In the earlier stages of CKD, the serum P concentration remains within the normal range because a reduction in kidney filtration of P is compensated by a reduction in tubular reabsorption of P which is mediated by the action of fibroblast growth factor-23 (FGF23) and parathyroid hormone (PTH); both hormones are increased even in moderate renal failure [3,4,5]. This evidence concerns the gene PTH and chronic kidney disease.