Hyperuricemia in acute gastroenteritis is caused by decreased urate excretion via ABCG2

• DOI: 10.1038/srep31003
• Publication Date: 2016-08-30T09:20:46Z
• Authors: Hirotaka Matsuo; Tomoyuki Tsunoda; Keiko Ooyama; Masayuki Sakiyama; Tsuyoshi Sogo; Tappei Takada; Akio Nakashima; Akiyoshi Nakayama; Makoto Kawaguchi; Toshihide Higashino; Kenji Wakai; Hiroshi Ooyama; Ryota Hokari; Hiroshi Suzuki; Kimiyoshi Ichida; Ayano Inui; Shin Fujimori; Nariyoshi Shinomiya
• Keywords: Serum; 0301 basic medicine; 0303 health sciences; Hyperuricemia; Article; Gastroenteritis; Neoplasm Proteins; Uric Acid; 3. Good health; 03 medical and health sciences; Intestinal Elimination; ATP Binding Cassette Transporter, Subfamily G, Member 2; Humans; Intestinal Mucosa

AbstractTo clarify the physiological and pathophysiological roles of intestinal urate excretion via ABCG2 in humans, we genotyped ABCG2 dysfunctional common variants, Q126X (rs72552713) and Q141K (rs2231142), in end-stage renal disease (hemodialysis) and acute gastroenteritis patients, respectively. ABCG2 dysfunction markedly increased serum uric acid (SUA) levels in 106 hemodialysis patients (P = 1.1 × 10−4), which demonstrated the physiological role of ABCG2 for intestinal urate excretion because their urate excretion almost depends on intestinal excretion via ABCG2. Also, ABCG2 dysfunction significantly elevated SUA in 67 acute gastroenteritis patients (P = 6.3 × 10−3) regardless of the degree of dehydration, which demonstrated the pathophysiological role of ABCG2 in acute gastroenteritis. These findings for the first time show ABCG2-mediated intestinal urate excretion in humans, and indicates the physiological and pathophysiological importance of intestinal epithelium as an excretion pathway besides an absorption pathway. Furthermore, increased SUA could be a useful marker not only for dehydration but also epithelial impairment of intestine.