[The uric acid cardio-nephropathy].

Uric acid is a product of purine catabolism formed by the activity of xanthine-oxidase and prevalently excreted by the kidney. In vivo, urate is known to have both an anti- or pro-oxidant role depending on several biological conditions. New evidence suggests that chronic hyperuricemia can contribute to hypertension development, kidney disease and cardiovascular risk. The pathophysiologic mechanisms are various, such as endothelial dysfunction and oxidative stress, vasoconstriction and stimulation of renin angiotensin system. These processes act at the kidney level, within arterioles and tubular cells, as well as at the systemic vasculature and tissue level causing hypertension, atherosclerosis and myocardial dysfunction. In recent years evidence has grown that asymptomatic hyperuricemia is a possible risk factor for the development of hypertension, diabetes as well as renal and cardiovascular events. Preliminary clinical evidence suggests that lowering uric acid levels by the use of xanthine-oxidase inhibitors may improve cardiovascular and renal risk. Several ongoing trials, both with allopurinol and febuxostat, will clarify this issue in the upcoming years.