[URATE AS A POTENTIAL RISK FACTOR OF CARDIOVASCULAR AND RENAL DISEASES]

Abstract

Although asymptomatic hyperuricemia is rather often in laboratory reports, it cannot be considered a disease. Despite the high prevalence of hyperuricemia in patients with arterial hypertension (AH), chronic kidney disease (CKD), cardiovascular disease (CVD) or metabolic syndrome, hyperuricemia is not confirmed as a causative factor of these disorders. The aim is to point to the latest studies of the importance of urate as a possible cardiorenal risk factor. The literature published in 2015 and 2016 was searched for the possible impact of urate level on the development of cardiorenal diseases. The PubMed, Cochrane, Medline, and UpToDate databases were searched for the literature published between November 2009 and October 2016 using the following key words: urate, hyperuricemia, cardiovascular disease, and chronic kidney disease. Causative correlation of hyperuricemia is confirmed only in disorders where deposits of monosodium urate crystals are present. Results of recent studies do not justify routine use of xanthine oxidase inhibitors in asymptomatic hyperuricemia. Some studies with small numbers of patients and short follow up report on endothelial function improvement on therapy with xanthine oxidase inhibitors. Nonpharmacological intervention by changing unhealthy lifestyle is preferred. Treatment of asymptomatic hyperuricemia in CKD is still debated, and additional studies are necessary to demonstrate the benefit of lowering urate level in CKD. Family doctors (general practitioners) should be familiar with the recommended approach to patients with asymptomatic hyperuricemia. Evidence based medicine still does not recommend target determination of serum urate level for identifying CVD and CKD risk factors. Recent studies suggest the possible effect of uric acid in cardiorenal diseases and that treatment of asymptomatic hyperuricemia with xanthine oxidase inhibitors may also be useful in CVD prevention. Additional studies are needed to prove this statement.