SLC34A1 and chronic kidney disease: A gain-of-function mechanism might explain the hyperphosphatemia in patients with CKD, especially in light of its recent identification as a prominent CKD locus.176 People who tend toward lower fractional excretions of phosphate might exhibit increased levels of NaPi2a.167 The high and inducible levels of expression suggest that variant versions differ in folding and may trigger an “endoplasmic reticulum associated stress response (ERAD).”177