The origin of uric acid, metabolic pathways of purine metabolism and the disposition of uric acid in normal man are reviewed. Two thirds of the uric acid is normally excreted through the kidney while one third gains entrance to the gut where it undergoes uricolysis. The pathogenesis of hyperuricemia in primary and secondary gout is discussed. Increased production or decreased excretion of uric acid are the two principal mechanisms of hyperuricemia. The known biochemical defects associated with primary overproduction gout are outlined. Extrarenal uricolysis assumes a greater role when the renal excretion of uric acid is compromised.