted for therapeutic intervention.</p>
]]></description>
<dc:creator><![CDATA[Mujais, S. K., Story, K., Brouillette, J., Takano, T., Soroka, S., Franek, C., Mendelssohn, D., Finkelstein, F. O.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05541008</dc:identifier>
<dc:title><![CDATA[Health-related Quality of Life in CKD Patients: Correlates and Evolution over Time]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1301</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1293</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1302?rss=1">
<title><![CDATA[Chronic Renal Insufficiency Cohort (CRIC) Study: Baseline Characteristics and Associations with Kidney Function]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1302?rss=1</link>
<description><![CDATA[
<p>Background and objectives: The Chronic Renal Insufficiency Cohort (CRIC) Study was established to examine risk factors for the progression of chronic kidney disease (CKD) and cardiovascular disease (CVD) in patients with CKD. We examined baseline demographic and clinical characteristics.</p>
<p>Design, setting, participants, &amp; measurements: Seven clinical centers recruited adults who were aged 21 to 74 yr and had CKD using age-based estimated GFR (eGFR) inclusion criteria. At baseline, blood and urine specimens were collected and information regarding health behaviors, diet, quality of life, and functional status was obtained. GFR was measured using radiolabeled iothalamate in one third of participants.</p>
<p>Results: A total of 3612 participants were enrolled with mean age &plusmn; SD of 58.2 &plusmn; 11.0 yr; 46% were women, and 47% had diabetes. Overall, 45% were non-Hispanic white, 46% were non-Hispanic black, and 5% were Hispanic. Eighty-six percent reported hypertension, 22% coronary disease, and 10% heart failure. Mean body mass index was 32.1 &plusmn; 7.9 kg/m<sup>2</sup>, and 47% had a BP &gt;130/80 mmHg. Mean eGFR was 43.4 &plusmn; 13.5 ml/min per 1.73 m<sup>2</sup>, and median (interquartile range) protein excretion was 0.17 g/24 h (0.07 to 0.81 g/24 h). Lower eGFR was associated with older age, lower socioeconomic and educational level, cigarette smoking, self-reported CVD, peripheral arterial disease, and elevated BP.</p>
<p>Conclusions: Lower level of eGFR was associated with a greater burden of CVD as well as lower socioeconomic and educational status. Long-term follow-up of participants will provide critical insights into the epidemiology of CKD and its relationship to adverse outcomes.</p>
]]></description>
<dc:creator><![CDATA[Lash, J. P., Go, A. S., Appel, L. J., He, J., Ojo, A., Rahman, M., Townsend, R. R., Xie, D., Cifelli, D., Cohan, J., Fink, J. C., Fischer, M. J., Gadegbeku, C., Hamm, L. L., Kusek, J. W., Landis, J. R., Narva, A., Robinson, N., Teal, V., Feldman, H. I., the Chronic Renal Insufficiency Cohort (CRIC) Study Group]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00070109</dc:identifier>
<dc:title><![CDATA[Chronic Renal Insufficiency Cohort (CRIC) Study: Baseline Characteristics and Associations with Kidney Function]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1311</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1302</prism:startingPage>
<prism:section>Chronic Kidney Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1312?rss=1">
<title><![CDATA[Complement Inhibitor Eculizumab in Atypical Hemolytic Uremic Syndrome]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1312?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Atypical hemolytic uremic syndrome (aHUS) is associated with a congenital or acquired dysregulation of the complement alternative pathway that leads to continuous complement activation on host cells causing inflammation and damage. Eculizumab, a humanized mAb against complement protein C5, inhibits activation of the terminal complement pathway.</p>
<p>Design, setting, participants, &amp; measurements: We report an adolescent with relapsing unclassified aHUS. On admission, a high plasma creatinine level indicated a poor prognosis, and hemodialysis had to be started. Plasma exchanges were initially effective against the microangiopathic hemolytic activity and allowed a temporary improvement of renal function with termination of hemodialysis after 7 wk. Subsequently, plasma exchanges (three times per week) failed to prevent ongoing aHUS activity and progressive renal failure. After 12 wk, aHUS treatment was switched to eculizumab.</p>
