Uric acid: bystander or culprit in hypertension and progressive renal disease?

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In humans, uric acid is the main urinary metabolite of purines. Serum levels are higher compared with other mammalians. Uric acid is an antioxidant and perhaps helps to control blood pressure during a low Na+ diet through stimulation of the renin–angiotensin system. Serum uric acid is also considered a marker of tubular reabsorption and ‘effective’ circulating blood volume. Moreover, hyperuricemia seems to be a cofactor in Na+-sensitive hypertension, a marker and possibly itself responsible for microvascular damage through stimulation of the renin–angiotensin system, inhibition of endothelial nitric oxide, and proliferative effects on vascular smooth muscle. As fructose-rich diets increase uric acid levels, hyperuricemia may also play a role in the metabolic syndrome, triggering insulin resistance and hypertension.

A number of studies on rats rendered hyperuricemic by administration of uricase inhibitors have recently confirmed induction of arterial hypertension and microvascular injury, particularly in the remnant kidney or in cyclosporine-induced renal fibrosis.

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