FGF23 and kidney disorder: Using genetic and pharmacologic approaches to increase DMP1 concentrations in bone of WT and Col4a3−/− mice with CKD, we also show that restoration of DMP1 in bone prevents CKD-associated bone disease by reducing osteocyte apoptosis, lowers FGF23 production via an NFAT signaling pathway, attenuates LVH, and prolongs survival despite unchanged severity of kidney disease and worsened hyperphosphatemia.