As CKD progresses, tubular phosphate excretion is less effective, leading to hyperphosphatemia, which in turn contributes to the increased release of PTH and FGF-23 to maintain normophosphatemia by increasing the phosphaturic effect (this action becomes insufficient starting from stage 4 CKD) [11] and activity of renal CYP24A1, which encodes the 24-hydroxylase, resulting in calcitriol inactivation and acting as a main inhibitor of 1-alpha hydroxylase [5]. This evidence concerns the gene FGF23 and hyperphosphatemia.