Uric acid as a cardiovascular risk factor in arterial hypertension

Publisher Website
Google Scholar
Abstract
Increased serum urate concentrations is a frequent finding in patients with hypertension. Since hyperuricaemia is associated with obesity, renal disease, hyperlipidaemia, and atherosclerosis the question as to whether 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 hyperuricaemia is deleterious. Several arguments favour the concept that increased serum urate in hypertensive patients most likely reflects renal vascular involvement. Hyperuricaemia is accompanied by a relatively diminished uric acid excretion rate in hypertensive patients. Selective insulin resistance and hyperinsulinism estimulates the tubular sodium—hydrogen exchanger and facilitates the active reabsorption of urate. In addition to the renal (urolithiasis) and articular disturbances that hyperuricaemia may cause, vascular damage due to arterial hypertension may limit the availability of oxygen for ATP synthesis. Tissue hypoxia determines increased adenine nucleotide degradation which ends in uric acid overproduction. The formation of uric acid is accompanied by an enhanced synthesis of reactive oxygen species which play a significant role in tissue damage. The hypothesis that hyperuricaemia indicates hypertensive vascular damage is plausible and if unequivocally demonstrated may contribute to delineate evidence-based therapeutic strategies for hypertensive-hyperuricaemic patients.