Renal handling of uric acid

Uric acid is the end product of purine catabolism in humans. The plasma concentration is the result of an intricate and partially known process that regulates its synthesis and excretion. Plasma levels range from 3 to 7 mg/dl, and are influenced by diet rich in purines, cell turnover and reduced renal excretion. The kidney plays a pivotal role in acid uric homeostasis, and the pathogenesis of hyperuricemia often correlates with a reduction in the amount of renal excretion, as happens in chronic kidney failure or as a result of certain drugs. Physiologically, uric acid is freely filtered by glomerulus; along the proximal tubule it is reabsorbed and secreted, with a fractional excretion equal to 6-12%. During the last decades many efforts have led to a better understanding of the molecular basis of renal urate handling. The present study analyzes the most recent evidences that demonstrate the role of several proteins involved in urate transport. Understanding this physiological mechanisms had a great impact in clinical practice, providing advances in our knowledge of drug action and genetic associations in hyperuricemic patients; contextually it opened new avenues for drug development.