<p>Results: Eculizumab was effective in terminating the microangiopathic hemolytic process in two aHUS relapses; however, after normalization of complement activity, aHUS recurred and ultimately led to anuric end-stage renal failure.</p>
<p>Conclusions: In this patient, complement inhibition by eculizumab temporarily terminated the microangiopathic hemolytic activity. Nevertheless, renal damage as a result of preceding and subsequent aHUS activity resulted in end-stage renal failure; therefore, therapeutic success may depend on early administration of eculizumab. The optimal duration of treatment may be variable and remains to be determined.</p>
]]></description>
<dc:creator><![CDATA[Mache, C. J., Acham-Roschitz, B., Fremeaux-Bacchi, V., Kirschfink, M., Zipfel, P. F., Roedl, S., Vester, U., Ring, E.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01090209</dc:identifier>
<dc:title><![CDATA[Complement Inhibitor Eculizumab in Atypical Hemolytic Uremic Syndrome]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1316</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1312</prism:startingPage>
<prism:section>Clinical Immunology and Pathology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1317?rss=1">
<title><![CDATA[Rituximab Treatment of Adult Patients with Steroid-Resistant Focal Segmental Glomerulosclerosis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1317?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Isolated case reports have shown a beneficial effect of rituximab on pediatric patients with primary FSGS, but there is no information about rituximab treatment of FSGS in adults.</p>
<p>Design, setting, participants, &amp; measurements: All patients who had biopsy-proven FSGS and were treated with rituximab in Spain were identified, independent of their positive or negative response, among the nephrology departments that belong to the Spanish Group for the Study of Glomerular Diseases (GLOSEN). Their characteristics and outcome after rituximab treatment were studied.</p>
<p>Results: Eight patients were identified. Rituximab failed to improve nephrotic syndrome in five of eight patients, who continued to show massive proteinuria and exhibited a rapidly deteriorating renal function in two cases. Among the remaining three patients, two of them showed an improvement of renal function and a remarkable proteinuria reduction and one experienced a beneficial but transitory effect after rituximab. There were no differences in clinical or laboratory characteristics or in the CD20 B lymphocyte count after rituximab between these three patients and the five who had a negative response. The only difference was in the regimen of rituximab administration: Whereas the five patients with a negative response received only four weekly consecutive infusions of 375 mg/m<sup>2</sup>, the three remaining patients received additional doses of rituximab.</p>
<p>Conclusions: Only a minority (three of eight) of patients in our series of adult patients with FSGS showed a positive influence of rituximab. More studies are necessary to characterize further the optimal dosages and the mechanisms of action of rituximab in FSGS.</p>
]]></description>
<dc:creator><![CDATA[Fernandez-Fresnedo, G., Segarra, A., Gonzalez, E., Alexandru, S., Delgado, R., Ramos, N., Egido, J., Praga, M., for the Grupo de Trabajo de Enfermedades Glomerulares de la Sociedad Espanola de Nefrologia (GLOSEN)]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00570109</dc:identifier>
<dc:title><![CDATA[Rituximab Treatment of Adult Patients with Steroid-Resistant Focal Segmental Glomerulosclerosis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1323</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1317</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1324?rss=1">
<title><![CDATA[Does Timing of Dialysis in Patients with ESRD and Acute Myocardial Infarcts Affect Morbidity or Mortality?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1324?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Patients with ESRD have an increased incidence of coronary events with a relatively higher risk for mortality after acute myocardial infarction (AMI). We evaluated whether it is safer to delay dialysis in AMI or if delay poses separate risks.</p>
<p>Design, setting, participants, &amp; measurements: We conducted a retrospective review of 131 long-term hemodialysis patients who had AMI and were admitted between 1997 and 2005 at three New York City municipal hospitals. Patients were separated into three groups on the basis of time between cardiac symptoms and first dialysis (&lt;24 h, 24 to 48 h, and &gt;48 h).</p>
