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ative role of UA in CV risk is primarily supported by in vitro study results demonstrating that exposure of cultured endothelial cells to UA induces NADPH oxidase activity and the production of reactive oxygen species.4 Conversely, the association between hyperuricemia and CV disease is only marginal or may be cofounded by other risk factors, such as hypertension, gout, and male sex. Likewise, hyperuricemia could be a consequence of impaired kidney function, diuretic therapy or oxidative stress, and as such, the role of SUA in conditions associated with oxidative stress is not entirely clear.2 Increasing experimental and clinical evidence shows that SUA has an antioxidant role in vivo that protects the CV system. Studies have shown a J-shaped relationship of SUA with CV events.5,6 For instance, the rate of CV events tended to be higher in SUA quartile 1 than in SUA quartile 2 in the PIUMA study ric acid (UA) is the endproduct of purine metabolism in humans. Most serum UA (SUA) is freely filtered in the glomerulus, and approximately 90% of the filtered SUA is reabsorbed, implying that SUA is likely to have a physiological role, rather than simply being a waste of purine metabolism.1 Furthermore, the SUA level in humans is almost 10-fold higher than those in the majority of other mammals, which supports the hypothesis that the SUA level increased during human evolution as an advantage to humans.1

Extremely Low Levels of Serum Uric Acid Are Associated With Endothelial Dysfunction in Humans