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[Role of uric acid in hypertension and in the progression of chronic renal disease].

In humans, uric acid (UA) is the main urinary metabolite of purines, whereas in other species (avians) it is the chief nitrogen compound excreted in the urine. The absence of uricase, due to nonsense or splice mutations occurring during the evolution of primates, results in blood urate levels much higher in humans than in other mammalians. This could have favorable implications, including protection from oxidative damage, as well as possibly allowing better blood pressure (BP) control in settings of low dietary Na+ intake. UA is a stimulus of the renin-angiotensin system (RAS). Moreover, blood UA levels are a major marker of proximal tubular function and overall volume status. On the other hand, hyperuricemia is a co-factor in Na+ -sensitive arterial hypertension, a marker and perhaps itself responsible for microvascular and systemic damage through RAS stimulation, inhibitory effects on endothelial cells, and the proliferation of perivascular smooth muscle cells. Recent studies in rats rendered hyperuricemic through administration of oxonic acid demonstrate the induction of hypertension and severe microvascular damage when associated with subtotal nephrectomy or chronic cyclosporine treatment. The opportunity to pharmacologically manipulate blood UA levels through inhibitors of synthesis (allopurinol), uricosuric agents (benziodarone), or recombinant urate oxidase (rasburicase) provides a relevant therapeutic potential in UA metabolism disorders, tumor lysis syndrome, and possibly in essential hypertension, as well as chronic progressive renal disease.