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<title>Clinical Journal of the American Society of Nephrology</title>
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<title><![CDATA[The Declaration of Istanbul on Organ Trafficking and Transplant Tourism]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1227?rss=1</link>
<description><![CDATA[
<P><I>Organ commercialism, which targets vulnerable populations (such as illiterate and impoverished persons, undocumented immigrants, prisoners, and political or economic refugees) in resource-poor countries, has been condemned by international bodies such as the World Health Organization for decades. Yet in recent years, as a consequence of the increasing ease of Internet communication and the willingness of patients in rich countries to travel and purchase organs, organ trafficking and transplant tourism have grown into global problems. For example, as of 2006, foreigners received two-thirds of the 2000 kidney transplants performed annually in Pakistan</I>.</P>
<P><I>The</I> Istanbul Declaration <I>proclaims that the poor who sell their organs are being exploited, whether by richer people within their own countries or by transplant tourists from abroad. Moreover, transplant tourists risk physical harm by unregulated and illegal transplantation. Participants in the Istanbul Summit concluded that transplant commercialism, which targets the vulnerable, transplant tourism, and organ trafficking should be prohibited. And they also urged their fellow transplant professionals, individually and through their organizations, to put an end to these unethical activities and foster safe, accountable practices that meet the needs of transplant recipients while protecting donors</I>.</P>
<P><I>Countries from which transplant tourists originate, as well as those to which they travel to obtain transplants, are just beginning to address their respective responsibilities to protect their people from exploitation and to develop national self-sufficiency in organ donation. The</I> Declaration <I>should reinforce the resolve of governments and international organizations to develop laws and guidelines to bring an end to wrongful practices. "The legacy of transplantation is threatened by organ trafficking and transplant tourism. The</I> Declaration of Istanbul <I>aims to combat these activities and to preserve the nobility of organ donation. The success of transplantation as a life-saving treatment does not require&mdash;nor justify&mdash;victimizing the world's poor as the source of organs for the rich" (Steering Committee of the Istanbul Summit)</I>.</P>
]]></description>
<dc:creator><![CDATA[Participants in the International Summit on Transplant Tourism and Organ Trafficking Convened by The Transplantation Society and International Society of Nephrology in Istanbul, Turkey, April 30 through May 2, 2008]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03320708</dc:identifier>
<dc:title><![CDATA[The Declaration of Istanbul on Organ Trafficking and Transplant Tourism]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1231</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1227</prism:startingPage>
<prism:section>Special Articles</prism:section>
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<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1232?rss=1">
<title><![CDATA[Pulmonary Hypertension, Right Ventricular Failure, and Kidney: Different from Left Ventricular Failure?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1232?rss=1</link>
<description><![CDATA[
<P>In this article, the pathophysiology of left ventricular failure is reviewed. By contrast, the paucity of information about pulmonary arterial hypertension and right ventricular failure is acknowledged. The potential mechanisms whereby renal sodium and water retention in right ventricular failure secondary to pulmonary arterial hypertension can occur, despite normal left ventricular function, are discussed. With right ventricular failure as the primary cause of death in patients with pulmonary hypertension, more information about the mechanisms of renal sodium and water retention in these patients is direly needed. Specifically, studies to examine the activation of the neurohumoral axis at various stages of pulmonary arterial hypertension and right ventricular failure, including inhibition of mineralocorticoid and V2 vasopressin receptors, are indicated.</P>
]]></description>
<dc:creator><![CDATA[Schrier, R. W., Bansal, S.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01960408</dc:identifier>
<dc:title><![CDATA[Pulmonary Hypertension, Right Ventricular Failure, and Kidney: Different from Left Ventricular Failure?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1237</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1232</prism:startingPage>
<prism:section>Special Articles</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1238?rss=1">
<title><![CDATA[Helping Nephrologists Become Lifelong Learners]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1238?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Falk, R. J., Rosenberg, M. E., Yee, J., Murray, P. T., Ibrahim, T.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02980608</dc:identifier>
<dc:title><![CDATA[Helping Nephrologists Become Lifelong Learners]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1241</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1238</prism:startingPage>
<prism:section>Special Articles</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1242?rss=1">
<title><![CDATA[Contrast-Induced Acute Kidney Injury: Is There a Risk after Intravenous Contrast?]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1242?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Solomon, R.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03470708</dc:identifier>
<dc:title><![CDATA[Contrast-Induced Acute Kidney Injury: Is There a Risk after Intravenous Contrast?]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1243</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1242</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1244?rss=1">
<title><![CDATA[Fanconi or not Fanconi? Lowe Syndrome Revisited]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1244?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Kleta, R.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02880608</dc:identifier>
<dc:title><![CDATA[Fanconi or not Fanconi? Lowe Syndrome Revisited]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1245</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1244</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1246?rss=1">
<title><![CDATA[Interpreting Results of Clinical Trials: A Conceptual Framework]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1246?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Singh, A. K., Kelley, K., Agarwal, R.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03580807</dc:identifier>
<dc:title><![CDATA[Interpreting Results of Clinical Trials: A Conceptual Framework]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1252</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1246</prism:startingPage>
<prism:section>Editorials</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1253?rss=1">
<title><![CDATA[Nephrology Potpourri]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1253?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Ritz, E.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.03500708</dc:identifier>
<dc:title><![CDATA[Nephrology Potpourri]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1259</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1253</prism:startingPage>
<prism:section>Presse R&amp;eacute;nale</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1260?rss=1">
<title><![CDATA[Predicting Acute Renal Failure after Cardiac Surgery: External Validation of Two New Clinical Scores]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1260?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Different scores to predict acute kidney injury after cardiac surgery have been developed recently. The purpose of this study was to validate externally two clinical scores developed at Cleveland and Toronto.</P>
<P>Design, setting, participants, &amp; measurements: A retrospective analysis was conducted of a prospectively maintained database of all cardiac surgeries performed during a 5-yr period (2002 to 2006) at a University Hospital in Madrid, Spain. Acute kidney injury was defined as the need for renal replacement therapy. For evaluation of the performance of both models, discrimination and calibration were measured.</P>
<P>Results: Frequency of acute kidney injury after cardiac surgery was 3.7% in the cohort used to validate the Cleveland score and 3.8% in the cohort used to validate the Toronto score. Discrimination of both models was excellent, with values for the areas under the receiving operator characteristics curves of 0.86 (95% confidence interval 0.81 to 0.9) and 0.82 (95% confidence interval 0.76 to 0.87), respectively. Calibration was poor, with underestimation of the risk for acute kidney injury except for patients within the very-low-risk category. The performance of both models clearly improved after recalibration.</P>
<P>Conclusions: Both models were found to be very useful to discriminate between patients who will and will not develop acute kidney injury after cardiac surgery; however, before using the scores to estimate risk probabilities at a specific center, recalibration may be needed.</P>
]]></description>
<dc:creator><![CDATA[Candela-Toha, A., Elias-Martin, E., Abraira, V., Tenorio, M. T., Parise, D., de Pablo, A., Centella, T., Liano, F.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00560208</dc:identifier>
<dc:title><![CDATA[Predicting Acute Renal Failure after Cardiac Surgery: External Validation of Two New Clinical Scores]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1265</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1260</prism:startingPage>
<prism:section>Acute Renal Failure</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1266?rss=1">
<title><![CDATA[Preoperative Use of Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers Is Associated with Increased Risk for Acute Kidney Injury after Cardiovascular Surgery]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1266?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Acute kidney injury (AKI) occurs commonly after cardiac surgery. Most patients who undergo cardiac surgery receive long-term treatment with angiotensin-converting enzyme inhibitors (ACEI) or angiotensin II receptor blockers (ARB). The aim of this study was to determine whether long-term use of ACEI/ARB is associated with an increased incidence of AKI after cardiac surgery.</P>
<P>Design, setting, participants, &amp; measurements: This was a retrospective cohort study of 1358 adult patients who underwent cardiac surgery between January 1, 2001, and December 31, 2005, in two tertiary care hospitals in Buffalo, NY. The incidence of AKI was determined after cardiac surgery. Clinical data were collected using a standardized form that included comorbid condition, use of ACEI/ARB, and intraoperative and postoperative complications.</P>
<P>Results: Overall, 40.2% of patients developed AKI. Preoperative variables that were significantly associated with development of AKI included increasing age; nonwhite race; combined valve surgery and coronary artery bypass grafting compared with coronary artery bypass grafting alone; American Society of Anesthesiologists (ASA) Risk Score category 4/5 compared with 2 to 3; presence of diabetes, congestive heart failure, or neurologic disease at baseline; use of ACEI/ARB; and emergency surgery. Intra- and postoperative factors that were associated with postoperative AKI were hypotension during surgery, use of vasopressors, and postoperative hypotension. Multiple regression logistic model confirmed an independent and significant association of AKI and preoperative use of ACEI/ARB. This was confirmed using a bivariate-probit and propensity score model that adjusts for confounding by indication of use and selection bias.</P>
<P>Conclusions: Preoperative use of ACEI/ARB is associated with a 27.6% higher risk for AKI postoperatively. Stopping ACEI or ARB before cardiac surgery may reduce the incidence of AKI.</P>
]]></description>
<dc:creator><![CDATA[Arora, P., Rajagopalam, S., Ranjan, R., Kolli, H., Singh, M., Venuto, R., Lohr, J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05271107</dc:identifier>
<dc:title><![CDATA[Preoperative Use of Angiotensin-Converting Enzyme Inhibitors/Angiotensin Receptor Blockers Is Associated with Increased Risk for Acute Kidney Injury after Cardiovascular Surgery]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1273</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1266</prism:startingPage>
