Kidney Function

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.

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 & Participants: 110 adult hemodialysis patients with tunneled cuffed intravascular catheters inserted at 3 centers in Northwest England.Outcomes & 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.

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 & 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 <125% of 2004 Department of Health and Human Services guideline), higher SES (≥125% of guideline); white and African American race.Outcomes & Measurements: CKD defined as estimated glomerular filtration rate <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 <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.