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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/CJN.01750408v1?rss=1">
<title><![CDATA[Academic Etiquette for the Nephrologist]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01750408v1?rss=1</link>
<description><![CDATA[
<p>
<P>Academic etiquette is an underexplored and underemphasized topic. Yet, a collegial atmosphere is essential to accomplish the missions of an academic medical center. Appropriate social, personal, and cultural behaviors are not only desirable, but they are also necessary to practice and emulate. As faculty in an academic center, one may want to share these thoughts with peers, students, and other healthcare providers. As a trainee, one may want dedicated lectures on this topic and to observe the behaviors modeled by mentors. This article attempts to outline principles of appropriate etiquette in the academic workplace. These include issues of loyalty, collegiality, and collaboration in daily activities from research to clinical care. Approaching personal interactions with grace and integrity can be an essential tool in the pursuit of academic excellence and success.</P>

]]></description>
<dc:creator><![CDATA[Watnick, S.]]></dc:creator>
<dc:date>2008-08-20</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01750408</dc:identifier>
<dc:title><![CDATA[Academic Etiquette for the Nephrologist]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-20</prism:publicationDate>
<prism:section>MOVING POINTS IN NEPHROLOGY</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.03250708v1?rss=1">
<title><![CDATA[Arterial Intima and Media Calcification: Distinct Entities with Different Pathogenesis or All the Same?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.03250708v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Drueke, T. B.]]></dc:creator>
<dc:date>2008-08-13</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03250708</dc:identifier>
<dc:title><![CDATA[Arterial Intima and Media Calcification: Distinct Entities with Different Pathogenesis or All the Same?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-13</prism:publicationDate>
<prism:section>CONTROVERSIES IN NEPHROLOGY</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.02940608v1?rss=1">
<title><![CDATA[Oxalate Nephropathy Complicating Roux-en-Y Gastric Bypass: An Underrecognized Cause of Irreversible Renal Failure]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.02940608v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: The most common bariatric surgery is Roux-en-Y gastric bypass (RYGB), which has been associated with hyperoxaluria and nephrolithiasis. We report a novel association of RYGB with renal insufficiency as a result of oxalate nephropathy.</P>
<P>Design, setting, participants, &amp; measurements: Eleven cases of oxalate nephropathy after RYGB were identified from the Renal Pathology Laboratory of Columbia University. The clinical features, pathologic findings, and outcomes are described.</P>
<P>Results: Patients were predominantly white (72.7%) with a mean age of 61.3 yr. Indications for RYGB included morbid obesity (eight patients) and reconstruction after total gastrectomy for gastric cancer (three patients). All 11 patients had a history of hypertension, and 9 were diabetic. Patients presented with acute renal failure, often superimposed on mild chronic renal insufficiency (<I>n</I> = 7), at a median of 12 mo after RYGB. The mean creatinine at baseline, at discovery of acute renal failure, and at biopsy was 1.5, 5.0, and 6.5 mg/dl, respectively. Renal biopsies revealed diffuse tubular degenerative changes, abundant tubular calcium oxalate deposits, and varying degrees of tubulointerstitial scarring. In addition, seven biopsies had underlying diabetic glomerulosclerosis and two had glomerulosclerosis attributable to obesity and hypertension. Eight of 11 patients rapidly progressed to ESRD and required hemodialysis at a mean of 3.2 wk after renal biopsy. The remaining three patients were left with significant chronic kidney disease.</P>
<P>Conclusions: Oxalate nephropathy is an underrecognized complication of RYGB and typically results in rapid progression to ESRD. Patients with pre-existing renal disease may be at higher risk for this complication.</P>