<prism:section>Acute Renal Failure</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1274?rss=1">
<title><![CDATA[Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1274?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Most studies of contrast-induced acute kidney injury (CIAKI) have focused on patients undergoing angiographic procedures. The incidence and outcomes of CIAKI in patients undergoing nonemergent, contrast-enhanced computed tomography in the inpatient and outpatient setting were assessed.</P>
<P>Design, setting, participants, &amp; measurements: Patients with estimated glomerular filtration rates (GFRs) &lt;60 ml/min per 1.73 m<SUP>2</SUP> undergoing nonemergent computed tomography with intravenous iodinated radiocontrast at an academic VA Medical Center were prospectively identified. Serum creatinine was assessed 48 to 96 h postprocedure to quantify the incidence of CIAKI, and the need for postprocedure dialysis, hospital admission, and 30-d mortality was tracked to examine the associations of CIAKI with these medical outcomes.</P>
<P>Results: A total of 421 patients with a median estimated GFR of 53 ml/min per 1.73 m<SUP>2</SUP> were enrolled. Overall, 6.5% of patients developed an increase in serum creatinine &ge;25%, and 3.5% demonstrated a rise in serum creatinine &ge;0.5 mg/dl. Although only 6% of outpatients received preprocedure and postprocedure intravenous fluid, &lt;1% of outpatients with estimated GFRs &gt;45 ml/min per 1.73 m<SUP>2</SUP> manifested an increase in serum creatinine &ge;0.5 mg/dl. None of the study participants required postprocedure dialysis. Forty-six patients (10.9%) were hospitalized and 10 (2.4%) died by 30-d follow-up; however, CIAKI was not associated with these outcomes.</P>
<P>Conclusions: Clinically significant CIAKI following nonemergent computed tomography is uncommon among outpatients with mild baseline kidney disease. These findings have important implications for providers ordering and performing computed tomography and for future clinical trials of CIAKI.</P>
]]></description>
<dc:creator><![CDATA[Weisbord, S. D., Mor, M. K., Resnick, A. L., Hartwig, K. C., Palevsky, P. M., Fine, M. J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01260308</dc:identifier>
<dc:title><![CDATA[Incidence and Outcomes of Contrast-Induced AKI Following Computed Tomography]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1281</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1274</prism:startingPage>
<prism:section>Acute Renal Failure</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1282?rss=1">
<title><![CDATA[Pauci-immune Crescentic Glomerulonephritis Superimposed on Diabetic Glomerulosclerosis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1282?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Pauci-immune necrotizing and crescentic glomerulonephritis (PNCGN) superimposed on diabetic glomerulosclerosis (DGS) is a rare occurrence. Only limited data on this dual glomerulopathy are available.</P>
<P>Design, setting, participants, &amp; measurements: Twenty-three cases of PNCGN superimposed on DGS were identified from the archives of the Renal Pathology Laboratory of Columbia University. The clinical features, pathologic findings, and outcomes are described.</P>
<P>Results: The majority of patients were white, elderly, and had longstanding diabetes. Patients presented with acute renal failure and an active urine sediment. Antinuclear cytoplasmic autoantibody (ANCA) testing was positive by indirect immunofluorescence in 18 of 22 patients. Sixteen patients had a P-ANCA pattern, 9 of whom underwent further testing and were found to be MPO-ANCA positive by enzyme-linked immunosorbent assay. Among the two patients with C-ANCA by indirect immunofluorescence, enzyme-linked immunosorbent assay was performed in one and revealed PR3-ANCA. Eight patients had extrarenal manifestations of vasculitis, including 6 with pulmonary hemorrhage. At the time of presentation and renal biopsy, 11 patients required hemodialysis. The mean percentages of glomeruli with cellular crescents, fibrous crescents, and necrosis were 24.9, 8.4, and 12.9, respectively. Most patients were treated with cyclophosphamide and prednisone. At a mean follow-up of 14.6 mo (available in 21 patients), 8 patients had died and 8 of the remaining 13 patients had reached end-stage renal disease. Correlates of end-stage renal disease were hemodialysis at presentation and the degree of DGS.</P>
<P>Conclusions: PNCGN may occur superimposed on DGS. The prognosis for this dual glomerulopathy is dismal despite aggressive therapy.</P>
]]></description>
<dc:creator><![CDATA[Nasr, S. H., D'Agati, V. D., Said, S. M., Stokes, M. B., Appel, G. B., Valeri, A. M., Markowitz, G. S.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00740208</dc:identifier>
<dc:title><![CDATA[Pauci-immune Crescentic Glomerulonephritis Superimposed on Diabetic Glomerulosclerosis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1288</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1282</prism:startingPage>
<prism:section>Clinical Immunology and Pathology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1289?rss=1">
<title><![CDATA[Coronary Artery Calcification, ADMA, and Insulin Resistance in CKD Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1289?rss=1</link>
<description><![CDATA[
<P>Background and objectives: It is known that coronary artery calcification (CAC) develops in chronic kidney disease (CKD) before initiation of renal replacement therapy, and factors associated with CKD mineral and bone disorders (CKD-MBDs) are involved. However, little information is available about any association between plasma levels of asymmetric dimethylarginine (ADMA), insulin resistance, and CAC.</P>
<P>Design, setting, participants, &amp; measurements: A total of 111 CKD patients (79 men, 32 women; glomerular filtration rate [GFR] median, 33.7 ml/min per 1.73 m<SUP>2</SUP>), free of cardiovascular disease, were consecutively recruited along with 30 age-matched healthy subjects. Coronary artery calcification scores (CACS) were measured by multidetector-row CT according to Agatston score.</P>
<P>Results: In CKD patients, CACS was distributed widely from 0 to 2901, while in age-matched, healthy control subjects (<I>n</I> = 30), CACS showed a range from 0 to 307. GFR had a significant negative correlation with CACS. Plasma ADMA levels were negatively correlated with GFR and positively correlated with CACS. When CACS was divided into quartiles (&lt;50, <I>n</I> = 56; 50 to 300, <I>n</I> = 24; 300 to 600, <I>n</I> = 14; &gt;600, <I>n</I> = 17), the patients with CACS &gt;600 had significantly higher values of HOMA-IR, plasma ADMA levels, and fibrinogen along with serum levels of phosphorus, compared with those in patients having CACS &lt;50. Multivariate regression analysis determined HOMA-IR as an independent contributing factor to CACS.</P>
<P>Conclusions: CAC becomes more prevalent and severe with a decline in GFR, and plasma ADMA levels and insulin resistance, independent of factors associated with CKD-MBD, are correlated with CAC.</P>
]]></description>
<dc:creator><![CDATA[Kobayashi, S., Oka, M., Maesato, K., Ikee, R., Mano, T., Hidekazu, M., Ohtake, T.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00010108</dc:identifier>
<dc:title><![CDATA[Coronary Artery Calcification, ADMA, and Insulin Resistance in CKD Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1295</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1289</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1296?rss=1">
<title><![CDATA[Prevalence of Subclinical Hypothyroidism in Patients with Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1296?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Subclinical primary hypothyroidism is highly prevalent in the general population, especially in the elderly. However, the prevalence of subclinical primary hypothyroidism in persons with chronic kidney disease (CKD) not requiring chronic dialysis is not well defined.</P>
<P>Design, setting, participants, and measurements: Cross-sectional data from 3089 adult outpatients, who were consecutively referred by general practitioners for routine blood testing over the last two years, were analyzed. Glomerular filtration rate (GFR) was estimated by the abbreviated Modification of Diet in Renal Disease equation. Multivariable logistic regression was used to evaluate the independent association between prevalent subclinical primary hypothyroidism and estimated GFR.</P>
<P>Results: Among 3089 adult participants, 293 (9.5%) had subclinical primary hypothyroidism and 277 (9%) had an estimated GFR &lt;60 ml/min per 1.73 m<SUP>2</SUP>. The prevalence of subclinical primary hypothyroidism increased from 7% at an estimated GFR &ge;90 ml/min per 1.73 m<SUP>2</SUP> to 17.9% at an estimated GFR &lt;60 ml/min per 1.73 m<SUP>2</SUP> (<I>P</I> &lt; 0.0001 for trend). Compared with participants with an estimated GFR &ge;60 ml/min per 1.73 m<SUP>2</SUP>, those with estimated GFR &lt;60 ml/min per 1.73 m<SUP>2</SUP> had an increased odds of subclinical primary hypothyroidism after adjusting for age, gender, fasting plasma glucose, total cholesterol, and triglyceride concentrations.</P>
<P>Conclusions: These findings suggest that subclinical primary hypothyroidism is a relatively common condition (~18%) among persons with CKD not requiring chronic dialysis, and it is independently associated with progressively lower estimated GFR in a large cohort of unselected outpatient adults.</P>
]]></description>
<dc:creator><![CDATA[Chonchol, M., Lippi, G., Salvagno, G., Zoppini, G., Muggeo, M., Targher, G.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00800208</dc:identifier>
<dc:title><![CDATA[Prevalence of Subclinical Hypothyroidism in Patients with Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1300</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1296</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1301?rss=1">
<title><![CDATA[Effect of Tonsillectomy Plus Steroid Pulse Therapy on Clinical Remission of IgA Nephropathy: A Controlled Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1301?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Few well-designed investigations have examined how tonsillectomy plus steroid pulse therapy affects IgA nephropathy. A prospective, controlled study therefore was performed to compare the effects of combined therapy with those of steroid pulse alone in patients with IgA nephropathy.</P>
<P>Design, setting, participants, &amp; measurements: Fifty-five patients were followed up for 54.0 &plusmn; 21.2 mo. Thirty-five of them underwent tonsillectomy and steroid pulse therapy (group C), and 20 received steroid pulse monotherapy (group M). Both groups received methylprednisolone intravenously, followed by oral prednisolone (initial dosage 0.5 mg/kg per d) for 12 to 18 mo. Primary evaluation items were a 100% increase in serum creatinine from baseline levels or the disappearance of urinary protein (UP) and/or occult blood (UOB) indicating clinical remission.</P>
<P>Results: At 24 mo after the initial treatment, the ratios of the UP and UOB disappearance were higher in group C than in group M, and the therapeutic effect persisted until the final observation. None of group C achieved a 100% increase in serum creatinine from the baseline level, whereas one patient in group M developed ESRD during the observation period. The histologic findings of repeated biopsy specimens from 18 patients revealed that mesangial proliferation and IgA deposition were significantly more reduced in group C than in group M. The Cox regression model showed that the combined therapy was approximately six-fold more effective in causing the disappearance of UP than steroid pulse monotherapy.</P>
<P>Conclusion: Tonsillectomy combined with steroid pulse treatment can induce clinical remission in patients with IgA nephropathy.</P>
]]></description>
<dc:creator><![CDATA[Komatsu, H., Fujimoto, S., Hara, S., Sato, Y., Yamada, K., Kitamura, K.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00310108</dc:identifier>
<dc:title><![CDATA[Effect of Tonsillectomy Plus Steroid Pulse Therapy on Clinical Remission of IgA Nephropathy: A Controlled Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1307</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1301</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1308?rss=1">
<title><![CDATA[Feasibility and Impact of the Measurement of Extracellular Fluid Volume Simultaneous with GFR by 125I-Iothalamate]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1308?rss=1</link>
<description><![CDATA[
