| [ Summary ] |
After phosphate intake, FGF23 is secreted from the bones and acts on the kidneys through its cell-surface receptor Klotho. FGF23 increases phosphate excretion by nephrons and decreases the active form of vitamin D (1,25D3), thereby maintaining phosphate homeostasis. In the early stages of CKD, FGF23 increases in order to compensate for decreased nephron quantity. FGF23 reduces 1,25D3 and then increases PTH. PTH further increases FGF23, thereby forming a vicious cycle, leading to CKD-MBD characterized by high FGF23, low 1,25D3, and high PTH. Hoped for interventions which may disrupt this vicious cycle are expected to be novel therapeutic methods for CKD treatment. |