Uric acid as a cardiovascular risk factor in arterial hypertension

Background Increased serum urate concentrations is a frequent finding in pa tients with hypertension. Since hyperuricaemia is associated with obesity, renal disease, hyperlipidaemia, and atherosclerosis the question as to whet her serum urate is a cardiovascular risk factor per se has remained elusive . In considering the relationship between uric acid and hypertension three aspects should be answered: (a) the significance of hyperuricaemia; (b) the pathophysiological mechanism of the association; and (c) whether hyperuric aemia is deleterious. Significance of hyperuricaemia Several arguments favour the concept that in creased serum urate in hypertensive patients most likely reflects renal vas cular involvement. Pathophysiological mechanism Hyperuricaemia is accompanied by a relatively diminished uric acid excretion rate in hypertensive patients. Selective ins ulin resistance and hyperinsulinism estimulates the tubular sodium-hydrogen exchanger and facilitates the active reabsorption of urate. Is hyperuricaemia deleterious? In addition to the renal (urolithiasis) and articular disturbances that hyperuricaemia may cause, vascular damage due t o arterial hypertension may limit the availability of oxygen for ATP synthe sis. Tissue hypoxia determines increased adenine nucleotide degradation whi ch ends in uric acid overproduction. The formation of uric acid is accompan ied by an enhanced synthesis of reactive oxygen species which play a signif icant role in tissue damage. The hypothesis that hyperuricaemia indicates h ypertensive vascular damage is plausible and if unequivocally demonstrated may contribute to delineate evidence-based therapeutic strategies for hyper tensive-hyperuricaemic patients. I Hypertens 1999, 17:869-872 (C) Lippincot t Williams & Wilkins.