<P>The feasibility, validity, and possible applications of the assessment of extracellular fluid volume (ECFV) simultaneous with glomerular filtration rate (GFR) were assessed in a series of validation studies using the constant infusion method of <SUP>125</SUP>I-iothalamate (IOT). In 48 subjects with a broad range of GFR, distribution volume (V<SUB>d</SUB>) of IOT corresponded well with V<SUB>d</SUB> bromide (16.71 &plusmn; 3.0 and 16.73 &plusmn; 3.2 l, respectively, not significant), with a strong correlation (<I>r</I> = 0.933, <I>P</I> &lt; 0.01) and without systematic deviations. Reproducibility assessment in 25 healthy male subjects showed coefficients of variation of 8.6% of duplicate measurement of V<SUB>d</SUB> IOT during strictly standardized (50 mmol Na<SUP>+</SUP>/d) sodium intake. An increase in dietary sodium intake (200 mmol Na<SUP>+</SUP>/d) induced a corresponding rise in V<SUB>d</SUB> IOT of 1.11 &plusmn; 1.5 l (<I>P</I> &lt; 0.01). In 158 healthy prospective kidney donors, the impact of indexing of GFR to ECFV was analyzed. Age, gender, height, and body surface area (BSA) were determinants of GFR. Whereas GFR, GFR/BSA, and GFR/height were gender-dependent, GFR/ECFV was gender-independent and not related to height or BSA. This supports the potential of normalizing GFR by ECFV. Thus, ECFV can be simultaneously assessed with GFR by the constant infusion method using IOT. After appropriate validation, also other GFR tracers could be used for such a simultaneous estimation, providing a valuable resource of data on ECFV in renal studies and, moreover, allowing GFR to be indexed to the body fluid compartment it clears: the ECFV.</P>
]]></description>
<dc:creator><![CDATA[Visser, F. W., Muntinga, J. H. J., Dierckx, R. A., Navis, G.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05501207</dc:identifier>
<dc:title><![CDATA[Feasibility and Impact of the Measurement of Extracellular Fluid Volume Simultaneous with GFR by 125I-Iothalamate]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1315</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1308</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1316?rss=1">
<title><![CDATA[Socioeconomic Status and Chronic Kidney Disease at Presentation to a Renal Service in the United Kingdom]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1316?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Low socioeconomic status (SES) is associated with both development and progression of chronic kidney disease (CKD). The impact of SES on severity of CKD at presentation to a renal service is less well known. This study investigated the relationship between SES and severity of CKD in a retrospective, cross-sectional analysis involving 1657 patients at the Sheffield Kidney Institute (Sheffield, UK).</P>
<P>Design, setting, participants, &amp; measurements: SES was assigned to each patient according to electoral ward of residence by postcode and ranked according to the corresponding British Index of Multiple Deprivation score, which comprises five deprivation quintiles (Q1, least deprived; Q5, most deprived). National Kidney Foundation Kidney Disease Outcomes Quality Initiative classification of CKD was used for stratification and analysis. Binary logistic regression analysis was applied for the association of variables/risk factors with CKD (lower GFR) at presentation.</P>
<P>Results: The age-adjusted prevalence of diagnosed CKD at presentation by area of residence, across the five deprivation quintiles, per million population was Q1 = 1495, Q2 = 3530, Q3 = 3398, Q4 = 3989, and Q5 = 19,599. Logistic regression models showed that living in the lowest SES quintile area (Q5) as compared with the highest SES (Q1) was associated with a greater risk for presenting with a lower estimated GFR, after adjustment for sociodemographic, lifestyle, and clinical variables.</P>
<P>Conclusions: Low SES is related to severity of CKD at presentation. Further studies are needed to examine this issue across the various SES categories in the United Kingdom.</P>
]]></description>
<dc:creator><![CDATA[Bello, A. K., Peters, J., Rigby, J., Rahman, A. A., El Nahas, M.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00680208</dc:identifier>
<dc:title><![CDATA[Socioeconomic Status and Chronic Kidney Disease at Presentation to a Renal Service in the United Kingdom]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1323</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1316</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1324?rss=1">
<title><![CDATA[Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects of Amiloride]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1324?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Polyuria, polydipsia, and nephrogenic diabetes insipidus have been associated with use of psychotropic medications, especially lithium.</P>
<P>Design, setting, participants, &amp; measurements: The impact of psychotropic medications on urinary concentrating ability and urinary aquaporin 2 (AQP2) excretion was investigated after overnight fluid deprivation, and over 6 h after 40 &micro;g of desmopressin (dDAVP), in patients on lithium (<I>n</I> = 45), compared with those on alternate psychotropic medications (<I>n</I> = 42).</P>
<P>Results: Those not on lithium demonstrated normal urinary concentrating ability (958 &plusmn; 51 mOsm/kg) and increased urinary excretion of AQP2 (98 &plusmn; 21 fmol/&micro;mol creatinine) and cAMP (410 &plusmn; 15 pmol/&micro;mol creatinine). Participants taking lithium were divided into tertiles according to urinary concentrating ability: normal, &gt;750 mOsm/kg; partial nephrogenic diabetes insipidus (NDI), 750 to 300 mOsm/kg; full NDI, &lt;300 mOsm/kg. Urinary AQP2 concentrations were 70.9 &plusmn; 13.6 fmol/&micro;mol creatinine (normal), 76.5 &plusmn; 10.4 fmol/&micro;mol creatinine (partial NDI), and 27.3 fmol/&micro;mol creatinine (full NDI). Impaired urinary concentrating ability and reduced urinary AQP2, cAMP excretion correlated with duration of lithium therapy. Other psychotropic agents did not impair urinary concentrating ability. Eleven patients on lithium were enrolled in a randomized placebo-controlled crossover trial investigating the actions of amiloride (10 mg daily for 6 wk) on dDAVP-stimulated urinary concentrating ability and AQP2 excretion. Amiloride increased maximal urinary osmolality and AQP2 excretion.</P>
<P>Conclusions: By inference, amiloride-induced reduction of lithium uptake in the principal cells of the collecting duct improves responsiveness to AVP-stimulated translocation of AQP2 to the apical membrane of the principal cells.</P>
]]></description>
<dc:creator><![CDATA[Bedford, J. J., Weggery, S., Ellis, G., McDonald, F. J., Joyce, P. R., Leader, J. P., Walker, R. J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01640408</dc:identifier>
<dc:title><![CDATA[Lithium-induced Nephrogenic Diabetes Insipidus: Renal Effects of Amiloride]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1331</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1324</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1332?rss=1">
<title><![CDATA[A Comparison of Change in Measured and Estimated Glomerular Filtration Rate in Patients with Nondiabetic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1332?rss=1</link>
<description><![CDATA[
<P>Background and objectives: All glomerular filtration rate (GFR) estimating equations have been developed from cross-sectional data. The aims of this study were to examine the concordance between use of measured GFR (mGFR) and estimated GFR (eGFR) in tracking changes in kidney function over time among patients with moderately severe chronic kidney disease.</P>
<P>Design, setting, participants, &amp; measurements: A retrospective cohort study of subjects who had been enrolled in the MDRD Study A and who had two or more contemporaneous assessments of mGFR and eGFR (<I>n</I> = 542; mGFR range, 25 to 55 ml/min per 1.73 m<SUP>2</SUP>) during the chronic phase (month 4 and afterwards). mGFR was based on urinary iothalamate clearance; eGFR was based on the 4-variable MDRD Study equation. Temporal changes in GFR were assessed by within-subject linear regression of time on GFR.</P>
<P>Results: Median follow-up time for all subjects was 2.6 yr; median number of GFR measurements was six. The eGFR slope tended to underestimate measured decrements in GFR. The absolute value of the difference in mGFR and eGFR slopes was &le;2 ml/min per 1.73 m<SUP>2</SUP> per yr among 58.3% of subjects; the remainder of subjects had larger absolute differences. Among the 22 variables studied, none predicted a systematic difference between mGFR slope and eGFR slope.</P>
<P>Conclusions: Although eGFR and mGFR exhibited similar relationships to 22 baseline variables, the overall bias seen in the full cohort suggests that clinicians and researchers should exercise caution when interpreting eGFR slope as a marker of progression of kidney disease.</P>
]]></description>
<dc:creator><![CDATA[Xie, D., Joffe, M. M., Brunelli, S. M., Beck, G., Chertow, G. M., Fink, J. C., Greene, T., Hsu, C.-y., Kusek, J. W., Landis, R., Lash, J., Levey, A. S., O'Conner, A., Ojo, A., Rahman, M., Townsend, R. R., Wang, H., Feldman, H. I.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.05631207</dc:identifier>
<dc:title><![CDATA[A Comparison of Change in Measured and Estimated Glomerular Filtration Rate in Patients with Nondiabetic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1338</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1332</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1339?rss=1">
<title><![CDATA[Renal Lesions Associated with IgM-Secreting Monoclonal Proliferations: Revisiting the Disease Spectrum]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1339?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Since the first description of pathology of the kidney in Waldenstr&ouml;m disease in 1970, there have been few reports on kidney complications of IgM-secreting monoclonal proliferations. Here, we aimed to revisit the spectrum of renal lesions occurring in patients with a serum monoclonal IgM.</P>
<P>Design, setting, participants, &amp; measurements: Fourteen patients with a circulating monoclonal IgM and a kidney disease related to B cell proliferation were identified retrospectively. Demographic, clinical, and laboratory data were assessed for each patient at the time of kidney biopsy.</P>
<P>Results: Seven patients had a nephrotic syndrome. Patients without nephrotic syndrome all had impaired renal function. Mean serum creatinine was 238 &micro;mol/L. For five patients, the diagnosis of monoclonal IgM preceded the kidney disease by 28.8 mo (range 12 to 60). Seven patients had Waldenstr&ouml;m disease, two had a small B cell non-Hodgkin lymphoma, one had an IgM-excreting multiple myeloma, one had a marginal zone B cell lymphoma, and three had an IgM-related disorder. Renal lesions included (<I>1</I>) intracapillary monoclonal deposits disease with granular, electron-dense IgM thrombi occluding capillary lumens (5); (<I>2</I>) atypical membranoproliferative glomerulonephritis (3); (<I>3</I>)  light chain amyloidosis (2) associated with &micro; deposits in one patient; (<I>4</I>) acute tubular necrosis (1); and (<I>5</I>) CD20<SUP>+</SUP> lymphomatous infiltration (3). Remission of the nephrotic syndrome was attained in three of seven patients, and renal function improved after chemotherapy.</P>
<P>Conclusions: Although renal complications of IgM proliferations are rare, a wide spectrum of kidney lesions is observed, without correlation with the type of hematologic disorder.</P>
]]></description>
<dc:creator><![CDATA[Audard, V., Georges, B., Vanhille, P., Toly, C., Deroure, B., Fakhouri, F., Cuvelier, R., Belenfant, X., Surin, B., Aucouturier, P., Mougenot, B., Ronco, P.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01600408</dc:identifier>
<dc:title><![CDATA[Renal Lesions Associated with IgM-Secreting Monoclonal Proliferations: Revisiting the Disease Spectrum]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1349</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1339</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1350?rss=1">
<title><![CDATA[Impact of Renal Failure on the Outcome of Dengue Viral Infection]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1350?rss=1</link>
<description><![CDATA[
<P>Background and objectives: In the 2002 dengue outbreak in Taiwan, some fatal cases had the underlying disease of renal failure (RF). Physicians faced difficulty in diagnosis and treatment of these patients; however, the impacts of RF on the clinical presentations and outcomes of dengue infection have not been reported previously.</P>
<P>Design, setting, participants, &amp; measurements: A retrospective review was conducted of medical records, clinical presentations, laboratory findings, and underlying diseases for all cases of dengue infection in a medical center. Characteristics and outcomes of dengue-infected patients with and without RF were compared.</P>
