ABCG2 dysfunction causes hyperuricemia due to both renal urate underexcretion and renal urate overload

作者：Matsuo Hirotaka^*; Nakayama Akiyoshi; Sakiyama Masayuki; Chiba Toshinori; Shimizu Seiko; Kawamura Yusuke; Nakashima Hiroshi; Nakamura Takahiro; Takada Yuzo; Oikawa Yuji; Takada Tappei; Nakaoka Hirofumi; Abe Junko; Inoue Hiroki; Wakai Kenji; Kawai Sayo; Guang Yin; Nakagawa Hiroko; Ito Toshimitsu; Niwa Kazuki; Yamamoto Ken; Sakurai Yutaka; Suzuki Hiroshi; Hosoya Tatsuo; Ichida Kimiyoshi; Shimizu Toru; Shinomiya Nariyoshi

来源：Scientific Reports, 2014, 4(1): 3755.

DOI：10.1038/srep03755

Gout is a common disease which results from hyperuricemia. We have reported that the dysfunction of urate exporter ABCG2 is the major cause of renal overload (ROL) hyperuricemia, but its involvement in renal underexcretion (RUE) hyperuricemia, the most prevalent subtype, is not clearly explained so far. In this study, the association analysis with 644 hyperuricemia patients and 1,623 controls in male Japanese revealed that ABCG2 dysfunction significantly increased the risk of RUE hyperuricemia as well as overall and ROL hyperuricemia, according to the severity of impairment. ABCG2 dysfunction caused renal urate underexcretion and induced hyperuricemia even if the renal urate overload was not remarkable. These results show that ABCG2 plays physiologically important roles in both renal and extra-renal urate excretion mechanisms. Our findings indicate the importance of ABCG2 as a promising therapeutic and screening target of hyperuricemia and gout.

• 出版日期2014-1-20