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	<title>Kidney Function</title>
	<link>http://kidneyfunction.org</link>
	<description>Renal Information</description>
	<lastBuildDate>Mon, 08 Mar 2010 18:00:00 +0000</lastBuildDate>
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	<language>en</language>
	
	<item>
		<title>Poverty, Race, and CKD in a Racially and Socioeconomically Diverse Urban Population &#8211; Corrected Proof</title>
		<description><![CDATA[Background: Low socioeconomic status (SES) and African American race are both independently associated with end-stage renal disease and progressive chronic kidney disease (CKD). However, despite their frequent co-occurrence, the effect of low SES independent of race has not been well studied in CKD.Study Design: Cross-sectional study.Setting &#38; Participants: 2,375 community-dwelling adults aged 30-64 years residing within 12 neighborhoods selected for both socioeconomic and racial diversity in Baltimore City, MD.Predictors: Low SES (self-reported household income &#60;125% of 2004 Department of Health and Human Services guideline), higher SES (≥125% of guideline); white and African American race.Outcomes &#38; Measurements: CKD defined as estimated glomerular filtration rate &#60;60 mL/min/1.73 m2. Logistic regression used to calculate ORs for relationship between poverty and CKD, stratified by race.Results: Of 2,375 participants, 955 were white (347 low SES and 608 higher SES) and 1,420 were African American (713 low SES and 707 higher SES). 146 (6.2%) participants had CKD. Overall, race was not associated with CKD (OR, 1.05; 95% CI, 0.57-1.96); however, African Americans had a much greater odds of advanced CKD (estimated glomerular filtration rate &#60;30 mL/min/1.73 m2). Low SES was independently associated with 59% greater odds of CKD after adjustment for demographics, insurance status, and comorbid disease (OR, 1.59; 95% CI, 1.27-1.99). However, stratified by race, low SES was associated with CKD in African Americans (OR, 1.91; 95% CI, 1.54-2.38), but not whites (OR, 0.95; 95% CI, 0.58-1.55; P for interaction = 0.003).Limitations: Cross-sectional design; findings may not be generalizable to non-urban populations.Conclusions: Low SES has a profound relationship with CKD in African Americans, but not whites, in an urban population of adults, and its role in the racial disparities seen in CKD is worthy of further investigation.]]></description>
		<link>http://kidneyfunction.org/poverty-race-and-ckd-in-a-racially-and-socioeconomically-diverse-urban-population-corrected-proof/</link>
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		<title>A Randomized Double-Blind Controlled Trial of Taurolidine-Citrate Catheter Locks for the Prevention of Bacteremia in Patients Treated With Hemodialysis &#8211; Corrected Proof</title>
		<description><![CDATA[Background: Bacteremia is a major cause of morbidity in patients using intravascular catheters. Interdialytic locking with antibiotics decreases the incidence of bacteremia, but risks antibiotic resistance. Taurolidine is a nontoxic broad-spectrum antimicrobial agent that has not been associated with resistance. Preliminary evidence suggests that taurolidine-citrate locks decrease bacteremia, but cause flow problems in established catheters.Study Design: Double-blind randomized controlled trial.Intervention: Interdialytic locking with taurolidine and citrate (1.35% taurolidine and 4% citrate) compared with heparin (5,000 U/mL) started at catheter insertion.Setting &#38; Participants: 110 adult hemodialysis patients with tunneled cuffed intravascular catheters inserted at 3 centers in Northwest England.Outcomes &#38; Measurements: Primary end points were time to first bacteremia episode from any cause and time to first use of thrombolytic therapy.Results: There were 11 bacteremic episodes in the taurolidine-citrate group and 23 in the heparin group (1.4 and 2.4 episodes/1,000 patient-days, respectively; P = 0.1). There was no significant benefit of taurolidine-citrate versus heparin for time to first bacteremia (hazard ratio, 0.66; 95% CI, 0.2-1.6: P = 0.4). Taurolidine-citrate was associated with fewer infections caused by Gram-negative organisms than heparin (0.2 vs 1.1 infections/1,000 patient-days; P = 0.02); however, there was no difference for Gram-positive organisms (1.1 vs 1.2 infections/1,000 patient-days; P = 0.8). There was a greater need for thrombolytic therapy in the taurolidine-citrate versus heparin group (hazard ratio, 2.5; 95% CI, 1.3-5.2; P = 0.008).Limitations: Small sample size. The study included bacteremia from all causes and was not specific for catheter-related bacteremia.Conclusions: Taurolidine-citrate use did not decrease all-cause bacteremia and was associated with a greater need for thrombolytic treatment. There was a decrease in infections caused by Gram-negative organisms and a trend to a lower frequency of bacteremia, which warrants further study.]]></description>