<P>Results: From January 2002 through January 2003, 519 dengue-infected patients were enrolled, including 412 patients with classical dengue fever (DF) and 107 patients with dengue hemorrhagic fever (DHF)/dengue shock syndrome (DSS). Twelve patients died in this outbreak, and all had DHF/DSS. Twenty-one (4.0%) patients were defined as being in the RF group. The RF group had a higher mortality rate than non-RF group (28.6 <I>versus</I> 1.2%; <I>P</I> &lt; 0.001). The severity of GFR impairment was associated with higher percentages of DHF/DSS (<I>P</I> = 0.029) and mortality (<I>P</I> &lt; 0.001). Differences in symptoms/signs and laboratory abnormalities between DF and DHF/DSS were significant in the non-RF group but not apparent in the RF group.</P>
<P>Conclusions: The diagnosis and management of dengue infection among patients with RF must be cautious, because complicated clinical courses with a higher mortality rate were well observed.</P>
]]></description>
<dc:creator><![CDATA[Kuo, M.-C., Lu, P.-L., Chang, J.-M., Lin, M.-Y., Tsai, J.-J., Chen, Y.-H., Chang, K., Chen, H.-C., Hwang, S.-J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00020108</dc:identifier>
<dc:title><![CDATA[Impact of Renal Failure on the Outcome of Dengue Viral Infection]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1356</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1350</prism:startingPage>
<prism:section>Clinical Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1357?rss=1">
<title><![CDATA[Interferon-{gamma} Release Assays for Diagnosing Mycobacterium tuberculosis Infection in Renal Dialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1357?rss=1</link>
<description><![CDATA[
<P>Background and objectives: End-stage renal disease (ESRD) patients are at high risk for tuberculosis (TB). IFN- release assays that assess immune responses to specific TB antigens offer potential advantages over tuberculin skin testing (TST) in screening such patients for <I>Mycobacterium tuberculosis</I> infection. This study sought to determine whether IFN- release assay results are more closely associated with recent TB exposure than TST results.</P>
<P>Design, setting, participants, and measures: Prospective cohort investigation of patients at a hemodialysis center with a smear-positive case of TB. Patients without a history of TB underwent initial and repeat testing with TST, and with the IFN- assays QuantiFERON-TB Gold&reg; (QFT-G) and ELISPOT test. Outcome measures included the prevalence of positive test results, identification of factors associated with positive results, and test result discordance.</P>
<P>Results: A total of 100 (47% foreign born; median age, 55 yr; age range, 18 to 83 yr) of 124 eligible patients were enrolled. Twenty-six persons had positive TST results, 21 had positive QFT-G results, and 27 had positive ELISPOT results. Patients with TB case contact were likely to have a positive QFT-G result (<B><I>P</I></B> = 0.02) and ELISPOT results (<B><I>P</I></B> = 0.04), whereas TB case contact was not associated with positive TST results (<B><I>P</I></B> = 0.7). Positive TST results were associated with foreign birth (<B><I>P</I></B> = 0.04) and having had a TST in the previous year (<B><I>P</I></B> = 0.04).</P>
<P>Conclusions: Positive IFN- assay results were more closely associated with recent TB exposure than were positive TST results. QFT-G and ELISPOT might offer a better method for detecting TB infection in ESRD patients.</P>
]]></description>
<dc:creator><![CDATA[Winthrop, K. L., Nyendak, M., Calvet, H., Oh, P., Lo, M., Swarbrick, G., Johnson, C., Lewinsohn, D. A., Lewinsohn, D. M., Mazurek, G. H.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01010208</dc:identifier>
<dc:title><![CDATA[Interferon-{gamma} Release Assays for Diagnosing Mycobacterium tuberculosis Infection in Renal Dialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1363</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1357</prism:startingPage>
<prism:section>Diagnosis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1364?rss=1">
<title><![CDATA[Diagnosing Hypertension by Intradialytic Blood Pressure Recordings]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1364?rss=1</link>
<description><![CDATA[
<P>Background and objectives: The diagnosis of hypertension among hemodialysis patients by predialysis or postdialysis blood pressure (BP) recordings is imprecise and biased and has poor test-retest reliability. The use of intradialytic BP measurements to diagnose hypertension is unknown.</P>
<P>Design, setting, participants, &amp; measurements: A diagnostic-test study was done with interdialytic ambulatory BP as reference standard. Index BP recordings tested were: predialysis (method 1), postdialysis (method 2), intradialytic (method 3), intradialytic including predialyis and postdialysis (method 4), and the average of predialysis and postdialysis (method 5). Each index BP was recorded over six consecutive dialysis treatments.</P>
<P>Results: There were differences among index BP measurements in reproducibility, bias, precision, and accuracy. Method 4 was the most reproducible (intraclass correlation coefficient = 0.70 for systolic and diastolic BP). All 5 measurement methods overestimated 44-h ambulatory systolic BP. Methods 2, 3, or 4 overestimated ambulatory systolic BP by only a small amount. Method 4 was the most precise and accurate. For diagnosis of hypertension, BP cut-point by method 4 of 135/75 mmHg, had a sensitivity of 90.4% and specificity of 75.9% for systolic BP (area under ROC curve 0.90). Median cut-off systolic BP of 140 mmHg from a single dialysis provides approximately 80% sensitivity and 80% specificity in diagnosing systolic hypertension; a median cut-off diastolic BP of 80 mmHg provides approximately 75% sensitivity and 75% specificity in diagnosing diastolic hypertension.</P>
<P>Conclusions: Consideration of intradialytic BP measurements together with predialysis and postdialysis BP measurements improves the reproducibility, bias, precision, and accuracy of BP measurement compared with predialysis or postdialysis measurements.</P>
]]></description>
<dc:creator><![CDATA[Agarwal, R., Metiku, T., Tegegne, G. G., Light, R. P., Bunaye, Z., Bekele, D. M., Kelley, K.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01510308</dc:identifier>
<dc:title><![CDATA[Diagnosing Hypertension by Intradialytic Blood Pressure Recordings]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1372</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1364</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1373?rss=1">
<title><![CDATA[Consistent Aspirin Use Associated with Improved Arteriovenous Fistula Survival among Incident Hemodialysis Patients in the Dialysis Outcomes and Practice Patterns Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1373?rss=1</link>
<description><![CDATA[
<P>Background and objectives: The relationship between aspirin use and arteriovenous fistula (AVF) survival has been lacking. The aim of this study was to evaluate the association between AVF survival and aspirin use.</P>
<P>Design, setting, participants, &amp; measurements: Data on 2815 incident hemodialysis patients (on dialysis &le; 30 d) using an AVF at enrollment into the Dialysis Outcomes and Practice Patterns Study between 1996 and 2004 were analyzed. Cox regression was used to examine the association between aspirin use and the risk of final AVF failure, first AVF failure, and a gastrointestinal bleeding event. Aspirin use was determined at baseline and one year later. Patients using aspirin at baseline and one year later were considered consistent aspirin users. All models accounted for facility clustering effects and were adjusted for age, race, gender, body mass index, prior permanent access failure, prior placement of a catheter, 10 comorbid conditions, laboratory data, and other medications, and stratified by regions.</P>
<P>Results: Consistent aspirin use was significantly related to a lower risk of final AVF failure. Facility-level analysis, which may reduce confounding by indication, also showed a nearly significant trend of reduced risk of final AVF failure with greater prevalence of consistent aspirin use within dialysis facilities (<I>P</I> for trend = 0.07). The occurrence of a new gastrointestinal bleeding event during the study period was not associated with aspirin use.</P>
<P>Conclusions: These results suggest that consistent aspirin use may be beneficial for AVF survival among incident hemodialysis patients.</P>
]]></description>
<dc:creator><![CDATA[Hasegawa, T., Elder, S. J., Bragg-Gresham, J. L., Pisoni, R. L, Yamazaki, S., Akizawa, T., Jadoul, M., Hugh, R. C., Port, F. K, Fukuhara, S.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00130108</dc:identifier>
<dc:title><![CDATA[Consistent Aspirin Use Associated with Improved Arteriovenous Fistula Survival among Incident Hemodialysis Patients in the Dialysis Outcomes and Practice Patterns Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1378</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1373</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1379?rss=1">
<title><![CDATA[Utility of the "Surprise" Question to Identify Dialysis Patients with High Mortality]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1379?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Dialysis patients are increasingly characterized by older age, multiple comorbidities, and shortened life expectancy. This study investigated whether the "surprise" question, "Would I be surprised if this patient died in the next year?" identifies patients who are at high risk for early mortality.</P>
<P>Design, setting, participants, &amp; measurements: This prospective cohort study of 147 patients in three hemodialysis dialysis units classified patients into "yes" and "no" groups on the basis of the "surprise" question response and tracked patient status (alive or dead) at 12 mo. Demographics, Charlson Comorbidity Index score, and Karnofsky Performance Status score were measured.</P>
<P>Results: Initially, 34 (23%) patients were classified in the "no" group. Compared with the 113 patients in the "yes" group, the patients in the "no" group were older (72.5 &plusmn; 12.8 <I>versus</I> 64.5 &plusmn; 14.9), had a higher comorbidity score (7.1 &plusmn; 2.3 <I>versus</I> 5.8 &plusmn; 2.1), and had a lower performance status score (69.7 &plusmn; 17.1 <I>versus</I> 81.6 &plusmn; 15.8). At 12 mo, 22 (15%) patients had died; the mortality rate for the "no" group was 29.4% and for the "yes" group was 10.6%. The odds of dying within 1 yr for the patients in the "no" group were 3.5 times higher than for patients in the "yes" group, (odds ratio 3.507, 95% CI 1.356 to 9.067, <I>P</I> = 0.01).</P>
<P>Conclusions: The "surprise" question is effective in identifying sicker dialysis patients who have a high risk for early mortality and should receive priority for palliative care interventions.</P>
]]></description>
<dc:creator><![CDATA[Moss, A. H., Ganjoo, J., Sharma, S., Gansor, J., Senft, S., Weaner, B., Dalton, C., MacKay, K., Pellegrino, B., Anantharaman, P., Schmidt, R.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00940208</dc:identifier>
<dc:title><![CDATA[Utility of the "Surprise" Question to Identify Dialysis Patients with High Mortality]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1384</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1379</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1385?rss=1">
<title><![CDATA[Hepatitis C Is Less Aggressive in Hemodialysis Patients than in Nonuremic Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1385?rss=1</link>
<description><![CDATA[
<P>Background and objectives: The severity of liver disease among hepatitis C patients on hemodialysis is controversial. The aim of this study was to compare the clinical, biochemical, and liver histologic characteristics of hepatitis C virus (HCV) in hemodialysis patients and in those with normal renal function.</P>
<P>Design, setting, participants, &amp; measurements: A case-control study was carried out with 36 HCV patients on hemodialysis and 37 HCV patients with normal renal function matched for gender, age at infection, and estimated time of infection.</P>
<P>Results: HCV patients on hemodialysis had lower levels of alanina aminotransferase and lower viral load. Hepatic fibrosis was significantly higher in the patients with normal renal function (73%) than in hemodialysis patients (47.2%, <I>P</I> &lt; 0.025); the same was observed for inflammatory activity (control group 59.5% <I>versus</I> hemodialysis patients 27.7%, <I>P</I> = 0.003). In addition, the risk of tissue inflammation was four times lower in hemodialysis patients (odds ratio = 0.23, <I>P</I> &lt; 0.004), and severe inflammatory activity on biopsy was the only independent risk factor for fibrosis (<I>P</I> &lt; 0.001).</P>
