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.
aDepartment of Clinical Sciences, Italy
bDivision of Nephrology, Italy
cDivision of Dialysis, Sant'Andrea University Hospital, University ‘La Sapienza’ of Rome, Rome, Italy
Received 17 May, 2008
Revised 21 June, 2008
Accepted 25 June, 2008
Correspondence to Paolo Menè, MD, Department of Clinical Sciences, U.O.C. Nefrologia, Azienda Ospedaliera Sant'Andrea, Via di Grottarossa 1035-1039, 00189 Rome, Italy Tel: +39 06 3377 5949; fax: +39 06 3377 5866; e-mail: Paolo.Mene@uniroma1.it