<p>Results: A total of 17 (13%) patients died, 10 (59%) of whom had either hypotension or an arrhythmia during their first cardiac care unit dialysis. Although these groups were comparable in acuity and cardiac status, there were no findings of increased morbidity (26, 36, and 20%, respectively) or mortality (11, 18, and 13%, respectively), despite differences in the timing of each group's dialysis. We found that previous cardiac disease, predialysis K<sup>+</sup>, K<sup>+</sup> after dialysis, and APACHE scores were significantly higher in patients with peridialysis morbidity.</p>
<p>Conclusions: We conclude that there is no increased morbidity with early dialysis in AMI, but rather close attention needs to be paid to the rate of decrease in serum potassium in patients with ESRD and their level of acuity when undergoing dialysis.</p>
]]></description>
<dc:creator><![CDATA[Coritsidis, G., Sutariya, D., Stern, A., Gupta, G., Carvounis, C., Arora, R., Balmir, S., Acharya, A.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04470908</dc:identifier>
<dc:title><![CDATA[Does Timing of Dialysis in Patients with ESRD and Acute Myocardial Infarcts Affect Morbidity or Mortality?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1330</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1324</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1331?rss=1">
<title><![CDATA[HFE Mutations Modulate the Effect of Iron on Serum Hepcidin-25 in Chronic Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1331?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Increased serum hepcidin has been reported in patients receiving chronic hemodialysis, and hypothesized to contribute to the alterations of iron metabolism of end-stage renal disease. However, no quantitative assessment is available to date; the clinical determinants are still under definition; and the role of genetic factors, namely HFE mutations, has not yet been evaluated. The aim of this study was to quantitatively assess serum hepcidin-25 in hemodialysis patients <I>versus</I> controls, and analyze the relationship between hepcidin, iron indices, HFE genotype, and erythropoietic parameters.</p>
<p>Design, setting, participants &amp; measurements: Sixty-five hemodialysis patients and 57 healthy controls were considered. Hepcidin-25 was evaluated by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry, HFE genotype by restriction analysis.</p>
<p>Results: Serum hepcidin-25 was higher in hemodialysis patients compared with controls. In patients, hepcidin-25 correlated positively with ferritin and C reactive protein, and negatively with serum iron after adjustment for confounders. Hepcidin/ferritin ratio was lower in patients with (n = 25) than in those without (n = 40) HFE mutations. At multivariate analysis, hepcidin-25 was independently associated with ferritin and HFE status. In a subgroup of 22 "stable" patients, <I>i.e.,</I> with Hb levels on target, normal CRP levels, and absence of complications for at least 1 yr, hepcidin-25 was negatively correlated with Hb levels independently of confounders.</p>
<p>Conclusions: Serum hepcidin-25 is increased in hemodialysis patients, regulated by iron stores and inflammation, and relatively reduced in subjects carrying frequent HFE mutations. Hepcidin-25 may contribute to the pathogenesis of anemia by decreasing iron availability.</p>
]]></description>
<dc:creator><![CDATA[Valenti, L., Girelli, D., Valenti, G. F., Castagna, A., Como, G., Campostrini, N., Rametta, R., Dongiovanni, P., Messa, P., Fargion, S.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01370209</dc:identifier>
<dc:title><![CDATA[HFE Mutations Modulate the Effect of Iron on Serum Hepcidin-25 in Chronic Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1337</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1331</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1338?rss=1">
<title><![CDATA[Sustained Low Efficiency Dialysis in the Continuous Mode (C-SLED): Dialysis Efficacy, Clinical Outcomes, and Survival Predictors in Critically Ill Cancer Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1338?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Oliguric, hypotensive patients who require large amounts of fluids may benefit from sustained low-efficiency dialysis performed continuously (C-SLED). C-SLED through higher clearance may improve survival, or through greater nutritional loss may worsen survival. No studies have assessed survival on C-SLED. The objective was to examine patient outcomes and survival predictors on C-SLED.</p>