<P>Conclusions: The lower biochemical and inflammatory activities observed in hemodialysis patients suggest that hemodialysis and uremia may have a protective role against progression of the disease caused by HCV.</P>
]]></description>
<dc:creator><![CDATA[Trevizoli, J. E., de Paula Menezes, R., Ribeiro Velasco, L. F., Amorim, R., de Carvalho, M. B., Mendes, L. S., Neto, C. J., de Deus Macedo, J. R., de Assis, F., Neves, R.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01330308</dc:identifier>
<dc:title><![CDATA[Hepatitis C Is Less Aggressive in Hemodialysis Patients than in Nonuremic Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1390</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1385</prism:startingPage>
<prism:section>Dialysis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1391?rss=1">
<title><![CDATA[Chronic Kidney Disease Prevalence Estimates among Racial/Ethnic Groups: The Multi-Ethnic Study of Atherosclerosis]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1391?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Muscle mass is not a major determinant of serum cystatin C levels, and its use to estimate GFR may lead to more congruent estimates of chronic kidney disease (CKD) across gender and racial/ethnic groups.</P>
<P>Design, setting, participants, &amp; measurements: The Multi-Ethnic Study of Atherosclerosis is a population-based study of 6814 men and women who are aged 45 to 85 yr and do not have clinical cardiovascular disease. Estimated CKD prevalence, defined as an estimated GFR &lt;60 ml/min per 1.73 m<SUP>2</SUP> body surface area, was compared using three different GFR prediction equations: The abbreviated Modification of Diet in Renal Disease (MDRD) equation and two equations based on serum cystatin C.</P>
<P>Results: Among women, CKD prevalence estimates across the four racial/ethnic groups using the MDRD- or the cystatin C&ndash;based GFR equations, which include gender and race coefficients, varied by approximately two-fold (<I>P</I> &lt; 0.0001) but were more congruent with use of a serum cystatin C&ndash;based equation without the use of coefficients (<I>P</I> = 0.3). CKD prevalence estimates did not differ significantly across racial/ethnic groups among men with the MDRD (<I>P</I> = 0.07) or cystatin C formula without coefficients (<I>P</I> = 0.05) but did differ significantly with the cystatin C formula, which incorporates gender and race coefficients (<I>P</I> = 0.006).</P>
<P>Conclusions: CKD prevalence estimates vary across racial/ethnic groups, and the degree of variability depends on the method used to estimate GFR, especially among women. Further research is needed to determine the accuracy and precision of GFR prediction equations in racially diverse populations.</P>
]]></description>
<dc:creator><![CDATA[Kramer, H., Palmas, W., Kestenbaum, B., Cushman, M., Allison, M., Astor, B., Shlipak, M.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04160907</dc:identifier>
<dc:title><![CDATA[Chronic Kidney Disease Prevalence Estimates among Racial/Ethnic Groups: The Multi-Ethnic Study of Atherosclerosis]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1397</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1391</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1398?rss=1">
<title><![CDATA[Serum Phosphate Levels and Risk of Infection in Incident Dialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1398?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Hyperphosphatemia is highly prevalent in dialysis patients and may be associated with immune dysfunction. The association of serum phosphate level with infection remains largely unexamined.</P>
<P>Design, setting, participants, &amp; measurements: In an incident cohort of 1010 dialysis patients enrolled from 1995 to 1998 and treated in 80 US clinics, the association of phosphate level (low &lt;3.5; normal 3.5 to 5.5; high &gt;5.5 mg/dl) at baseline and during follow-up with the risk for incident inpatient and outpatient infection-related events was examined. Infectious events were identified from US Renal Data System data (mean follow-up 3.3 yr). Incidence rate ratios for all infections, sepsis, respiratory tract infections, and osteomyelitis were obtained using multivariable Poisson models, adjusting for potential confounders (age, race, gender, smoking, comorbidity, and laboratory values).</P>
<P>Results: Infections of any type (<I>n</I> = 1398) were more frequent among patients with high phosphate levels at baseline, relative to normal; this association was not changed by adjustment for parathyroid hormone level. Similarly, high <I>versus</I> normal baseline phosphate was associated with increased risk for sepsis and osteomyelitis but not respiratory tract infections. Associations with calcium were generally NS, and results with calcium-phosphate product mirrored the phosphate results.</P>
<P>Conclusions: High phosphate levels may be associated with increased risk for infection, contributing further to the rationale for aggressive management of hyperphosphatemia in dialysis patients.</P>
]]></description>
<dc:creator><![CDATA[Plantinga, L. C., Fink, N. E., Melamed, M. L., Briggs, W. A., Powe, N. R., Jaar, B. G.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00420108</dc:identifier>
<dc:title><![CDATA[Serum Phosphate Levels and Risk of Infection in Incident Dialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1406</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1398</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1407?rss=1">
<title><![CDATA[Age-related Blood Pressure Patterns and Blood Pressure Variability among Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1407?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Despite the high prevalence of cardiovascular disease among hemodialysis patients, the relationship between age and blood pressure (BP) is not well understood. It was postulated that the relationship of BP to age differs among hemodialysis patients <I>versus</I> the general population and that there is significant variability in dialysis unit BP measurements.</P>
<P>Design, setting, participants, &amp; measurements: To explore this hypothesis, the patterns of systolic, diastolic, mean arterial, and pulse pressures in the general population using data from National Health and Nutrition Examination Survey participants (<I>n</I> = 9242) were compared with those in a cohort of hemodialysis patients (<I>n</I> = 9849).</P>
<P>Results: In contrast to the increase in systolic BP with age in the general population, systolic BP was elevated in young hemodialysis patients and declined slightly among the elderly. The inverted "U"-shape relationship between age and diastolic BP in the general population was absent in hemodialysis patients. Diastolic BP was elevated among hemodialysis patients &lt;50 yr of age and declined with advancing age. Mean arterial and pulse pressures were elevated among young hemodialysis patients and exhibited less age dependency than in the general population. Variability in BP within patients was similar to that between patients.</P>
<P>Conclusions: The relationship of BP to age differed from that in the general population. The variability in dialysis unit BP measurements may limit their use in managing hypertension and predicting outcomes. Nevertheless, dialysis unit BP measurements are necessary to minimize acute complications during the dialysis procedure.</P>
]]></description>
<dc:creator><![CDATA[Rohrscheib, M. R., Myers, O. B., Servilla, K. S., Adams, C. D., Miskulin, D., Bedrick, E. J., Hunt, W. C., Lindsey, D. E., Gabaldon, D., Zager, P. G., for the DCI Medical Directors]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00110108</dc:identifier>
<dc:title><![CDATA[Age-related Blood Pressure Patterns and Blood Pressure Variability among Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1414</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1407</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1415?rss=1">
<title><![CDATA[Associations of Kidney Function with Cardiovascular Medication Use after Myocardial Infarction]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1415?rss=1</link>
<description><![CDATA[
<P>Background and objectives: It is unknown whether adherence to recommended medications after myocardial infarction (MI) differs by kidney function.</P>
<P>Design, setting, participants, &amp; measurements: This was a retrospective cohort study of older patients who were discharged after MI in two Eastern states between 1995 and 2004. Patients were categorized as having ESRD, having chronic kidney disease (CKD), and being free from diagnosed CKD. Use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (ACEI/ARB), &beta; blockers (BB), and statins was assessed within 30 d after discharge. Good adherence was defined as proportion of days covered &gt;80% during the first year after discharge.</P>
<P>Results: Compared with patients with no CKD, patients with CKD had 22% lower adjusted use of ACEI/ARB but similar rates of BB and statin use. Patients with ESRD experienced 43% lower ACEI/ARB and 17% lower statin use. Only 64% (BB), 57% (statins), and 54% (ACEI/ARB) of patients had good 1-yr adherence. Adherence was similar between patients with CKD and with no CKD for all study drugs. Fewer patients with ESRD had good adherence to BB.</P>
<P>Conclusions: With the exception of lower ACEI/ARB use in patients with CKD, we found no differences between patients with CKD and with no CKD in their use of and adherence to these cardiovascular medications after MI. Patients with ESRD experienced lower use of ACEI/ARB and statins and lower adherence to BB regimens. Postulated differences in medication use after MI across levels of kidney function are unlikely to explain the observed differences in long-term outcomes.</P>
]]></description>
<dc:creator><![CDATA[Winkelmayer, W. C., Levin, R., Setoguchi, S.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02010408</dc:identifier>
<dc:title><![CDATA[Associations of Kidney Function with Cardiovascular Medication Use after Myocardial Infarction]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1422</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1415</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1423?rss=1">
<title><![CDATA[Consistent Control of Mineral and Bone Disorder in Incident Hemodialysis Patients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1423?rss=1</link>
<description><![CDATA[
<P>Background and objectives: In 2003, the National Kidney Foundation introduced guidelines for the control of parathyroid hormone, calcium, and phosphorus in hemodialysis patients.</P>
<P>Design, setting, participants, &amp; measurements: A cohort study was conducted of 22,937 incident hemodialysis patients who were identified from a large national provider between July 1, 2000, and June 30, 2002, and followed through June 30, 2004. Consistent achievement was determined (<I>1</I>) as the simultaneous control of multiple markers over time and (<I>2</I>) as the time in target for each marker during the first year of dialysis. Mortality risk was assessed with Cox proportional hazards models.</P>
<P>Results: In the simultaneous control analysis, patients who achieved target for none of the markers had a 51% greater risk for death than those who achieved target for all three markers (reference group). Patients who achieved any target for any single marker had a 35 to 39% higher risk for death, and patients who achieved target for any two of the three markers had a 15 to 21% higher risk for death compared with the reference group. In the time in target analysis, patients with parathyroid hormone in target for 4 quarters had a 25% lower risk for death compared with those who did so for &le;1 quarter (reference group). Patients with calcium in target for 4 quarters had a 14% lower risk, and patients with phosphorus in target for 4 quarters had a 38% lower risk.</P>
<P>Conclusions: Consistent control of the markers of bone metabolism and disease within published targets is a strong predictor of survival in hemodialysis patients.</P>
]]></description>
<dc:creator><![CDATA[Danese, M. D., Belozeroff, V., Smirnakis, K., Rothman, K. J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01060308</dc:identifier>
<dc:title><![CDATA[Consistent Control of Mineral and Bone Disorder in Incident Hemodialysis Patients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1429</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1423</prism:startingPage>
<prism:section>Epidemiology and Outcomes</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1430?rss=1">
