On the other hand, recent studies suggested an increase in C-terminal FGF23 may precede an increase in intact FGF23 in the relatively early phase of CKD [39] and that cleavage of FGF23 might be a major determinant for FGF23 activity in various diseases [40,41,42]; therefore, serum levels of intact FGF23 should be assessed, especially among populations including patients without severe renal dysfunction, such as the current study sample. This evidence concerns the gene FGF23 and chronic kidney disease.