Since uric acid (urate), the final product of purine metabolism, exhibits antioxidative activity, its protective role against oxidative stress becomes attractive. Low serum urate levels have been associated with multiple sclerosis, Parkinsons disease, and Alzheimers disease. Despite its beneficial role, hyperuricemia is associated with gout, hypertension, cardiovascular diseases such as myocardial infarction and stroke, and renal diseases such as acute urate nephropathy and nephrolithiasis. The urate transport system of the kidney is an important determinant of the serum urate level, but clarification of its molecular mechanism remains incomplete. In 2002, our group identified URAT1 (SLC22A12), a renal apical urate/anion exchanger, leading to the accumulation of information concerning individual molecules involved in urate transport in the kidney. In 2008, we functionally characterized facilitatory glucose transporter family member GLUT9 (SLC2A9) as a voltage-driven urate transporter URATv1 and analysis of a renal hypouricemia patient with a genetic defect in SLC2A9 have established the main route of the urate reabsorption pathway at the basolateral side of renal proximal tubules, where urate in the urinary lumen is taken up via apical URAT1 and intracellular urate exits from the cell to the interstitium/blood space via basolateral URATv1. In this review, recent findings concerning these molecules are presented.