]]></description>
<dc:creator><![CDATA[Nasr, S. H., D'Agati, V. D., Said, S. M., Stokes, M. B., Largoza, M. V., Radhakrishnan, J., Markowitz, G. S.]]></dc:creator>
<dc:date>2008-08-13</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02940608</dc:identifier>
<dc:title><![CDATA[Oxalate Nephropathy Complicating Roux-en-Y Gastric Bypass: An Underrecognized Cause of Irreversible Renal Failure]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-13</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01760408v1?rss=1">
<title><![CDATA[Ratio of Paricalcitol Dosage to Serum Parathyroid Hormone Level and Survival in Maintenance Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01760408v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: Several observational studies have indicated that vitamin D receptor activators (VDRA), including paricalcitol, are associated with greater survival in maintenance hemodialysis (MHD) patients; however, patients with higher serum parathyroid hormone (PTH), indicative of a more severe secondary hyperparathyroidism and higher death risk, are usually given higher VDRA dosages, which can lead to confounding by medical indication and attenuated survival advantage of high VDRA dosages. It was hypothesized that the ratio of the administered paricalcitol dosage to serum PTH level discloses better the underlying dosage&ndash;survival association.</P>
<P>Design, setting, participants, &amp; measurements: The 3-yr mortality predictability of the administered paricalcitol during the first 3 mo of the cohort divided by averaged serum intact PTH during the same period was examined in 34,307 MHD patients from all DaVita dialysis clinics across the United States using Cox regression.</P>
<P>Results: MHD patients were 60.8 &plusmn; 15.4 yr of age and included 47% women, 34% black patients, and 47% patients with diabetes. Initially, the ratio of paricalcitol (&micro;g/wk) to PTH (pg/ml) was divided into four groups: 0 (reference), 1 to &lt;30, 30 to &lt;60, and &gt;60 x 10<SUP>-3</SUP>. Unadjusted, case mix&ndash;adjusted (demographics, comorbidity, and Kt/V), and malnutrition-inflammation complex syndrome&ndash;adjusted models, the death rate ratio for the paricalcitol/PTH index groups, were 0.99, 0.95, and 0.92. Restricted cubic splines analyses were consistent with a linear relation.</P>
<P>Conclusions: Higher weekly paricalcitol dosage per each unit of serum PTH seems to have an incremental association with greater survival in MHD patients. The observed dosage-response phenomenon needs to be confirmed in clinical trials.</P>

]]></description>
<dc:creator><![CDATA[Shinaberger, C. S., Kopple, J. D., Kovesdy, C. P., McAllister, C. J., van Wyck, D., Greenland, S., Kalantar-Zadeh, K.]]></dc:creator>
<dc:date>2008-08-13</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01760408</dc:identifier>
<dc:title><![CDATA[Ratio of Paricalcitol Dosage to Serum Parathyroid Hormone Level and Survival in Maintenance Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-13</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.02080508v1?rss=1">
<title><![CDATA[The Agony of Ecstasy: MDMA (3,4-Methylenedioxymethamphetamine) and the Kidney]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.02080508v1?rss=1</link>
<description><![CDATA[
<p>
<P>Ecstasy (MDMA, 3,4-methylenedioxymethamphetamine) is commonly used by college-aged individuals. Ecstasy leads to feelings of euphoria, emotional empathy, and increased energy. These effects come at a significant risk for complications. Ecstasy has been associated with acute kidney injury that is most commonly secondary to nontraumatic rhabdomyolysis but also has been reported in the setting of drug-induced liver failure and drug-induced vasculitis. More common, ecstasy has led to serious hyponatremia and hyponatremia-associated deaths. Hyponatremia in these cases is due to a "perfect storm" of ecstasy-induced effects on water balance. Ecstasy leads to secretion of arginine vasopressin as well as polydipsia as a result of its effects on the serotonergic nervous pathways. Compounding these effects are the ready availability of fluids and the recommendation to drink copiously at rave parties where ecstasy is used. The effects of ecstasy on the kidney as well as therapeutic measures for the treatment of ecstasy-induced hyponatremia are presented.</P>

