Abstract
Hyperuricemia, which has been considered as a cause of gout and nephrolithiasis has recently been suggested to be associated with hypertension, coronary heart disease, heart failure, atrial fibrillation, insulin resistance, and nonalcoholic fatty liver disease. Several clinical and experimental studies have supported uric acid (UA) as an independent risk factor for predicting disease development along with the traditional risk factors. The mechanism by which UA causes cardiometabolic disease has not been fully elucidated to date; however, it has been explained by several hypotheses such as oxidative stress, reduced nitric oxide bioavailability, inflammation, endothelial dysfunction, and so on. Although evidence of the preventive and therapeutic effects of UA lowering therapy on cardiometabolic diseases is still insufficient, it is expected to be considered as a new treatment strategy for such diseases through additional, carefully designed, large-scale clinical studies.