title: Advanced kidney failure and hyperuricemia.
abstract: 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.
authors.affiliation: Department of Internal Medicine, Section on Nephrology, Wake Forest School of Medicine, Winston-Salem, NC 27157-1053, USA. mmurea@wakehealth.edu
authors.forename: Mariana
authors.initials: M
authors.lastname: Murea
mesh_terms: D006073:Gout / Q000209:etiology* / Q000378:metabolism; D006801:Humans; D033461:Hyperuricemia / Q000378:metabolism* / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects*; D014527:Uric Acid / Q000097:blood* / Q000378:metabolism
chemical_list: D014527:Uric Acid