| Theme |
Testify the concepts of renal osteodystrophy and chronic kidney disease-bone and mineral disorder (CKD-MBD) |
| Title |
FGF23-Klotho system as biomarker |
| Author |
Yasuji Sugano |
Division of Nephrology, Endocrinology and Metabolism, Tokai University Hachioji Hospital / Kita Hachiouji Clinic |
| Author |
Takatoshi Kakuta |
Division of Nephrology, Endocrinology and Metabolism, Tokai University Hachioji Hospital |
| [ Summary ] |
Understanding the role of FGF23 requires some explanation. FGF23 is a phosphate diuretic hormone produced primarily in bone osteocytes. FGF23 decreases the expression of the type 1 sodium-phosphate cotransporters in the proximal tubule and accelerates urinary phosphate excretion. In addition, FGF23 decreases active vitamin D concentrations by downregulating the expression of 1-α-hydroxylase. These two actions of FGF23 synergistically reduce phosphorus concentrations. Moreover, FGF23 suppresses PTH secretion through its direct effects on parathyroid cells. FGF23 concentrations are elevated in CKD patients before serum phosphate, calcium or PTH concentrations change significantly. Thus, increased FGF23 concentrations in the early stages of CKD may promote urinary phosphate excretion and suppress PTH secretion, counteracting the increases in serum phosphate and PTH levels. These mechanisms, however, are inoperative in end-stage renal failure patients because the expression of FGFR1-Klotho coreceptors which mediate the actions of FGF23 which is downregulated in these patients. The role of the FGF23-Kloth system as a biomarker is considered. |