		<link>http://kidneyfunction.org/a-randomized-double-blind-controlled-trial-of-taurolidine-citrate-catheter-locks-for-the-prevention-of-bacteremia-in-patients-treated-with-hemodialysis-corrected-proof/</link>
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		<title>Hemolysis in a Patient With Alkaptonuria and Chronic Kidney Failure &#8211; Corrected Proof</title>
		<description><![CDATA[In alkaptonuria, the absence of homogentisic acid oxidase results in the accumulation of homogentisic acid (HGA) in the body. Fatal disease cases are infrequent, and death often results from kidney or cardiac complications. We report a 24-year-old alkaptonuric man with severe decreased kidney function who developed fatal metabolic acidosis and intravascular hemolysis. Hemolysis may have been caused by rapid and extensive accumulation of HGA and subsequent accumulation of plasma soluble melanins. Toxic effects of plasma soluble melanins, their intermediates, and reactive oxygen side products are increased when antioxidant mechanisms are overwhelmed. A decrease in serum antioxidative activity has been reported in patients with chronic decreased kidney function. However, despite administration of large doses of an antioxidant agent and ascorbic acid and intensive kidney support, hemolysis and acidosis could not be brought under control and hemolysis led to the death of the patient.]]></description>
		<link>http://kidneyfunction.org/hemolysis-in-a-patient-with-alkaptonuria-and-chronic-kidney-failure-corrected-proof/</link>
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		<title>Can Diabetics Receive Kidney Transplants?</title>
		<description><![CDATA[Short answer: Yes. Long answer&#8230;
If you suffer from diabetes, you can receive a kidney transplant form a living relative or from a deceased person. The amount of insulin that is required may increase as a result of the use of immunosupressant drugs to prevent rejection, an increased appetite for food and food intake and the [...]]]></description>
		<link>http://kidneyfunction.org/can-diabetics-receive-kidney-transplants/</link>
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		<title>Hemoglobin A1c and Fructosamine for Assessing Glycemic Control in Diabetic Patients With CKD Stages 3 and 4 &#8211; Corrected Proof</title>
		<description><![CDATA[Background: Hemoglobin A1c (HbA1c) and fructosamine can be used to monitor glycemic control in diabetic patients with normal kidney function, but their validity in patients with chronic kidney disease (CKD) has not been evaluated. In this study, we evaluated the correlation and accuracy of these 2 measures of glycemic control in type 2 diabetic patients with CKD stages 3-4.Study Design: Diagnostic test study.Setting &#38; Participants: Type 2 diabetic patients with normal (n = 30) and abnormal kidney function (n = 30) were recruited in Taipei Veterans General Hospital, Taiwan.Index Tests: HbA1c and fructosamine.Reference Test: Self-monitoring of blood glucose levels.Measurements: Blood glucose measurements consisted of 6 preprandial, 6 postprandial, and 2 bedtime assessments in a week with a cycle of 4-week intervals for 12 weeks.Results: Correlation coefficients between HbA1c level or fructosamine-albumin ratio and mean blood glucose levels were 0.836 and 0.645 in participants with normal kidney function and 0.813 and 0.649 in participants with CKD stages 3-4, respectively. In patients with CKD stages 3-4, mean blood glucose levels in weeks 1-12 were 21.9 mg/dL (95% CI, 11.6-32.5) higher than estimated average glucose (eAG) levels calculated from HbA1c levels in participants with normal kidney function. In patients with CKD stages 3-4, mean blood glucose levels in weeks 10-12 were 15.5 mg/dL (95% CI, 5.2-30.5) higher than eAG levels calculated from fructosamine levels in participants with normal kidney function, but without statistical significance when eAG calculated from fructosamine level was corrected for serum albumin level (difference of 5.6 mg/dL; 95% CI, −8.6 to 19.8).Limitations: Relatively small number of participants with limited amount of blood glucose measurement data.Conclusion: Our data show that eAG calculated from HbA1c and fructosamine levels might underestimate mean blood glucose levels in patients with CKD stages 3-4. References ranges may need to be modified when interpreting results of measurements of glycemic control in type 2 diabetic patients with CKD.]]></description>
		<link>http://kidneyfunction.org/hemoglobin-a1c-and-fructosamine-for-assessing-glycemic-control-in-diabetic-patients-with-ckd-stages-3-and-4-corrected-proof-2/</link>
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		<title>Pulse Cyclophosphamide Therapy and Clinical Remission in Atypical Hemolytic Uremic Syndrome With Anti–Complement Factor H Autoantibodies &#8211; Corrected Proof</title>
