Uric acid is a metabolite of purine degradation and hyperuricemia is strongly associated with gout and kidney stones, and has been linked to several other pathological conditions such as hypertension, the metabolic syndrome and inflammation. GLUT9 (SLC2A9) is a newly identified urate transporter, initially cloned by homology with the glucose transporter family. GLUT9 mutations in humans have been shown to be causative for the familial renal hypouricemia, a condition in which affected patients present hypouricemia, renal uric acid wasting, kidney stone and a propensity to acute renal failure during strenuous exercise. The in vivo role of GLUT9 has been recently unravelled in the mouse. Mice with whole body deletion of Glut9 are hyperuricemic and display severe nephropathy that results from intratubular uric acid precipitation. Mice in which GLUT9 has been deleted only in the liver present with hyperuricemia, due to the role of GLUT9 in facilitating the entry of uric acid in the hepatocyte for its degradation by the enzyme uricase. By contrast, the role of GLUT9 in the kidney remains largely unknown. In particular, the exact localization of GLUT9 (proximal vs. distal tubules, apical vs. basolateral side of the epithelium), and the precise mode of urate transport have not been solved yet. In order to address these points, we generated mouse models carrying kidney-specific disruption in different parts of the tubules and showed that GLUT9 is essential for proper urate reabsorption in the mouse kidney. Indeed, tetracycline-inducible whole nephron deletion of GLUT9 led to hyperuricosuria. These results point out GLUT9 as a crucial partner in the renal handling of uric acid and designate it as a new target for uricosuric agent.