FGF23 and hyperphosphatemia: Deficiency of klotho also appears to reduce osteoblastic population andinterfere with bone mineralization.7 Together, the FGF receptor–Klotho complex inhibits sodium-dependent phosphateuptake and 1α-hydroxylase activity in the proximal tubule of the kidney, leading tohypophosphatemia and inappropriate low 1,25(OH)2D.8 In contrast, a deficiency of either FGF23 or klotho results in the oppositephenotype of hyperphosphatemia and elevated production of 1, 25(OH)2D,further confirming the role of FGF23 in regulation of serum phosphate and1,25(OH)2D levels.