The role of hyperuricemia in vascular disorders

The role of uric acid as a mediator of vascular damage is not a new idea but has only recently gained widespread acceptance. Uric acid has previously been viewed as a benign solute in serum until it exceeds its saturation level. Others have viewed it as an important antioxidant. These opinions have given way to strong epidemiologic evidence that uric acid elevation may damage endothelial cells and cause significant medical problems.

The comorbidities associated with gout include hypertension, renal failure, obesity and diabetes. Multiple large epidemiologic studies cited in this review show that uric acid itself may play an important role in initiating the vascular endothelial dysfunction associated with this cluster of medical problems and ultimately lead to stroke, coronary artery disease and chronic kidney disease. These studies are supported by experiments in animals demonstrating how uric acid can gain entrance into cells and function as a 'pro-oxidant'.

Uric acid has been long recognized as the cause of gouty arthritis and kidney stones. There is mounting evidence that it may also have an important role in the development of vascular conditions such as coronary heart disease, stroke and kidney disease. These findings have important implications for the way we view asymptomatic hyperuricemia and for future therapeutic interventions.