Sodium-dependent anion transport by SMCT1 and SMCT2 increases intracellular concentrations of monovalent anions that exchange with luminal urate (URAT1/OAT10). OAT4 appears to exchange urate with divalent anions. GLUT9 is the exit pathway for urate at the basolateral membrane.
Courtesy of David B Mount, MD, 2012.
Updated with information from:
- Johnson RJ, Bakris GL, Borghi C, et al. Hyperuricemia, Acute and Chronic Kidney Disease, Hypertension, and Cardiovascular Disease: Report of a Scientific Workshop Organized by the National Kidney Foundation. Am J Kidney Dis 2018; 71:851.
- Mandal AK, Mount DB. The molecular physiology of uric acid homeostasis. Annu Rev Physiol 2015; 77:323.