<title><![CDATA[Renal Phenotype in Lowe Syndrome: A Selective Proximal Tubular Dysfunction]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1430?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Lowe syndrome is defined by congenital cataracts, mental retardation, and proximal tubulopathy and is due to mutations in <I>OCRL</I>. Recently, mutations in <I>OCRL</I> were found to underlie some patients with Dent disease, characterized by low molecular weight proteinuria, hypercalciuria, and nephrocalcinosis. This phenotypic heterogeneity is poorly understood.</P>
<P>Design, setting, participants, &amp; measurements: The renal phenotype of 16 patients with Lowe syndrome (10.9 &plusmn; 7.0 yr) under care of the authors was characterized to define overlap of symptoms with Dent disease and infer clues about OCRL function. Medical charts of patients were reviewed for data regarding glomerular filtration rate and markers of proximal tubular function.</P>
<P>Results: All patients had low molecular weight proteinuria and albuminuria. Lysosomal enzymuria was elevated in all 11 patients assessed. Fifteen patients had hypercalciuria, and 14 aminoaciduria. Seven patients required bicarbonate and three required phosphate replacement; all others maintained normal serum values without supplementation. None of the patients had detectable glycosuria, and none had clinically overt rickets. GFR was mildly to moderately impaired and highly variable, with a trend of deterioration with age.</P>
<P>Conclusions: Patients with Lowe syndrome do not have renal Fanconi syndrome but a selective proximal tubulopathy, variable in extent and dominated by low molecular weight proteinuria and hypercalciuria, the classical features of Dent disease. These findings suggest that OCRL and ClC-5, the chloride channel mutated in Dent disease, are involved in similar reabsorption pathways in the proximal tubule.</P>
]]></description>
<dc:creator><![CDATA[Bockenhauer, D., Bokenkamp, A., van't Hoff, W., Levtchenko, E., Kist-van Holthe, J. E., Tasic, V., Ludwig, M.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00520108</dc:identifier>
<dc:title><![CDATA[Renal Phenotype in Lowe Syndrome: A Selective Proximal Tubular Dysfunction]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1436</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1430</prism:startingPage>
<prism:section>Hereditary Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1437?rss=1">
<title><![CDATA[Higher Strength Lanthanum Carbonate Provides Serum Phosphorus Control With a Low Tablet Burden and Is Preferred by Patients and Physicians: A Multicenter Study]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1437?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Management of hyperphosphatemia, a predictor of mortality in chronic kidney disease, is challenging. Nonadherence to dietary phosphate binders, in part, contributes to uncontrolled serum phosphorus levels. This phase IIIb trial assessed the efficacy of increased dosages (3000 to 4500 mg/d) of reformulated lanthanum carbonate (500-, 750-, and 1000-mg tablets) in nonresponders to dosages of up to 3000 mg/d.</P>
<P>Design, setting, participants, &amp; measurements: This 8-wk study with a 4-mo open-label extension enrolled 513 patients who were undergoing maintenance hemodialysis. Patients who achieved serum phosphorus control at week 4 with &le;3000 mg/d lanthanum carbonate entered cohort A; nonresponders were randomly assigned to receive 3000, 3750, or 4500 mg/d (cohort B). The primary outcome measure was the control rate for predialysis serum phosphorus levels at the end of week 8, among patients in cohort B.</P>
<P>Results: At the end of week 4, 54% of patients achieved serum phosphorus control at dosages &le;3000 mg/d administered as one tablet per meal. Among patients who entered cohort B, control rates of 25, 38, and 32% for patients who were randomly assigned to 3000, 3750, or 4500 mg/d lanthanum carbonate, respectively, were achieved, with no increase in adverse events. Patients and physicians reported significantly higher levels of satisfaction with reformulated lanthanum carbonate compared with previous phosphate binders, partly because of reduced tablet burden with higher dosage strengths. Physicians and patients also expressed a preference for lanthanum carbonate over previous medication.</P>
<P>Conclusions: Reformulated lanthanum carbonate is an effective phosphate binder that may reduce daily tablet burden.</P>
]]></description>
<dc:creator><![CDATA[Mehrotra, R., Martin, K. J., Fishbane, S., Sprague, S. M., Zeig, S., Anger, M., for the Fosrenol Overview Research Evaluation Study for Early Experience (FORESEE) Study Group]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04741107</dc:identifier>
<dc:title><![CDATA[Higher Strength Lanthanum Carbonate Provides Serum Phosphorus Control With a Low Tablet Burden and Is Preferred by Patients and Physicians: A Multicenter Study]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1445</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1437</prism:startingPage>
<prism:section>Mineral Metabolism and Bone Disease</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1446?rss=1">
<title><![CDATA[RANKL Is a Mediator of Bone Resorption in Idiopathic Hypercalciuria]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1446?rss=1</link>
<description><![CDATA[
<P>Background and objectives: This study aimed to determine the expression of osteoprotegerin, receptor activator of nuclear factor B ligand, interleukin-1, transforming growth factor-&beta;, and basic fibroblast growth factor in stone-forming patients with idiopathic hypercalciuria.</P>
<P>Design, setting, participants, &amp; measurements: Immunohistochemical analysis was performed in undecalcified bone samples previously obtained from 36 transiliac bone biopsies of patients who had idiopathic hypercalciuria and whose histomorphometry had shown lower bone volume, increased bone resorption, and prolonged mineralization lag time.</P>
<P>Results: Bone expression of receptor activator of nuclear factor B ligand and osteoprotegerin was significantly higher in patients with idiopathic hypercalciuria <I>versus</I> control subjects. Transforming growth factor-&beta; immunostaining was lower in patients with idiopathic hypercalciuria than in control subjects and correlated directly with mineralization surface. Interleukin-1 and basic fibroblast growth factor staining did not differ between groups. Receptor activator of nuclear factor B ligand bone expression was significantly higher in patients who had idiopathic hypercalciuria and exhibited higher <I>versus</I> normal bone resorption.</P>
<P>Conclusion: A higher expression of receptor activator of nuclear factor B ligand in bone tissue suggests that increased bone resorption in patients with idiopathic hypercalciuria is mediated by receptor activator of nuclear factor B ligand. Osteoprotegerin bone expression might have been secondarily increased in an attempt to counteract the actions of receptor activator of nuclear factor B ligand. The low bone expression of transforming growth factor-&beta; could contribute to the delayed mineralization found in such patients.</P>
]]></description>
<dc:creator><![CDATA[Gomes, S. A., dos Reis, L. M., Noronha, I. L., Jorgetti, V., Heilberg, I. P.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00240108</dc:identifier>
<dc:title><![CDATA[RANKL Is a Mediator of Bone Resorption in Idiopathic Hypercalciuria]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1452</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1446</prism:startingPage>
<prism:section>Nephrolithiasis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1453?rss=1">
<title><![CDATA[Determinants of 24-hour Urinary Oxalate Excretion]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1453?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Higher levels of urinary oxalate substantially increase the risk of calcium oxalate kidney stones. However, the determinants of urinary oxalate excretion are unclear. The objective was to examine the impact of dietary factors, age, body size, diabetes, and urinary factors on 24-h urinary oxalate.</P>
<P>Design, setting, participants, and measurements: We conducted a cross-sectional study of 3348 stone forming and non&ndash;stone-forming participants in the Health Professionals Follow-up Study (men), the Nurses&rsquo; Health Study (older women), and the Nurses&rsquo; Health Study II (younger women).</P>
<P>Results: Median urinary oxalate was 39 mg/d in men, 27 mg/d in older women, and 26 mg/d in younger women. Participants in the highest quartile of dietary oxalate excreted 1.7 mg/d more urinary oxalate than participants in the lowest quartile (<I>P</I> trend 0.001). The relation between dietary and urinary oxalate was similar in individuals with and without nephrolithiasis. Participants consuming 1000 mg/d or more of vitamin C excreted 6.8 mg/d more urinary oxalate than participants consuming &lt;90 mg/d (<I>P</I> trend &lt; 0.001). Body mass index, total fructose intake, and 24-h urinary potassium, magnesium, and phosphorus levels also were positively associated with urinary oxalate. Calcium intake and age were inversely associated with urinary oxalate. After adjustment for body size, participants with diabetes excreted 2.0 mg/d more urinary oxalate than those without diabetes (<I>P</I> &lt; 0.01).</P>
<P>Conclusions: The impact of dietary oxalate on urinary oxalate appears to be small. Further investigation of factors influencing urinary oxalate may lead to new approaches to prevent calcium kidney stones.</P>
]]></description>
<dc:creator><![CDATA[Taylor, E. N., Curhan, G. C.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01410308</dc:identifier>
<dc:title><![CDATA[Determinants of 24-hour Urinary Oxalate Excretion]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1460</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1453</prism:startingPage>
<prism:section>Nephrolithiasis</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1461?rss=1">
<title><![CDATA[High-Dosage Intravenous Immunoglobulin-Associated Macrovacuoles Are Associated with Chronic Tubulointerstitial Lesion Worsening in Renal Transplant Recipients]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1461?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Intravenous immunoglobulins (IVIg) may induce acute renal failure associated with tubular vacuolization. Although the use of IVIg is increasing in kidney transplantation, their impact on graft histology and function remains unknown.</P>
<P>Design, setting, participants, &amp; measurements: Twenty-seven kidney transplant recipients who had high immunologic risk and were treated with four courses of IVIg after transplantation were studied retrospectively at a transplant center, and findings were compared with those of 27 control subjects. Protocol kidney biopsies were performed at time of transplantation and at 3 mo and 1 yr after transplantation.</P>
<P>Results: No episode of IVIg-related acute renal failure occurred. Nevertheless, screening biopsies revealed the presence of "microvacuoles" and "macrovacuoles." Widespread microvacuolizations were often detected (70%) on preimplantation biopsy and not associated with IVIg. Macrovacuoles, which were absent on preimplantation biopsies, were observed exclusively in IVIg-treated patients. Macrovacuoles among IVIg-treated patients were seen in kidneys from older donors and were associated with chronic tubulointerstitial changes at 3 mo, with similar trends at 1 yr. Macrovacuoles were associated with lower creatinine clearance at last follow-up in IVIg-treated patients.</P>
<P>Conclusions: IVIg frequently induce tubular macrovacuoles in kidney transplant recipients. These are more frequently observed in grafts from older donors, suggesting a higher vulnerability to IVIg. These data suggest a deleterious impact of IVIg-induced macrovacuoles on chronic tubulointerstitial changes and long-term renal function.</P>
]]></description>
<dc:creator><![CDATA[Bollee, G., Anglicheau, D., Loupy, A., Zuber, J., Patey, N., Gregor, D. M., Martinez, F., Mamzer-Bruneel, M.-F., Snanoudj, R., Thervet, E., Legendre, C., Noel, L.-H.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00500108</dc:identifier>
<dc:title><![CDATA[High-Dosage Intravenous Immunoglobulin-Associated Macrovacuoles Are Associated with Chronic Tubulointerstitial Lesion Worsening in Renal Transplant Recipients]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1468</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1461</prism:startingPage>
<prism:section>Renal Transplantation</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1469?rss=1">
<title><![CDATA[Pauci-immune and Immune Glomerular Lesions in Kidney Transplants for Systemic Lupus Erythematosus]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1469?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Glomerular lesions in allografts in recipients with end-stage nephritis resulting from systemic lupus erythematosus (SLE) were examined to determine the spectrum of glomerular pathology in recurrent glomerulonephritis (GN).</P>
