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A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
Published on: November 7, 2017
Hyperuricemia and cardiovascular disease risk
Claudio Borghi1, Federico Maria Verardi, Ilenia Pareo
1Department of Medical and Surgical Science, S. Orsola-Malpighi University Hospital, University of Bologna, Via Albertoni 15 - Pad. 2, 40138 Bologna, Italy.
Abstract:
Uric acid (UA) is the final end product of purine catabolism and is formed from xanthines and hypoxanthines. Hyperuricemia can be secondary to either an exaggerated production of UA that follows high cellular turnover conditions or, most frequently, to a low renal excretion in patients with impaired renal function. Recent data suggest that serum UA (SUA) at high-normal level is associated with cardiovascular disease risk factors and cardiovascular disease, often being a predictor of incident events. Preliminary data suggest that the reduction of SUA level in subjects with normal-high SUA could prevent at least a part of target-organ damage related to high SUA, especially when xanthine oxidase is selectively inhibited.
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