<p>Design, setting, participants, &amp; measurements: The data of 199 consecutive cancer patients treated with C-SLED were analyzed. The median duration of C-SLED was 50 h. With 48 h of C-SLED, the blood urea nitrogen (BUN) and serum creatinine levels had decreased by 80% and 73%, respectively. The mean arterial pressure (MAP) was maintained despite higher ultrafiltration and reduced vasopressor use. The 30-d mortality rate was 65%. Despite excellent dialysis, the sequential organ failure assessment (SOFA) score remained predictive of mortality. In the univariate model, higher SOFA scores and lower values for MAP, blood pH, and serum albumin and creatinine levels were associated with higher mortality. Administration of total parenteral nutrition (TPN) was, however, associated with lower mortality.</p>
<p>Results: In the multivariate model, the higher SOFA score and lower blood pH, MAP and C-SLED duration were associated with higher mortality. In a subset analysis of 129 patients who received C-SLED for at least 48 h, those with higher BUN levels, which were associated with higher TPN infusion, had a lower mortality risk.</p>
<p>Conclusion: This first detailed report on C-SLED indicates that C-SLED can be effective and suggests a link between nutrition and survival.</p>
]]></description>
<dc:creator><![CDATA[Salahudeen, A. K., Kumar, V., Madan, N., Xiao, L., Lahoti, A., Samuels, J., Nates, J., Price, K.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02130309</dc:identifier>
<dc:title><![CDATA[Sustained Low Efficiency Dialysis in the Continuous Mode (C-SLED): Dialysis Efficacy, Clinical Outcomes, and Survival Predictors in Critically Ill Cancer Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1346</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1338</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1347?rss=1">
<title><![CDATA[Antiplatelet Medications in Hemodialysis Patients: A Systematic Review of Bleeding Rates]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1347?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Patients with end stage renal disease (ESRD) are often prescribed antiplatelet medications. However, these patients are also at increased risk of bleeding compared with the general population, and an aim was made to quantify this risk with antiplatelet agents.</p>
<p>Design, setting, participants, &amp; measurements: A systematic review of the literature (Medline, EMBASE, Cochrane CENTRAL and Google Scholar databases) was done to determine the bleeding risk in ESRD patients prescribed antiplatelet therapy. The secondary outcome was the effect on access thrombosis. All case series, cohort studies and clinical trials were considered if they included ten or more ESRD patients, assessed bleeding risk with antiplatelet agents, and lasted for more than 3 mo.</p>
<p>Results: Sixteen studies, including 40,676 patients, were identified that met predefined inclusion criteria. Due to study heterogeneity and weaknesses in methodology, bleeding rates were not pooled across studies. However, the bleeding risk appears to be increased for hemodialysis patients treated with combination antiplatelet therapy. The results are mixed for studies using a single antiplatelet agent. Antiplatelet agents appear to be effective in preventing shunt and central venous catheter thrombosis, but not for preventing thrombosis of arteriovenous grafts.</p>
<p>Conclusion: The risks and benefits of antiplatelet agents in ESRD patients remain poorly defined. Until a clinical trial addresses this in the dialysis population, individual risk stratification taking into account the increased risk of bleeding should be considered before initiating antiplatelet agents, especially in combination therapy.</p>
]]></description>
<dc:creator><![CDATA[Hiremath, S., Holden, R. M., Fergusson, D., Zimmerman, D. L.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00810209</dc:identifier>
<dc:title><![CDATA[Antiplatelet Medications in Hemodialysis Patients: A Systematic Review of Bleeding Rates]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1355</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1347</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1356?rss=1">