<P>Design, setting, participants, &amp; measurements: A total of 156 biopsy samples, from 49 serial allografts in 43 recipients with end-stage lupus nephritis, were examined by light microscopy, and by immunofluorescence and electron microscopy in selected cases. These were compared with control allografts (<I>n</I> = 35).</P>
<P>Results: Glomerular lesions best explained by recurrent lupus nephritis were observed in 19 of 49 allografts (38.8%) in lupus recipients. Three categories of glomerulopathies were identified: 1) immune complex glomerulopathies, including mesangial GN (28%) and membranous GN (4%); 2) atypical glomerulopathies, including acute proliferative GN (32%) and focal segmental glomerulosclerosis (12%), with scant immune deposits in glomerular capillaries, frequent endothelial tubuloreticular inclusions, and thrombotic microangiopathy; and 3) transplant-associated glomerulopathies (24%).</P>
<P>Conclusions: Allografts from recipients with SLE had typical immune complex-mediated GN and atypical pauci-immune, proliferative GN and segmental glomerular sclerosis. Atypical glomerulopathies like these suggest a role for nonimmune complex-mediated glomerular injury in recurrent lupus GN.</P>
]]></description>
<dc:creator><![CDATA[Meehan, S. M., Chang, A., Khurana, A., Baliga, R., Kadambi, P. V., Javaid, B.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00790208</dc:identifier>
<dc:title><![CDATA[Pauci-immune and Immune Glomerular Lesions in Kidney Transplants for Systemic Lupus Erythematosus]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1478</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1469</prism:startingPage>
<prism:section>Renal Transplantation</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1479?rss=1">
<title><![CDATA[Circulating Anti-endothelial Cell Antibodies Are Associated with Poor Outcome in Renal Allograft Recipients with Acute Rejection]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1479?rss=1</link>
<description><![CDATA[
<P>Background and objectives: Anti-endothelial cell antibody (AECA) can cause hyperacute rejection and immediate graft loss after renal transplantation; however, its prevalence and significance during acute rejection are unknown. Previous studies suggested that AECA may be detected in recipients with acute vascular rejection (AVR).</P>
<P>Design, setting, participants, &amp; measurements: We retrospectively analyzed 653 cadaveric renal transplant recipients; circulating AECA was positive in 13 of 47 cases of AVR; another two cases of hyperacute rejection also had detectable AECA. Twenty-six cases of AVR without circulating AECA were selected as controls.</P>
<P>Results: AECA-positive AVR usually occurred within 1 yr after transplantation and mostly was resistant to steroid treatment. Compared with the control group, the AECA-positive group was associated with a significantly lower 1-yr graft survival rate (46.7 <I>versus</I> 80.5%; <I>P</I> = 0.038), and more patients had histologic interstitial plasma cell infiltration (53.8 <I>versus</I> 11.5%; <I>P</I> = 0.005). More patients with AECA-positive AVR experienced another one or more episodes of acute rejection during 1 yr of follow-up (75.0 <I>versus</I> 13.0%; <I>P</I> = 0.003). AECA-positive AVR with C4d deposition in peri-tubular capillaries had the worst outcome in this cohort, and it accounted for 38.5% graft loss in AVR. AECA in turn accounted for 71.4% of graft loss in C4d<SUP>+</SUP> AVR.</P>
<P>Conclusions: Circulating AECA is associated with poor outcome in renal allograft recipients with acute rejection and should be monitored regularly.</P>
]]></description>
<dc:creator><![CDATA[Sun, Q., Liu, Z., Chen, J., Chen, H., Wen, J., Cheng, D., Li, L.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04451007</dc:identifier>
<dc:title><![CDATA[Circulating Anti-endothelial Cell Antibodies Are Associated with Poor Outcome in Renal Allograft Recipients with Acute Rejection]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1486</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1479</prism:startingPage>
<prism:section>Renal Transplantation</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1487?rss=1">
<title><![CDATA[Epidemiology of Acute Infections among Patients with Chronic Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1487?rss=1</link>
<description><![CDATA[
<P>The objectives of this review were (<I>1</I>) to review recent literature on the rates, risk factors, and outcomes of infections in patients who had chronic kidney disease (CKD) and did or did not require renal replacement therapy; (<I>2</I>) to review literature on the efficacy and use of selected vaccines for patients with CKD; and (<I>3</I>) to outline a research framework for examining key issues regarding infections in patients with CKD. Infection-related hospitalizations contribute substantially to excess morbidity and mortality in patients with ESRD, and infection is the second leading cause of death in this population. Patients who have CKD and do not require renal replacement therapy seem to be at higher risk for infection compared with patients without CKD; however, data about patients who have CKD and do not require dialysis therapy are very limited. Numerous factors potentially predispose patients with CKD to infection: advanced age, presence of coexisting illnesses, vaccine hyporesponsiveness, immunosuppressive therapy, uremia, dialysis access, and the dialysis procedure. Targeted vaccination seems to have variable efficacy in the setting of CKD and is generally underused in this population. In conclusion, infection is a primary issue when caring for patients who receive maintenance dialysis. Very limited data exist about the rates, risk factors, and outcomes of infection in patients who have CKD and do not require dialysis. Future research is needed to delineate accurately the epidemiology of infections in these populations and to develop effective preventive strategies across the spectrum of CKD severity.</P>
]]></description>
<dc:creator><![CDATA[Dalrymple, L. S., Go, A. S.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01290308</dc:identifier>
<dc:title><![CDATA[Epidemiology of Acute Infections among Patients with Chronic Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1493</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1487</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1494?rss=1">
<title><![CDATA[Adverse Renal and Metabolic Effects Associated with Oral Sodium Phosphate Bowel Preparation]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1494?rss=1</link>
<description><![CDATA[
<P>Colorectal cancer can be prevented by the removal of adenomatous polyps during screening colonoscopy, but adequate bowel preparation is required. Oral sodium phosphate (OSP), an effective bowel purgative, is available over the counter and requires a substantially lower volume than polyethylene glycol-based preparative agents. Accumulating reports implicate OSP in electrolyte disturbances as well as acute kidney injury (AKI) in a syndrome termed phosphate nephropathy (a form of nephrocalcinosis). Despite published case reports and case series, the actual incidence, risk factors, and natural history of phosphate nephropathy remain largely undefined. Several recent observational studies have provided new information on these important issues while supporting a link between OSP and acute phosphate nephropathy as well as the development of chronic kidney disease in elderly patients, many of whom had a normal serum creatinine at the time of OSP ingestion. This review summarizes current knowledge about the renal complications of OSP, risk factors for its development, and the pathophysiology of acute and chronic kidney damage in nephrocalcinosis.</P>
]]></description>
<dc:creator><![CDATA[Heher, E. C., Thier, S. O., Rennke, H., Humphreys, B. D.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02040408</dc:identifier>
<dc:title><![CDATA[Adverse Renal and Metabolic Effects Associated with Oral Sodium Phosphate Bowel Preparation]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1503</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1494</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1504?rss=1">
<title><![CDATA[Vitamin K-dependent Proteins, Warfarin, and Vascular Calcification]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1504?rss=1</link>
<description><![CDATA[
<P>Vitamin K-dependent proteins (VKDPs) require carboxylation to become biologically active. Although the coagulant factors are the most well-known VKDPs, there are many others with important physiologic roles. Matrix Gla Protein (MGP) and Growth Arrest Specific Gene 6 (Gas-6) are two particularly important VKDPs, and their roles in vascular biology are just beginning to be understood. Both function to protect the vasculature; MGP prevents vascular calcification and Gas-6 affects vascular smooth muscle cell apoptosis and movement. Unlike the coagulant factors, which undergo hepatic carboxylation, MGP and Gas-6 are carboxylated within the vasculature. This peripheral carboxylation process is distinct from hepatic carboxylation, yet both are inhibited by warfarin administration. Warfarin prevents the activation of MGP and Gas-6, and in animals, induces vascular calcification. The relationship of warfarin to vascular calcification in humans is not fully known, yet observational data suggest an association. Given the high risk of vascular calcification in those patients with chronic kidney disease, the importance of understanding warfarin's effect on VKDPs is paramount. Furthermore, recognizing the importance of VKDPs in vascular biology will stimulate new areas of research and offer potential therapeutic interventions.</P>
]]></description>
<dc:creator><![CDATA[Danziger, J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00770208</dc:identifier>
<dc:title><![CDATA[Vitamin K-dependent Proteins, Warfarin, and Vascular Calcification]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1510</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1504</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1511?rss=1">
<title><![CDATA[Angiotensin Converting Enzyme Insertion/Deletion Polymorphism and Renoprotection in Diabetic and Nondiabetic Nephropathies]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1511?rss=1</link>
<description><![CDATA[
<P>Despite the huge amount of studies looking for candidate genes, the ACE gene remains the unique, well-characterized locus clearly associated with pathogenesis and progression of chronic kidney disease, and with response to treatment with drugs that directly interfere with the renin angiotensin system (RAS), such as angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor antagonists (ARA). The II genotype is protective against development and progression of type I and type II nephropathy and is associated with a slower progression of nondiabetic proteinuric kidney disease. ACE inhibitors are particularly effective at the stage of normoalbuminuria or microalbuminuria in both type I and type II diabetics with the II genotype, whereas the DD genotype is associated with a better response to ARA therapy in overt nephropathy of type II diabetes and to ACE inhibitors in male patients with nondiabetic proteinuric nephropathies. The role of other RAS or non-RAS polymorphisms and their possible interactions with different <I>ACE</I> I/D genotypes are less clearly defined. Thus, evaluating the <I>ACE</I> I/D polymorphism is a reliable tool to identify patients at risk and those who may benefit the most of renoprotective therapy with ACE inhibitors or ARA. This may guide pharmacologic therapy in individual patients and help design clinical trials in progressive nephropathies. Moreover, it might help optimize prevention and intervention strategies at population levels, in particular, in countries where resources are extremely limited and 1 million patients continue to die every year of cardiovascular or renal disease.</P>
]]></description>
<dc:creator><![CDATA[Ruggenenti, P., Bettinaglio, P., Pinares, F., Remuzzi, G.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.04140907</dc:identifier>
<dc:title><![CDATA[Angiotensin Converting Enzyme Insertion/Deletion Polymorphism and Renoprotection in Diabetic and Nondiabetic Nephropathies]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1525</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1511</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1526?rss=1">
<title><![CDATA[Aspects of Immune Dysfunction in End-stage Renal Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1526?rss=1</link>
<description><![CDATA[
