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Open Access Highly Accessed Review

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

David Gustafsson1* and Robert Unwin2

Author Affiliations

1 Bioscience, CVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden

2 University College London, UCL Centre for Nephrology, Royal Free Campus, London, UK

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BMC Nephrology 2013, 14:164  doi:10.1186/1471-2369-14-164

Published: 29 July 2013

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.

Keywords:
Uric acid; Urate; Hypertension; Chronic kidney disease; Congestive heart failure; Type 2 diabetes mellitus; Metabolic syndrome; Cardiovascular events; Atherosclerosis