Hyperuricemia and cardiovascular disease risk

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.

Keywords::

• allopurinol
• cardiovascular disease risk
• epidemiology
• febuxostat
• pathophysiology
• serum uric acid
• xanthine-oxidase inhibitors

Financial & competing interests disclosure

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.

Key issues

• Recent data suggest that high–normal serum uric acid (SUA) levels are often associated to a large number of known cardiovascular disease (CVD) risk factors.

• High–normal SUA is also often associated to CVD and cognitive decline.

• High–normal SUA also seems to be an independent risk factor for CVD and Type 2 diabetes.

• Renin-angiotensin system activation seems at least partly responsible for SUA-related cardiovascular damage.

• Preliminary data suggest that the reduction in SUA levels in subjects with normal–high SUA could prevent at least a part of target organ damage related to high SUA.

• Selective inhibition of xanthine oxidase appears to be a promising pharmacological tool to reduce SUA levels and CVD risk associated to high–normal SUA levels.

• Future trials are needed to understand how the integration of SUA in risk stratification charts will improve the early detection of subjects at high cardiovascular risk and how SUA reduction will decrease the risk.