Crystal deposition diseases: Edited by Michael BeckerControl of renal uric acid excretion and goutTaniguchi, Atsuo; Kamatani, Naoyuki Author Information Institute of Rneumatology, Tokyo Women's Medical University, Tokyo, Japan Correspondence to Atsuo Taniguchi, Institute of Rheumatology, Tokyo Women's Medical University, 10-22 Kawada-cho, Shinjuku-ku, Tokyo 162-0054, Japan Tel: +81 3 5269 1725; fax: +81 3 5269 1726; e-mail: [email protected] Current Opinion in Rheumatology: March 2008 - Volume 20 - Issue 2 - p 192-197 doi: 10.1097/BOR.0b013e3282f33f87 Buy Metrics Abstract Purpose of review Impaired renal uric acid excretion is the major mechanism of hyperuricemia in patients with primary gout. This review highlights recent advances in the knowledge of normal mechanisms of renal uric acid handling and derangement of these mechanisms in uric acid underexcretion. Recent findings The discovery of URAT1 has facilitated identification of other molecules potentially involved in uric acid transport in the renal tubules. Some of these molecules show gender differential expression in animal experiments. Sodium-dependent monocarboxylate cotransporters have been shown to transport lactate and butyrate, and may have roles in hyperuricemia associated with diabetic ketoacidosis and alcohol ingestion. Certain polymorphisms in SLC22A12 may be associated with the development of hyperuricemia or gout, although confirmation is needed. Mechanisms of hyperuricemia associated with uric acid underexcretion in patients with familial juvenile hyperuricemic nephropathy also remain to be clarified. Distal tubular salt wasting and compensatory upregulation of the resorption of sodium and uric acid in the proximal tubule may explain the hyperuricemia associated with this disorder. Summary Much progress has been made in understanding the mechanisms of renal uric acid handling. Elucidation of the mechanisms of hyperuricemia in patients with familial juvenile hyperuricemic nephropathy will shed light on the function of uromodulin, functional impairment of which eventually results in diminished uric acid excretion. © 2008 Lippincott Williams & Wilkins, Inc.