Do We Need Another Look at Serum Uric Acid in Cardiovascular Disease? Serum Uric Acid as a Predictor of Outcomes in Acute Myocardial Infarction

In humans and other higher primates, uric acid (UA) is the end product of purine metabolism generated by oxidation of xanthine catalyzed by xantine oxidase (XO) (EC 1.17.3.2) (Figure 1). In other mammals, UA is further oxidized by uricase (EC 1.7.3.3) to yield highly soluble allantoin, which is then excreted from the body. From the evolutionary standpoint, the reasons for the mutations resulting in a nonfunctioning uricase gene (pseudogene) in higher mammals are still unclear. In contrast to allantoin, uric acid is poorly hydrosoluble (water solubility of its salts, the urates, is slightly higher) and when its serum concentrations exceed the theoretical limit of solubility (around 415 mol/L, or 7 mg/dL), urate crystals are likely to be formed. Approximately two thirds of the daily UA turnover is eliminated by the kidney (glomerular filtration, tubular re-absorption and secretion) and one third via the gastrointestinal system.