Although hyperphosphatemia, a typical serological feature of CKD patients, acts as an independent risk factor for cardiovascular death14,27, we are aware that altering phosphate homeostasis in vivo may lead to changes in FGF23, PTH, Klotho, and VitD, which can also contribute to myocardial hypertrophy and energy metabolism changes24,25. This evidence concerns the gene PTH and chronic kidney disease.