Hyperuricemia and deterioration of kidney function; a mini-review to the pathophysiological mechanisms

Abstract

Uric acid, as the end-product of purine metabolism, is excreted principally by the renal proximal tubules. Abnormal serum level of uric acid are owing to modifications in excretion or production. Uric acid may be a principal factor in the pathogenesis of acute renal failure, aggravation of diabetic kidney disease, aggravation of chronic renal failure and hypertension. Uric acid may not only be a sign but also a potential therapeutic target in various renal disease. Elevated serum uric acid levels initiates an endothelial cell dysfunction through activating the renin–angiotensin system, and inhibiting nitric oxide synthase and then producing a pro-inflammation state resulted to change the morphology of  endothelial and vascular smooth muscle cells, and finally contributing to atherosclerosis.