		<description><![CDATA[We report 3 children with atypical hemolytic uremic syndrome associated with anti–complement factor H (CFH) autoantibodies who presented with sustained remission with low antibody titers and normal kidney function after plasma exchanges (PEs) and cyclophosphamide pulses. The 3 children initially presented with acute vomiting, fatigue, gross hematuria, hypertension, hemolytic anemia, thrombocytopenia, nephrotic syndrome, and acute kidney injury. C3 levels were normal in patients 1 and 3 and low in patient 2 (0.376 mg/mL [0.376 g/L]). CFH antibody titers were increased (15,000 to &#62; 32,000 arbitrary units [AU]). Patient 1, an 11-year-old boy, was treated with 12 PEs, leading to a decrease in CFH antibody titer (to 800 AU). A first relapse 1 month later was treated with 6 PEs and 4 rituximab infusions. A second relapse 3 months later required 5 PEs, and the patient received oral steroids (0.5 mg/d/kg body weight) and 5 cyclophosphamide pulses (1 g/1.73 m2), leading to sustained remission with normal kidney function (estimated glomerular filtration rate [eGFR], 120 mL/min/1.73 m2 [2.0 mL/s/1.73 m2]) and a stable decrease in CFH antibody titer (to 2,000 AU) 3 years later. Patient 2, a 5-year-old boy, required dialysis therapy for 2 weeks. He received 3 plasma infusions without remission. Six PEs associated with 2 cyclophosphamide pulses (0.5 g/1.73 m2) and steroids (1 mg/d/kg body weight) led to rapid remission, with eGFR of 107 mL/min/1.73 m2 [1.78 mL/s/1.73 m2] and a prolonged decrease in CFH antibody titer after 15 months (1,300 AU). Patient 3, a 16-month-old boy, was treated with oral steroids (1 mg/d/kg body weight), 2 PEs, and 2 cyclophosphamide pulses (0.5 g/1.73 m2), resulting in a stable decrease in CFH antibody titer to 276 AU. Kidney function quickly normalized (eGFR, 110 mL/min/1.73 m2 [1.83 mL/s/1.73 m2]) and has remained normal after 14 months. All 3 patients show a homozygous deletion mutation of the CFHR1 and CFHR3 genes. Cyclophosphamide pulses with PE may lead to a prolonged decrease in CFH antibody titers and a favorable outcome of atypical hemolytic uremic syndrome and kidney function.]]></description>
		<link>http://kidneyfunction.org/pulse-cyclophosphamide-therapy-and-clinical-remission-in-atypical-hemolytic-uremic-syndrome-with-anti%e2%80%93complement-factor-h-autoantibodies-corrected-proof/</link>
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		<title>Molecular Mechanisms of Hepcidin Regulation: Implications for the Anemia of CKD &#8211; Corrected Proof</title>
		<description><![CDATA[Anemia is prevalent in patients with chronic kidney disease (CKD) and is associated with lower quality of life and higher risk of adverse outcomes, including cardiovascular disease and death. Anemia management in patients with CKD currently revolves around the use of erythropoiesis-stimulating agents and supplemental iron. However, many patients do not respond adequately and/or require high doses of these medications. Furthermore, recent clinical trials have shown that targeting higher hemoglobin levels with conventional therapies leads to increased cardiovascular morbidity and mortality, particularly when higher doses of erythropoiesis-stimulating agents are used and in patients who are poorly responsive to therapy. One explanation for the poor response to conventional therapies in some patients is that these treatments do not fully address the underlying cause of the anemia. In many patients with CKD, as with patients with other chronic inflammatory diseases, poor absorption of dietary iron and the inability to use the body's iron stores contribute to the anemia. Recent research suggests that these abnormalities in iron balance may be caused by increased levels of the key iron regulatory hormone hepcidin. This article reviews the pathogenesis of anemia in CKD, the role and regulation of hepcidin in systemic iron homeostasis and the anemia of CKD, and the potential diagnostic and therapeutic implications of these findings.]]></description>
		<link>http://kidneyfunction.org/molecular-mechanisms-of-hepcidin-regulation-implications-for-the-anemia-of-ckd-corrected-proof/</link>
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		<title>ADMA, C-Reactive Protein, and Albuminuria in Untreated Essential Hypertension: A Cross-sectional Study &#8211; Corrected Proof</title>
		<description><![CDATA[Background: Asymmetric dimethylarginine (ADMA) and subclinical inflammation are associated with atherosclerosis progression, whereas microalbuminuria is an established index of hypertensive organ damage.Study Design: Cross-sectional.Setting &#38; Participants: In an outpatient hypertensive unit, 296 nondiabetic and untreated participants with hypertension were studied. Participants with atherosclerotic cardiovascular disease, severe valvulopathy, congestive heart failure, presence of neoplastic or other concurrent systemic disease, atrial fibrillation, serum creatinine level &#62; 1.5 mg/dL in men and &#62; 1.4 mg/dL in women, and urinary albumin excretion &#62; 300 mg/24 h were excluded.Predictors: ADMA and high-sensitivity C-reactive protein (hs-CRP) levels.Outcome Variable: : Albuminuria assessed using albumin-creatinine ratio (ACR).Measurements: Participants underwent