The pathophysiology of hyperuricaemia and its possible relationship to cardiovascular disease, morbidity and mortality

BMC Nephrol. 2013 Jul 29;14:164. doi: 10.1186/1471-2369-14-164.

Abstract

Uric acid is the end product of purine metabolism in humans. High levels are causative in gout and urolithiasis. Hyperuricaemia has also been implicated in the pathophysiology of hypertension, chronic kidney disease (CKD), congestive heart failure (CHF), the metabolic syndrome, type 2 diabetes mellitus (T2DM), and atherosclerosis, with or without cardiovascular events. This article briefly reviews uric acid metabolism and summarizes the current literature on hyperuricaemia in cardiovascular disease and related co-morbidities, and emerging treatment options.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / epidemiology
  • Cardiovascular Diseases / mortality*
  • Cardiovascular Diseases / physiopathology*
  • Humans
  • Hyperuricemia / epidemiology
  • Hyperuricemia / mortality*
  • Hyperuricemia / physiopathology*
  • Morbidity