]]></description>
<dc:creator><![CDATA[Campbell, G. A., Rosner, M. H.]]></dc:creator>
<dc:date>2008-08-06</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02080508</dc:identifier>
<dc:title><![CDATA[The Agony of Ecstasy: MDMA (3,4-Methylenedioxymethamphetamine) and the Kidney]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-06</prism:publicationDate>
<prism:section>IN-DEPTH REVIEWS</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01730408v1?rss=1">
<title><![CDATA[Effects of Rituximab on Morphofunctional Abnormalities of Membranous Glomerulopathy]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01730408v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: In idiopathic membranous nephropathy (IMN), CD<SUB>20</SUB> B-cell depletion by rituximab may induce nephrotic syndrome (NS) remission. Whether this is associated with kidney function restoration and regression of the glomerular pathology was evaluated.</P>
<P>Design, setting, participants, &amp; measurements: Treatment-induced morphofunctional changes were evaluated in 7 IMN patients consenting to repeat functional and morphologic evaluations after stable disease remission achieved by four weekly rituximab (375 mg/m<SUP>2</SUP>) infusions.</P>
<P>Results: Over a median of 21 mo from rituximab administration, NS remission was associated with 8.5-fold increase <I>versus</I> baseline in sodium fractional clearance from 1.56 to 13.25, decrease in renal plasma flow from 440.8 to 276.6 ml/min per 1.73 m<SUP>2</SUP>, stable glomerular filtration rate, and increased renal vascular resistances. Changes in sodium fractional clearance and hemoglobin concentration were positively correlated (<I>r</I> = 0.82). Biopsy reevaluations showed complete or partial reabsorption of subepithelial deposits. Median (interquartile range) IgG4 staining score decreased from 3 (3&ndash;3) to 1 (0&ndash;2), whereas total numbers of slit diaphragms (0.27; range, 0.19 to 0.30 <I>versus</I> 0.86; range, 0.53 to 1.16 slits/&micro;m glomerular basement membrane) and percentages of those with electron-dense diaphragm (55.2; range, 42.0 to 62.0 <I>versus</I> 78.5; range, 73.0 to 82.7 of all slits) significantly increased in parallel with amelioration of glomerular ultrastructural changes. Changes in slit frequency and albumin fractional clearance were negatively correlated (r = -0.79).</P>
<P>Conclusions: In human IMN, treatment-induced NS remission is associated with restoration of sodium homeostasis and kidney hemodynamics, and regression of the glomerular changes underlying proteinuria. These effects are likely to translate into long-term renoprotection.</P>

]]></description>
<dc:creator><![CDATA[Ruggenenti, P., Cravedi, P., Sghirlanzoni, M. C., Gagliardini, E., Conti, S., Gaspari, F., Marchetti, G., Abbate, M., Remuzzi, G.]]></dc:creator>
<dc:date>2008-08-06</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01730408</dc:identifier>
<dc:title><![CDATA[Effects of Rituximab on Morphofunctional Abnormalities of Membranous Glomerulopathy]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-06</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01120308v1?rss=1">
<title><![CDATA[Course of Depression and Anxiety Diagnosis in Patients Treated with Hemodialysis: A 16-month Follow-up]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01120308v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: There is growing identification of the need to seriously study the psychiatric presentations of end-stage renal disease patients treated with hemodialysis. This study reports on the course of depression and anxiety diagnoses and their impact on quality of life and health status.</P>
<P>Design, setting, participants, &amp; measurements: The 16-mo course of psychiatric diagnoses in 50 end-stage renal disease patients treated with hemodialysis was measured by structured clinical interview.</P>
<P>Results: Three different pathways were identified: one subset of patients not having a psychiatric diagnosis at either baseline or 16-mo follow-up (68% for depression, 51% for anxiety), one group having an intermittent course (21% for depression, 34% for anxiety), and one group having a persistent course (11% for depression, 15% for anxiety), with diagnoses at both time 1 and time 2. For depression, the people with the persistent course showed marked decreases in quality of life and self-reported health status compared with the nondepressed and intermittently depressed cohorts. The most powerful predictor of depression at time 2 is degree of depressive affect at time 1(<I>P</I> &lt; 0.05).</P>
<P>Conclusions: Patients at risk for short- and long-term complications of depression can be potentially identified by high levels of depressive affect even at a single time point. As nearly 20% of the sample had chronic depression or anxiety, identifying a psychiatric diagnosis in hemodialysis patients and then offering treatment are important because, in the absence of intervention, psychiatric disorders are likely to persist in a substantial proportion of patients.</P>

