Journal
ADVANCES IN CHRONIC KIDNEY DISEASE
Volume 19, Issue 6, Pages 419-424Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.ackd.2012.07.008
Keywords
Chronic kidney disease; Gout; Hyperuricemia
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Metabolic end products accumulate in kidney failure, including uric acid (UA), a terminal product of purine catabolism. Hyperuricemia (HUA) can cause gout and has been increasingly linked with cardiovascular (CV) morbidity and mortality, outcomes that are highly prevalent in patients with kidney disease. Serum UA levels rise as glomerular filtration declines, whereas the frequency of gouty attacks declines and the incidence of CV death rises precipitously. Herein, we review the kinetics of UA metabolism in CKD and dialysis and discuss the possible mechanisms of gout mitigation in kidney failure and the potential contribution of hyperuricemic milieu to CV outcomes in patients with kidney disease. (C) 2012 by the National Kidney Foundation, Inc. All rights reserved.
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