G protein-coupled pH-sensing receptor OGR1 and metabolic acidosis-induced hypercalciuria

Abstract

Nearly a century ago it was discovered that metabolic acidosis promotes hypercalciuria. Studies have described intrarenal and extrarenal mechanisms underlying calcium wasting in acidosis, in part by altering bone metabolism but also by directly inhibiting renal calcium transport. In this issue of Kidney International, Imenez Silva et al. report that ablation of the pH-sensing receptor ovarian cancer G protein-coupled receptor 1 in a murine model led to Na⁺/H⁺-exchanger isoform 3 redistribution in the kidney and dampens the hypercalciuric response to metabolic acidosis.