]]></description>
<dc:creator><![CDATA[Cukor, D., Coplan, J., Brown, C., Peterson, R. A., Kimmel, P. L.]]></dc:creator>
<dc:date>2008-08-06</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01120308</dc:identifier>
<dc:title><![CDATA[Course of Depression and Anxiety Diagnosis in Patients Treated with Hemodialysis: A 16-month Follow-up]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-08-06</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.02110508v1?rss=1">
<title><![CDATA[Academic Internal Medicine in the United States: Current Trends, Future Implications for Academic Nephrology]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.02110508v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ibrahim, T.]]></dc:creator>
<dc:date>2008-07-30</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02110508</dc:identifier>
<dc:title><![CDATA[Academic Internal Medicine in the United States: Current Trends, Future Implications for Academic Nephrology]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-30</prism:publicationDate>
<prism:section>MOVING POINTS IN NEPHROLOGY&amp;gt;</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01930408v1?rss=1">
<title><![CDATA[Accelerated Atherosclerotic Calcification and Monckeberg's Sclerosis: A Continuum of Advanced Vascular Pathology in Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01930408v1?rss=1</link>
<description><![CDATA[
<p>
<P>Autopsy studies have demonstrated the near universal presence of fatty streaks and fibroatheromas in the general population from which patients with chronic kidney disease (CKD) arise. The vast majority of patients with CKD have multiple conventional cardiovascular risk factors. Vascular atherosclerotic calcification develops in most patients as they transition from the general population to significant CKD as part of cholesterol crystallization within atherosclerotic lesions. Once present, however, atherosclerotic medial calcification can become prominent and has been previously identified as M&ouml;nckeberg&rsquo;s sclerosis. A unifying concept supported by the preponderance of pathologic evidence contends that M&ouml;nckeberg&rsquo;s sclerosis is a manifestation of accelerated atherosclerosis in patients with CKD. The term has also been used in rare cases to describe vascular calcinosis not related to CKD. This clarification is critical to advance the field in terms of pathologic diagnosis and treatment of CKD bone and mineral disorder. Factors that seem to promote the osteoblastic transformation of vascular smooth muscle cells and enhance deposition of calcium hydroxyapatite crystals include phosphorus activation of the Pit-1 receptor, bone morphogenic proteins 2 and 4, leptin, endogenous 1,25 dihydroxyvitamin D, vascular calcification activating factor, and measures of oxidative stress. These entities work to accelerate the atherosclerotic process in patients with CKD and may be future targets for diagnosis and treatment because randomized trials with hydroxymethylglutaryl-CoA reductase inhibitors have failed to attenuate the rate of progressive vascular calcification.</P>

]]></description>
<dc:creator><![CDATA[McCullough, P. A., Agrawal, V., Danielewicz, E., Abela, G. S.]]></dc:creator>
<dc:date>2008-07-30</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01930408</dc:identifier>
<dc:title><![CDATA[Accelerated Atherosclerotic Calcification and Monckeberg's Sclerosis: A Continuum of Advanced Vascular Pathology in Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-30</prism:publicationDate>
<prism:section>CONTROVERSIES IN NEPHROLOGY</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01820408v1?rss=1">
<title><![CDATA[Assessing the Validity of an Abdominal CT Scoring System in the Diagnosis of Encapsulating Peritoneal Sclerosis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01820408v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: Encapsulating peritoneal sclerosis (EPS) is a severe peritoneal fibrotic reaction in patients on long-term peritoneal dialysis (PD). The early clinical features may be nonspecific. The purpose of the study is to assess the reliability and diagnostic utility of abdominal CT scanning in the diagnosis of EPS.</P>
<P>Design, setting, participants, &amp; measurements: Abdominopelvic CT scans of 27 patients diagnosed with EPS on clinical and radiologic grounds in our unit from 1997 to 2006 were retrospectively analyzed. In addition, 35 control CT scans were scored: 15 from hemodialysis patients (HD controls) and 20 from patients on PD (PD controls). Scans were anonymized and scored independently by three radiologists.</P>
<P>Results: Inter-rater agreement was moderate to very good (kappa = 0.40 to 0.75) for peritoneal calcification, bowel distribution, bowel wall thickening, and bowel dilation but poorer for loculation of ascites and peritoneal thickening. There was a strongly significant difference between the total CT scan scores at EPS diagnosis and controls (<I>P</I> &lt; 0.00001). Each individual parameter also showed significant differences between EPS and controls (<I>P</I> &lt; 0.006). Bowel tethering and peritoneal calcification were the most specific parameters, and. loculation was the least discriminatory parameter. Interestingly, prediagnostic scans a median of 1.5 yr before EPS diagnosis were normal or near-normal in 9 of 13 EPS patients.</P>
<P>Conclusions: CT scanning is a valid and reliable adjunct to the diagnosis of EPS but may not be useful as a screening tool, as the prediagnostic scans did not show abnormalities in many patients who subsequently developed EPS.</P>