ambulatory blood pressure monitoring, echocardiography, routine assessment of metabolic profile, ADMA, and hs-CRP, whereas ACR was determined as the mean of 3 values in nonconsecutive morning spot urine samples.Results: 64 participants had an ACR of 30-300 mg/g. Stratification based on ADMA level showed that participants with hypertension in quartile [Q] 4 compared with those in Q3, Q2, and Q1 showed the highest ACRs (53.2 vs 31.2 vs 30.4 vs 16.7 mg/g; P &#60; 0.008 for all). Moreover, stratification based on hs-CRP level showed that participants with hypertension in Q4 (69.8% had microalbuminuria) showed the highest ACRs (72.2 vs 25.6, 16.2, and 19.2 mg/g for Q3, Q2, and Q1, respectively; P &#60; 0.008 for all). Stepwise regression analysis showed that age, 24-hour systolic blood pressure, hs-CRP level, ADMA level, and the interaction of hs-CRP with ADMA were independent predictors of ACR (R2 = 0.674; P &#60; 0.001).Limitations: Cross-sectional study.Conclusions: In patients with untreated essential hypertension, increased hs-CRP and ADMA levels are associated with microalbuminuria, suggesting the involvement of inflammation and endothelial dysfunction in vascular and kidney damage.]]></description>
		<link>http://kidneyfunction.org/adma-c-reactive-protein-and-albuminuria-in-untreated-essential-hypertension-a-cross-sectional-study-corrected-proof/</link>
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		<title>Carbohydrate Antigen 19-9 as a Diagnostic Marker for Hepatic Cyst Infection in Autosomal Dominant Polycystic Kidney Disease &#8211; Corrected Proof</title>
		<description><![CDATA[The diagnosis of hepatic cyst infection is difficult in patients with autosomal dominant polycystic kidney disease (ADPKD). We hypothesized that carbohydrate antigen 19-9 (CA 19-9), secreted by the biliary epithelium lining the cysts, is overproduced in the case of cyst infection. In this report, we describe 3 patients with ADPKD with hepatic cyst infection, all with functioning kidney transplants, who had markedly increased serum CA 19-9 levels. Furthermore, CA 19-9 level was extremely increased in cystic fluid obtained in 2 of these individuals. Corresponding with clinical improvement, there was a marked decrease in serum CA 19-9 level in all 3 patients. To assess the potential applicability of these findings, serum CA 19-9 was measured in asymptomatic patients with ADPKD with known liver cysts and in controls without ADPKD. Although serum CA 19-9 levels were significantly higher in asymptomatic patients with ADPKD than in controls, they were markedly increased in patients with cyst infection compared with either asymptomatic ADPKD patients or controls. Immunostaining for CA 19-9 showed strong positivity in biliary tree epithelia and cysts of polycystic livers from patients with ADPKD that appeared more intense than in normal livers. Although further study is necessary, these data suggest that serum CA 19-9 level is markedly increased during liver cyst infection in kidney transplant recipients with ADPKD and has potential utility as a diagnostic marker.]]></description>
		<link>http://kidneyfunction.org/carbohydrate-antigen-19-9-as-a-diagnostic-marker-for-hepatic-cyst-infection-in-autosomal-dominant-polycystic-kidney-disease-corrected-proof/</link>
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		<title>Multiple Listing in Kidney Transplantation &#8211; Corrected Proof</title>
		<description><![CDATA[The increasing number of patients with end-stage renal disease and the expanding waiting lists for various solid-organ transplants, particularly kidney transplants, has compelled prospective transplant recipients and their care teams to explore novel ways to accelerate this process, initiating the practice of multiple listing. Multiple listing is defined as being listed for an organ transplant at more than 1 transplant center. Current policy allows patients to be listed at more than 1 transplant center in 1 or more organ procurement organization. Multiple listing can be beneficial for different groups of transplant candidates. Current data support a beneficial effect for the patient on multiple waiting lists, most notably portending a survival advantage for transplant recipients. The kidney transplant list has the most patients who are multiply listed (4.7%), followed by the liver transplant list at 3.8%. The main potential downside of multiple listing is its effect on patients not on multiple lists, as well as the cost accrued to achieve multiple listings. With the newly clarified policy of the United Network for Organ Sharing, a pivotal role for nephrologists in educating patients about the option of multiple listing becomes more apparent. In this article, current practices and policies regarding multiple listing are reviewed and opinions and ethics relating to the practice are discussed.]]></description>
		<link>http://kidneyfunction.org/multiple-listing-in-kidney-transplantation-corrected-proof/</link>
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