Uric acid (UA) is the terminal product of purine catabolism and arises from both endogenous nucleic acid turnover and exogenous intake—particularly from diets rich in animal protein and fructose [1]. Accumulating evidence implicates elevated serum uric acid (SUA) as associated to an increase in the risk of cardiovascular disease (CVD), acting through multiple pathogenic mechanisms including endothelial dysfunction, oxidative stress, systemic inflammation, and impaired renal function—all of which are known to play a critical role in the development of adverse cardiovascular outcomes [2].