]]></description>
<dc:creator><![CDATA[Tarzi, R. M., Lim, A., Moser, S., Ahmad, S., George, A., Balasubramaniam, G., Clutterbuck, E. J., Gedroyc, W., Brown, E. A.]]></dc:creator>
<dc:date>2008-07-30</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01820408</dc:identifier>
<dc:title><![CDATA[Assessing the Validity of an Abdominal CT Scoring System in the Diagnosis of Encapsulating Peritoneal Sclerosis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-30</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01560408v1?rss=1">
<title><![CDATA[N-Acetylcysteine Effect on Serum Creatinine and Cystatin C Levels in CKD Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01560408v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: N-acetylcysteine (NAC) has been widely used as a prophylactic therapy for contrast-induced nephropathy (CIN). Its efficacy is controversial because of heterogeneity in study results and because of evidence that NAC can alter serum creatinine levels without affecting glomerular filtration rate. This confounding effect of N-acetylcysteine on serum creatinine has not been rigorously tested, however, in a population at risk for CIN and following doses of NAC currently recommended for prophylaxis of CIN.</P>
<P>Design, setting, participants, &amp; measurements: "Double-dose" NAC was administered in the absence of iodinated contrast media to 29 stage 3 to 5 stable chronic kidney disease patients. Serum creatinine and cystatin C were measured before and 4 h and 48 h after the last dose of NAC.</P>
<P>Results: There was no effect of NAC on either serum creatinine or cystatin C levels.</P>
<P>Conclusion: NAC, in doses currently recommended for prophylaxis of CIN, has no effect on serum creatinine or cystatin C levels. It is therefore unlikely that the heterogeneity seen in clinical trials of NAC prophylaxis for CIN is related to a confounding effect on serum creatinine.</P>

]]></description>
<dc:creator><![CDATA[Rehman, T., Fought, J., Solomon, R.]]></dc:creator>
<dc:date>2008-07-30</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01560408</dc:identifier>
<dc:title><![CDATA[N-Acetylcysteine Effect on Serum Creatinine and Cystatin C Levels in CKD Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-30</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.05691207v1?rss=1">
<title><![CDATA[Aggressive Immunosuppression Minimization Reduces Graft Loss Following Diagnosis of BK Virus-Associated Nephropathy: A Comparison of Two Reduction Strategies]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.05691207v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and Objectives: BK virus-associated nephropathy (BKVAN) has emerged as a leading cause of kidney graft loss, with no known predictors for graft loss and no consensus regarding treatment other than reduction of immunosuppression.</P>
<P>Design, setting, participants and measurements: A single-center retrospective analysis was performed of all cases of BKVAN from 1999 to 2005 for clinical predictors of graft loss, with evaluation of the impact of immunosuppression withdrawal (3-drug to 2-drug immunosuppression) within the first month <I>versus</I> reduction of immunosuppression.</P>
<P>Results: Of 910 kidney transplants, 35 (3.8%) cases of BKVAN were diagnosed at a median of 15 months after transplant (range, 5.5 to 90 months after transplant), 16 (46%) of which progressed to graft failure at a median of 11 months (range, 2 to 36 months) after diagnosis. Depleting antibody induction was a significant risk factor for graft loss on univariate analysis, whereas early drug withdrawal (&lt;1 mo following diagnosis) protected against graft loss. On multivariate analysis, these findings were independent predictors of graft outcomes. Additionally, when patients were comanaged by referring nephrologists and the transplant center before the diagnosis of BKVAN, the risk of graft loss was 11-fold higher (<I>P</I> = 0.03) than if patients were managed solely by the transplant center.</P>
<P>Conclusions: Increased awareness and early diagnosis of BKVAN, with aggressive tapering of immunosuppression once established, is critical to preserve kidney graft function. Early drug withdrawal to low-dose two-drug therapy maintenance may be preferable to a general reduction of agents.</P>