<title><![CDATA[A Large Family with a Gain-of-Function Mutation of Complement C3 Predisposing to Atypical Hemolytic Uremic Syndrome, Microhematuria, Hypertension and Chronic Renal Failure]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1356?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Atypical hemolytic uremic syndrome (aHUS) is associated with mutations in genes encoding complement-regulatory proteins factor H, I and B and membrane cofactor protein. Recently, heterozygous gain-of-function mutations in the complement C3 gene have been found in patients with aHUS.</p>
<p>Design, setting, participants, &amp; measurements: A large family with a C3 R570Q mutation is described. Clinical and laboratory findings of carriers of the mutation and unaffected family members are reported.</p>
<p>Results: The index patient suffered from recurrent aHUS at age 22 and developed end-stage renal failure. Of 24 family members, nine harbored the C3 R570Q mutation. Carriers showed reduced or borderline C3 levels. Arterial hypertension was found in six family members, microhematuria in five and chronic kidney disease stage 3 in two elderly carrier patients. Despite marked consumption of C3, serum terminal complement complex levels were not elevated in carriers compared with other family members.</p>
<p>Conclusions: The penetrance of the C3 R570Q mutation to induce aHUS is incomplete and lower compared with mutations in other genes predisposing to the disease. The mutation is possibly also associated with hypertension, hematuria and chronic kidney disease, all of which may represent consequences of long-term complement activation in the renal vasculature.</p>
]]></description>
<dc:creator><![CDATA[Lhotta, K., Janecke, A. R., Scheiring, J., Petzlberger, B., Giner, T., Fally, V., Wurzner, R., Zimmerhackl, L. B., Mayer, G., Fremeaux-Bacchi, V.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.06281208</dc:identifier>
<dc:title><![CDATA[A Large Family with a Gain-of-Function Mutation of Complement C3 Predisposing to Atypical Hemolytic Uremic Syndrome, Microhematuria, Hypertension and Chronic Renal Failure]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1362</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1356</prism:startingPage>
<prism:section>Hereditary Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1363?rss=1">
<title><![CDATA[Hypertension in Pediatric Long-term Hemodialysis Patients in the United States]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1363?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Data are limited regarding BP distribution and the prevalence of hypertension in pediatric long-term dialysis patients. This study aimed to examine BP distribution in U.S. pediatric long-term hemodialysis patients.</p>
<p>Design, setting, participants, &amp; measurements: This cross-sectional study of all U.S. pediatric (aged 0-&lt; 18 yr, n = 624) long-term hemodialysis patients was performed as part of the Centers for Medicare &amp; Medicaid Services End-Stage Renal Disease (ESRD) Clinical Performance Measures Project. BP and clinical information were collected monthly in October, November, and December 2001. Hypertension was defined as the mean of pre- and postdialysis systolic or diastolic BP above the 95th percentile for age, height, and sex, or antihypertensive medication use. Results were calculated by age, sex, race, ethnicity, ESRD duration, body mass index percentile, primary cause of ESRD, and laboratory data.</p>
<p>Results: Hypertension was present in 79% of patients; 62% used antihypertensive medication. Five percent of patients were prehypertensive (mean BP at 90th to 95th percentile). Hypertension was uncontrolled in 74% of treated patients. Characteristics associated with hypertension included acquired kidney disease, shorter duration of ESRD, and lower mean hemoglobin and calcium values. Characteristics associated with uncontrolled hypertension were younger age and shorter duration of ESRD.</p>
<p>Conclusions: Hypertension is common in U.S. pediatric long-term hemodialysis patients, uncontrolled in 74% of treated patients, and untreated in 21% of hypertensive patients. It is concluded that a more aggressive approach to treatment of hypertension is warranted in pediatric long-term hemodialysis patients.</p>
]]></description>
<dc:creator><![CDATA[Chavers, B. M., Solid, C. A., Daniels, F. X., Chen, S.-C., Collins, A. J., Frankenfield, D. L., Herzog, C. A.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01440209</dc:identifier>
