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uric acid and cvd

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Review QJM Uric acid as a risk factor for cardiovascular disease W.S. WARING, D.J. WEBB and S.R.J. MAXWELL From the Clinical Pharmacology Unit and Research Centre, Department of Medical Sciences, University of Edinburgh, Edinburgh, UK Introduction Over recent years there has been renewed debate about the nature of the association between raised serum uric acid concentration and cardiovascular disease. 1 Several large studies have identified the value, in populations, of serum uric acid concentra- tion in predicting the risk of cardiovascular events, such as myocardial infarction. This has directed research towards the potential mechanisms by which uric acid might have direct or indirect effects on the cardiovascular system. It has been difficult to identify the specific role of elevated serum uric acid because of its association with established cardio- vascular risk factors such as hypertension, diabetes mellitus, hyperlipidaemia and obesity. 2,3 Indeed, it is not even clear at this stage whether uric acid has a damaging or protective effect in these circum- stances. Increased understanding of the mechanisms underlying these associations may allow a clearer interpretation of the importance of elevated serum uric acid concentrations, and the potential value of specific urate-lowering treatment on cardiovascular disease. Uric acid synthesis Purines arise from metabolism of dietary and endo- genous nucleic acids, and are degraded ultimately to uric acid in man, through the action of the enzyme xanthine oxidase Figure 1). Uric acid is a weak acid pKa 5.8), distributed throughout the extracellular fluid compartment as sodium urate, and cleared from the plasma by glomerular filtration. 4 Around 90% of filtered uric acid is reabsorbed from the proximal renal tubule, while active secretion into the distal tubule by an ATPase-dependent mechanism contributes to overall clearance. 5 Serum uric acid concentration within the population has a Gaussian distribution, with a typical reference range 95% CI) of 120±420 mmol/l. For an individual, urate concen- tration is determined by a combination of the rate of purine metabolism both endogenous and exogenous) and the efficiency of renal clearance. Purine metabolism is influenced by dietary, as well as genetic factors regulating cell turnover. Uric acid is sparingly soluble in aqueous media, and persist- ent exposure to high serum levels predisposes to urate crystal deposition within soft tissues. 4 All species apart from man and higher apes express urate oxidase, an enzyme responsible for further metabolism of uric acid to allantoin a more sol- uble waste product) prior to excretion. 6 In man, the urate oxidase gene located on chromosome 1 is not expressed due to two non-sense mutations. 7 Loss of uric oxidase activity appears to have developed under evolutionary pressure, 7 suggesting that higher serum uric acid concentrations, or reduced urate oxidase may confer important advantages in man. Uric acid as a risk factor for cardiovascular disease An epidemiological link between elevated serum uric acid and an increased cardiovascular risk has ß Association of Physicians 2000 Address correspondence to Dr W.S. Waring, Clinical Pharmacology Unit, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh EH4 2LH. e-mail: [email protected] Q J Med 2000; 93:707±713

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