<P>End-stage renal disease (ESRD) is associated with significantly increased morbidity and mortality resulting from cardiovascular disease (CVD) and infections, accounting for 50% and 20%, respectively, of the total mortality in ESRD patients. It is possible that these two complications are linked to alterations in the immune system in ESRD, as uremia is associated with a state of immune dysfunction characterized by immunodepression that contributes to the high prevalence of infections among these patients, as well as by immunoactivation resulting in inflammation that may contribute to CVD. This review describes disorders of the innate and adaptive immune systems in ESRD, underlining the specific role of ESRD-associated disturbances of Toll-like receptors. Finally, based on the emerging links between the alterations of immune system, CVD, and infections in ESRD patients, it emphasizes the potential role of the immune dysfunction in ESRD as an underlying cause for the high mortality in this patient population and the need for more studies in this area.</P>
]]></description>
<dc:creator><![CDATA[Kato, S., Chmielewski, M., Honda, H., Pecoits-Filho, R., Matsuo, S., Yuzawa, Y., Tranaeus, A., Stenvinkel, P., Lindholm, B.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.00950208</dc:identifier>
<dc:title><![CDATA[Aspects of Immune Dysfunction in End-stage Renal Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1533</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1526</prism:startingPage>
<prism:section>In-Depth Reviews</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1534?rss=1">
<title><![CDATA[Introduction to Vitamin D Symposium, March 14, 2008]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1534?rss=1</link>
<description><![CDATA[
<P>A large body of work in diverse clinical and scientific areas has accumulated that supports a role for vitamin D in multiple organ systems and physiologic and molecular processes. The vitamin D receptor is distributed ubiquitously, and by binding with its receptor, vitamin D initiates a series of events that can affect cellular proliferation and differentiation, inflammation, the immune system, and the endocrine system, including the renin-angiotensin system, insulin resistance, and lipid metabolism.</P>
]]></description>
<dc:creator><![CDATA[Rostand, S. G., Warnock, D. G.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01130308</dc:identifier>
<dc:title><![CDATA[Introduction to Vitamin D Symposium, March 14, 2008]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1534</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1534</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1535?rss=1">
<title><![CDATA[Vitamin D in Health and Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1535?rss=1</link>
<description><![CDATA[
<P>Vitamin D functions in the body through both an endocrine mechanism (regulation of calcium absorption) and an autocrine mechanism (facilitation of gene expression). The former acts through circulating calcitriol, whereas the latter, which accounts for more than 80% of the metabolic utilization of the vitamin each day, produces, uses, and degrades calcitriol exclusively intracellularly. In patients with end-stage kidney disease, the endocrine mechanism is effectively disabled; however, the autocrine mechanism is able to function normally so long as the patient has adequate serum levels of 25(OH)D, on which its function is absolutely dependent. For this reason, calcitriol and its analogs do not constitute adequate replacement in managing vitamin D needs of such patients. Optimal serum 25(OH)D levels are greater than 32 ng/mL (80 nmol/L). The consequences of low 25(OH)D status include increased risk of various chronic diseases, ranging from hypertension to diabetes to cancer. The safest and most economical way to ensure adequate vitamin D status is to use oral dosing of native vitamin D. (Both daily and intermittent regimens work well.) Serum 25(OH)D can be expected to rise by about 1 ng/mL (2.5 nmol/L) for every 100 IU of additional vitamin D each day. Recent data indicate that cholecalciferol (vitamin D<SUB>3</SUB>) is substantially more potent than ergocalciferol (vitamin D<SUB>2</SUB>) and that the safe upper intake level for vitamin D<SUB>3</SUB> is 10,000 IU/d.</P>
]]></description>
<dc:creator><![CDATA[Heaney, R. P.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01160308</dc:identifier>
<dc:title><![CDATA[Vitamin D in Health and Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1541</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1535</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1542?rss=1">
<title><![CDATA[Vitamin D and Osteogenic Differentiation in the Artery Wall]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1542?rss=1</link>
<description><![CDATA[
<P>Vascular calcification is widespread, particularly in patients with chronic kidney disease, who receive, among other treatments, active vitamin D supplements. Emerging evidence indicates that vascular calcification is a regulated process that resembles embryonic endochondral osteogenesis, involving osteoblastic differentiation of vascular smooth muscle cells. In experimental animal models, high dosages of vitamin D consistently promote vascular calcification. In particular, the vitamin D&ndash;fed rat is frequently used as a model to assess putative regulators of calcific vasculopathy. The artery wall calcification in these animals most likely results from multiple mechanisms involving systems physiology of the complex, bone-vascular-renal-endocrine axis. Genetically engineered mice with upregulated vitamin D signaling pathways have also shed light on the molecular intermediaries, including fibroblast growth factor-23 and transcriptional intermediary factor 1-. In contrast to the studies of animals, studies of humans show that vitamin D has an inverse relationship or little effect. This difference between <I>in vitro</I> and <I>in vivo</I> findings is most likely, again, due to the complex, systemic feedback regulatory mechanisms that control calcium-phosphate metabolism. Recent epidemiologic evidence suggests that there is a narrow range of vitamin D levels in which vascular function is optimized. Levels above or below this range seem to confer a significant increase in risk for cardiovascular disease. There is some evidence to suggest that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages. These findings raise interesting questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk.</P>
]]></description>
<dc:creator><![CDATA[Hsu, J. J., Tintut, Y., Demer, L. L.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01220308</dc:identifier>
<dc:title><![CDATA[Vitamin D and Osteogenic Differentiation in the Artery Wall]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1547</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1542</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1548?rss=1">
<title><![CDATA[Vitamin D and Sunlight: Strategies for Cancer Prevention and Other Health Benefits]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1548?rss=1</link>
<description><![CDATA[
<P>Vitamin D deficiency is a worldwide health problem. The major source of vitamin D for most humans is sensible sun exposure. Factors that influence cutaneous vitamin D production include sunscreen use, skin pigmentation, time of day, season of the year, latitude, and aging. Serum 25-hydroxyvitamin D [25(OH)D] is the measure for vitamin D status. A total of 100 IU of vitamin D raises blood level of 25(OH)D by 1 ng/ml. Thus, children and adults who do not receive adequate vitamin D from sun exposure need at least 1000 IU/d vitamin D. Lack of sun exposure and vitamin D deficiency have been linked to many serious chronic diseases, including autoimmune diseases, infectious diseases, cardiovascular disease, and deadly cancers. It is estimated that there is a 30 to 50% reduction in risk for developing colorectal, breast, and prostate cancer by either increasing vitamin D intake to least 1000 IU/d vitamin D or increasing sun exposure to raise blood levels of 25(OH)D &gt;30 ng/ml. Most tissues in the body have a vitamin D receptor. The active form of vitamin D, 1,25-dihydroxyvitamin D, is made in many different tissues, including colon, prostate, and breast. It is believed that the local production of 1,25(OH)<SUB>2</SUB>D may be responsible for the anticancer benefit of vitamin D. Recent studies suggested that women who are vitamin D deficient have a 253% increased risk for developing colorectal cancer, and women who ingested 1500 mg/d calcium and 1100 IU/d vitamin D<SUB>3</SUB> for 4 yr reduced risk for developing cancer by &gt;60%.</P>
]]></description>
<dc:creator><![CDATA[Holick, M. F.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01350308</dc:identifier>
<dc:title><![CDATA[Vitamin D and Sunlight: Strategies for Cancer Prevention and Other Health Benefits]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1554</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1548</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1555?rss=1">
<title><![CDATA[Vitamin D and Kidney Disease]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1555?rss=1</link>
<description><![CDATA[
<P>Abnormalities in vitamin D metabolism play a major role in the pathogenesis of secondary hyperparathyroidism in chronic kidney disease. The gradual and progressive decline in 1,25-dihydroxyvitamin D in the course of chronic kidney disease is the result of several mechanisms that limit the ability of the failing kidney to maintain the levels of 1,25-dihydroxyvitamin D despite increasing levels of parathyroid hormone. Recent observations have indicated that chronic kidney disease seems to be associated with a high incidence of nutritional vitamin D insufficiency or deficiency as manifested by decreased levels of 25-hydroxyvitamin D. This contributes to the inability to maintain the levels of 1,25-dihydroxyvitamin D; therefore, current practice guidelines suggest repleting vitamin D status by the administration of native vitamin D as a first step in the therapy of the abnormalities of bone and mineral metabolism in chronic kidney disease. The efficacy of this therapy is extremely variable, and active vitamin D sterols may be required, especially as kidney disease progresses. The importance of the abnormal vitamin D metabolism is being investigated vigorously in view of the observations that vitamin D may have important biologic actions in many tissues in addition to bone and parathyroid. Thus, observational data have suggested potential survival benefits of vitamin D sterol administration in this clinical setting, and experimental data have suggested a potential beneficial effect of vitamin D sterols on the progression of kidney disease. Further work is required to define the mechanisms involved and to examine the effects of vitamin D therapy on outcomes in randomized, controlled trials.</P>
]]></description>
<dc:creator><![CDATA[Al-Badr, W., Martin, K. J.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.01150308</dc:identifier>
<dc:title><![CDATA[Vitamin D and Kidney Disease]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1560</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1555</prism:startingPage>
<prism:section>Moving Points in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1561?rss=1">
<title><![CDATA[Reporting eGFR]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1561?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Bennett, W. M.]]></dc:creator>
<dc:date>2008-08-26</dc:date>
<dc:identifier>info:doi/10.2215/CJN.02870608</dc:identifier>
<dc:title><![CDATA[Reporting eGFR]]></dc:title>
<dc:publisher>American Society of Nephrology</dc:publisher>
<prism:number>5</prism:number>
<prism:volume>3</prism:volume>
<prism:endingPage>1562</prism:endingPage>
<prism:publicationDate>2008-09-01</prism:publicationDate>
<prism:startingPage>1561</prism:startingPage>
<prism:section>Controversies in Nephrology</prism:section>
</item>

<item rdf:about="http://cjasn.asnjournals.org/cgi/content/short/3/5/1563?rss=1">
<title><![CDATA[Screening for CKD with eGFR: Doubts and Dangers]]></title>
<link>http://cjasn.asnjournals.org/cgi/content/short/3/5/1563?rss=1</link>
<description><![CDATA[
<P>The early identification of chronic kidney disease (CKD) is a legitimate enterprise if it provides meaningful opportunities for effective and safe interventions that reduce the risk of death, end-stage renal disease, or complications of renal dysfunction. The screening of <I>unselected</I> populations not already known to be at risk of CKD has the potential of harm and has not been shown to be cost-effective. The application of formulas for the estimation of GFR (eGFR) to the guidelines for staging of chronic kidney disease (Kidney Disease Outcomes Quality Initiative, K/DOQI) as universal screening tools is of dubious value and has inherent dangers. This conclusion is based both on the unreliability of curren