]]></description>
<dc:creator><![CDATA[Weiss, A. S., Gralla, J., Chan, L., Klem, P., Wiseman, A. C.]]></dc:creator>
<dc:date>2008-07-23</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05691207</dc:identifier>
<dc:title><![CDATA[Aggressive Immunosuppression Minimization Reduces Graft Loss Following Diagnosis of BK Virus-Associated Nephropathy: A Comparison of Two Reduction Strategies]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-23</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.01400308v1?rss=1">
<title><![CDATA[Renal Transplantation Is Not Associated with Regression of Left Ventricular Hypertrophy: A Magnetic Resonance Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.01400308v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: Patients with end-stage renal failure (ESRD) have an increased risk of premature cardiovascular (CV) disease. Left ventricular hypertrophy is an independent risk factor for CV events and death in ESRD. Renal transplantation has been associated with reduction in CV risk and echocardiographic regression of left ventricular hypertrophy. However, echocardiography overestimates LV mass in ESRD patients. Cardiac magnetic resonance (CMR) provides more detailed, volume-independent, measures of cardiac structure. Changes in LV mass measured by CMR after renal transplantation were studied.</P>
<P>Design, setting, participants, &amp; measurements: Fifty patients underwent CMR on two occasions. Twenty-five were transplanted before the second scan. CMR was performed to measure LV mass index (LVMI), ejection fraction, end-diastolic and end-systolic volumes. Changes were expressed as percentage change over time. Patients with CV events between scans (<I>e.g.</I>, acute coronary syndrome, myocardial infarction) were excluded. All transplant patients had serum creatinine &lt;150 &micro;mol/L.</P>
<P>Results: There was no significant change in LVMI between patients who underwent renal transplantation and those who remained on dialysis (transplanted mean, 2.75%/yr, &plusmn; 9.1 <I>versus</I> dialysis, -3.6%/yr &plusmn; 16.7). In addition, there were no significant changes in end-diastolic volume (transplant, 0.1%/yr &plusmn; 19.5 <I>versus</I> not transplanted, -3.4%/yr &plusmn; 31.5), end-systolic volume (transplanted mean, 15.2%/yr &plusmn; 65.2 <I>versus</I> not transplanted, 3.0%/yr &plusmn; 55.5), or ejection fraction (transplant, 2.1%/yr &plusmn; 11.9 <I>versus</I> not transplanted, -0.4%/yr &plusmn; 5.3).</P>
<P>Conclusions: Renal transplantation is not associated with significant regression of LVMI on CMR compared with patients who remain on the transplant waiting list.</P>

]]></description>
<dc:creator><![CDATA[Patel, R. K., Mark, P. B., Johnston, N., McGregor, E., Dargie, H. J., Jardine, A. G.]]></dc:creator>
<dc:date>2008-07-23</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01400308</dc:identifier>
<dc:title><![CDATA[Renal Transplantation Is Not Associated with Regression of Left Ventricular Hypertrophy: A Magnetic Resonance Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-23</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.00830208v1?rss=1">
<title><![CDATA[Clinicopathologic Correlation and Outcome of C1q Nephropathy]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.00830208v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: The number of patients with C1q nephropathy (C1qN) in previous reports is small and the duration of follow-up is short. Our study describes the clinicopathologic correlation and clinical outcome through the mean follow-up period of 7.2 yr in 61 patients.</P>
<P>Design, settings, participants, &amp; measurements: Sixty-one patients, 1 to 67 yr of age, with C1qN were enrolled in this study.</P>
<P>Results: According to presentation at onset, patients were divided into two groups: asymptomatic urinary abnormalities (asymptomatic) (<I>n</I> = 36) and nephrotic syndrome (NS) (<I>n</I> = 25). Light microscopy showed minimal change disease (MCD) in 46 patients (75%), mesangial proliferative glomerulonephritis in 7 (12%), and focal segmental glomerulosclerosis (FSGS) in 8 (13%). The prevalence of MCD was higher in the NS group than in the asymptomatic group. Nine patients in the asymptomatic group and all patients in the NS group were treated with prednisolone and/or cyclosporine. Normal urinalysis was found in 10 patients in asymptomatic group and 8 in NS group during the follow-up. Thirteen patients in the NS group were frequent relapsers at the latest follow-up. Three patients with FSGS developed chronic renal failure 8 to 15 yr after the diagnosis. C1q deposits disappeared in 3 of 8 patients receiving repeat biopsy, and 2 of these 3 showed FSGS.</P>
<P>Conclusions: The prognosis of C1qN is good, associated with MCD in a large number. In some patients, C1q deposits disappear through the follow-up period. FSGS may develop in some patients on repeat biopsies. Further investigation is critically needed to settle this issue.</P>

