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

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
DOI: 10.1038/srep31003 Publication Date: 2016-08-30T09:20:46Z
ABSTRACT
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.
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