<dc:title><![CDATA[Hypertension in Pediatric Long-term Hemodialysis Patients in the United States]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1369</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1363</prism:startingPage>
<prism:section>Hypertension</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1370?rss=1">
<title><![CDATA[Phosphorus and Potassium Content of Enhanced Meat and Poultry Products: Implications for Patients Who Receive Dialysis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1370?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Uncooked meat and poultry products are commonly enhanced by food processors using phosphate salts. The addition of potassium and phosphorus to these foods has been recognized but not quantified.</p>
<p>Design, setting, participants, &amp; measurements: We measured the phosphorus, potassium, and protein content of 36 uncooked meat and poultry products: Phosphorus using the Association of Analytical Communities (AOAC) official method 984.27, potassium using AOAC official method 985.01, and protein using AOAC official method 990.03.</p>
<p>Results: Products that reported the use of additives had an average phosphate-protein ratio 28% higher than additive free products; the content ranged up to almost 100% higher. Potassium content in foods with additives varied widely; additive free products all contained &lt;387 mg/100 g, whereas five of the 25 products with additives contained at least 692 mg/100 g (maximum 930 mg/100 g). Most but not all foods with phosphate and potassium additives reported the additives (unquantified) on the labeling; eight of 25 enhanced products did not list the additives. The results cannot be applied to other products. The composition of the food additives used by food processors may change over time.</p>
<p>Conclusions: Uncooked meat and poultry products that are enhanced may contain additives that increase phosphorus and potassium content by as much as almost two- and three-fold, respectively; this modification may not be discernible from inspection of the food label.</p>
]]></description>
<dc:creator><![CDATA[Sherman, R. A., Mehta, O.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02830409</dc:identifier>
<dc:title><![CDATA[Phosphorus and Potassium Content of Enhanced Meat and Poultry Products: Implications for Patients Who Receive Dialysis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1373</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1370</prism:startingPage>
<prism:section>Mineral Metabolism and Bone Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1374?rss=1">
<title><![CDATA[Calcium, Parathyroid Hormone, and Vitamin D: Major Determinants of Chronic Pain in Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1374?rss=1</link>
<description><![CDATA[
<p>Background and objectives: Pain is a frequent complaint of hemodialysis (HD) patients, yet information regarding its causes and frequency is relatively scarce. The aim of this study was to evaluate the frequency and possible causes of chronic pain in patients who are on long-term HD.</p>
<p>Design, setting, participants, &amp; measurements: We prospectively enrolled 100 patients who were undergoing maintenance HD for at least 3 mo. Pain was evaluated using the Brief Pain Inventory. Data collected on each participant included age, gender, ethnic origin, body mass index, smoking habits, time on dialysis, type of blood access, comorbidities, and biochemical and hematologic parameters.</p>
<p>Results: The average age was 64.5 yr; the average time on dialysis 40.4 mo. Forty-five patients were male. Thirty-one participants were of Arabic origin. Fifty-three patients had diabetes, 36 of whom had diabetic retinopathy. Although 51 patients experienced chronic pain, only 19.6% described the pain as severe. Musculoskeletal pain, neuropathic pain, and headache were the most prevalent forms of pain. The presence of diabetic retinopathy and neuropathy (but not diabetes <I>per se</I>) and levels of intact parathyroid hormone, calcium, and calcitriol (but not 25-hydroxyvitamin D<SUB>3</SUB>) differed significantly between those who experienced chronic pain and those who did not. On a logistic regression model, higher serum calcium levels and intact parathyroid hormone levels &gt;250 pg/ml were independently associated with chronic pain, as well as the presence of diabetic retinopathy. Calcitriol had a marginal effect.</p>
<p>Conclusions: Disturbed mineral metabolism is strongly associated with chronic pain in long-term HD patients, along with microangiopathy.</p>