]]></description>
<dc:creator><![CDATA[Hisano, S., Fukuma, Y., Segawa, Y., Niimi, K., Kaku, Y., Hatae, K., Saitoh, T., Takeshita, M., Iwasaki, H.]]></dc:creator>
<dc:date>2008-07-23</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00830208</dc:identifier>
<dc:title><![CDATA[Clinicopathologic Correlation and Outcome of C1q Nephropathy]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-23</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.00850208v1?rss=1">
<title><![CDATA[Natriuretic Peptides in Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.00850208v1?rss=1</link>
<description><![CDATA[
<p>
<P>Background and objectives: B-type natriuretic peptide (BNP) and amino-terminal pro-B-type natriuretic peptide (NT-proBNP) are biomarkers of cardiovascular disease that is common in patients with chronic kidney disease (CKD). Conflicting data on the influence of glomerular filtration rate (GFR) on BNP and NT-proBNP levels in CKD may stem from failure to account fully for the effects of coexistent cardiac disease, dysfunction, and volume overload.</P>
<P>Design, setting, participants, &amp; measurements: Prospective head-to-head comparison of plasma BNP and NT-proBNP in ambulatory euvolemic CKD patients with normal LV ejection fraction and no manifest cardiac or vascular disease. GFR was estimated by the Modification of Diet in Renal Disease formula, BNP and NT-proBNP measured using Abbott AxSYM and Roche Elecsys assays, respectively, and cardiac morphology and function assessed by transthoracic echocardiography.</P>
<P>Results: In 142 patients (42% female) of mean age 60 &plusmn; 11 yr, mean left ventricular ejection fraction was 71% &plusmn; 6%, GFR 38 &plusmn; 14 ml/min per 1.73 m<SUP>2</SUP>, and median BNP and NT-proBNP level 59 and 311 pg/ml, respectively. Multivariate predictors of NT-proBNP level were GFR, &beta;-blocker usage, LV mass index, and hemoglobin level. Plasma BNP was independently predicted by LV mass index and &beta;-blocker usage but not GFR. In the 74 patients without diastolic dysfunction, there was a significant rise in NT-proBNP but not BNP as GFR declined.</P>
<P>Conclusions: Unlike NT-proBNP, plasma BNP level is relatively independent of GFR. BNP may therefore be the more appropriate biomarker to screen for cardiac dysfunction in CKD.</P>

]]></description>
<dc:creator><![CDATA[Tagore, R., Ling, L. H., Yang, H., Daw, H.-Y., Chan, Y.-H., Sethi, S. K.]]></dc:creator>
<dc:date>2008-07-16</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00850208</dc:identifier>
<dc:title><![CDATA[Natriuretic Peptides in Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-07-16</prism:publicationDate>
<prism:section>ORIGINAL ARTICLES</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.05791207v1?rss=1">
<title><![CDATA[The Afterlife for Retiring Deans and Other Senior Medical Administrators]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.05791207v1?rss=1</link>
<description><![CDATA[
<p>
<P>Career options for individuals leaving the administrative role as dean of a school of medicine or other senior administrative positions are considered. Options discussed include retirement and a variety of other positions both within schools of medicines and in other venues. Many opportunities exist for a challenging and fulfilling career path after leaving the role as a senior administrator in an academic medical center.</P>

]]></description>
<dc:creator><![CDATA[Tannen, R. L.]]></dc:creator>
<dc:date>2008-03-05</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05791207</dc:identifier>
<dc:title><![CDATA[The Afterlife for Retiring Deans and Other Senior Medical Administrators]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-03-05</prism:publicationDate>
<prism:section>MOVING POINTS IN NEPHROLOGY</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/CJN.03900907v1?rss=1">
<title><![CDATA[New Challenges and Paradigms for Mid-Career Faculty in Academic Medical Centers: Key Strategies for Success for Mid-Career Medical School Faculty]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/CJN.03900907v1?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Golper, T. A., Feldman, H. I.]]></dc:creator>
<dc:date>2008-03-05</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03900907</dc:identifier>
<dc:title><![CDATA[New Challenges and Paradigms for Mid-Career Faculty in Academic Medical Centers: Key Strategies for Success for Mid-Career Medical School Faculty]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:publicationDate>2008-03-05</prism:publicationDate>
<prism:section>MOVING POINTS IN NEPHROLOGY</prism:section>
</item>

</rdf:RDF>