FGF23 and secondary hyperparathyroidism: The mechanisms how phosphate retention contributes to the development of secondary hyperparathyroidism are multifactorial (Figure 1) [18, 19], including (1) the induction of hypocalcemia, (2) diminished renal production of 1,25(OH)2D by inhibiting 1-alpha-hydroxylase activity, (3) increased PTH gene expression by reducing PTH mRNA degradation, (4) direct stimulation of parathyroid growth, and (5) stimulation of FGF23 production in bone.