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Abstract
Hyperuricemia is associated with an increased risk of developing gout. This increases with the degree and duration of hyperuricemia. Gout can be managed by dietary modification and pharmacologic urate-lowering therapies. The recent identification of the renal apical urate/anion exchanger URAT1 (SLC22A12) and several membrane proteins relevant to the transport of urate play an important role in gaining a better understanding of the mode of action of many drugs used to treat gout. As described in this review, therapeutics designed to modify URAT1 transport activities might be useful in treating pathologies associated with hyperuricemia such as gout and urolithiasis. Continuing studies into the urate transportsome hold promise for the development of new, more effective therapeutics for hyperuricemia.
Acknowledgments
The authors thank all the members of their laboratories who have contributed to much of the work discussed in this review. This work was supported in part by grants from the Ministry of Education, Culture, Sports, Science and Technology of Japan, the Japan Society for the Promotion of Science, Research on Health Sciences focusing on Drug Innovation from the Japan Health Sciences Foundation, Mutual Aid Corporation for Private Schools of Japan, the Salt Science Research Foundation (No. 0524, 0721), Gout Research Foundation of Japan, the Ichiro Kanehara Foundation, the Shimabara Science Promotion Foundation and the Kyorin University School of Medicine (Kyorin Medical Research Award 2006).