]]></description>
<dc:creator><![CDATA[Golan, E., Haggiag, I., Os, P., Bernheim, J.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00680109</dc:identifier>
<dc:title><![CDATA[Calcium, Parathyroid Hormone, and Vitamin D: Major Determinants of Chronic Pain in Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1380</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1374</prism:startingPage>
<prism:section>Mineral Metabolism and Bone Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1381?rss=1">
<title><![CDATA[Prehypertension: Is It Relevant for Nephrologists?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1381?rss=1</link>
<description><![CDATA[
<p>Prehypertension has been proposed as the diagnosis for the presence of blood pressures &gt;120/80 mmHg but &lt;140/90 mmHg. It covers more than 60 million people in the United States and nephrologists will increasingly be involved with them. This review describes its relevance to nephrologists.</p>
]]></description>
<dc:creator><![CDATA[Kaplan, N. M.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02340409</dc:identifier>
<dc:title><![CDATA[Prehypertension: Is It Relevant for Nephrologists?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1383</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1381</prism:startingPage>
<prism:section>Special Feature</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1384?rss=1">
<title><![CDATA[Hepcidin for Clinicians]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1384?rss=1</link>
<description><![CDATA[
<p>Despite the use of erythropoiesis-stimulating agents (ESAs), the anemia of chronic kidney disease (CKD) can be resistant to therapy. Both absolute and functional iron deficiency along with inflammation can contribute to ESA resistance and can be difficult to identify with current-day markers of iron storage. Hepcidin, a small peptide produced by the liver, is a recently discovered key regulator of iron homeostasis. <I>Via</I> regulation of ferroportin, hepcidin inhibits intestinal iron absorption and iron release from macrophages and hepatocytes. Because of its renal elimination and regulation by inflammation, it is possible that progressive renal insufficiency leads to altered hepcidin metabolism, subsequently affecting enteric absorption of iron and the availability of iron stores. Thus, hepcidin likely plays a major role in the anemia of CKD as well as ESA resistance. This article discusses the biologic actions and regulation of hepcidin along with reviewing studies of hepcidin in CKD.</p>
]]></description>
<dc:creator><![CDATA[Young, B., Zaritsky, J.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02190309</dc:identifier>
<dc:title><![CDATA[Hepcidin for Clinicians]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1387</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1384</prism:startingPage>
<prism:section>Mini-Review</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/4/8/1388?rss=1">
<title><![CDATA[Staphylococcus aureus Infections in Hemodialysis: What a Nephrologist Should Know]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/4/8/1388?rss=1</link>
<description><![CDATA[
<p><I>Staphylococcus aureus</I> is a formidable pathogen that has the ability to colonize approximately half the dialysis population without any sign of disease but is also capable of causing wound and tissue infections; fulminant septicemia; and chronic, difficult-to-eradicate and often foreign body-related infections. <I>S. aureus</I> is the main cause of infectious morbidity and mortality in hemodialysis patients. This review highlights the importance of <I>S. aureus</I> infections in daily hemodialysis practice from a clinical viewpoint, starting from some key issues in the pathogenesis of staphylococcal infections.</p>
]]></description>
<dc:creator><![CDATA[Vandecasteele, S. J., Boelaert, J. R., De Vriese, A. S.]]></dc:creator>
<dc:date>Tue, 04 Aug 2009 10:02:00 PDT</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01590309</dc:identifier>
<dc:title><![CDATA[Staphylococcus aureus Infections in Hemodialysis: What a Nephrologist Should Know]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>8</prism:number>
<prism:volume>4</prism:volume>
<prism:endingPage>1400</prism:endingPage>
<prism:publicationDate>2009-08-01</prism:publicationDate>
<prism:startingPage>1388</prism:startingPage>
<prism:section>In-Depth Review</prism:section>
</item>

</rdf:RDF>