The challenge of hyperphosphatemia control in chronic kidney disease

Mineral metabolism abnormalities in chronic kidney disease (CRK) have adverse effects, particularly on the skeleton and cardiovascular system. Among the classic biochemical abnormalities, hyperphosphoremia plays a significant role. It stimulates parathyroid hormone production by the parathyroid gland both directly (it increases PTH synthesis and secretion and induces cell proliferation) and indirectly (it suppresses calcitriol synthesis by the kidneys and reduces vitamin D receptor and calcium sensor expression). It induces phenotypical activation of vascular smooth muscle cells, causing them to acquire an osteoblastic profile and produce procalcifying factors. As a result of both effects, numerous studies (retrospective) have shown an increase in mortality associated with hyperphosphoremia (usually P > 5.5 mg/dL). Finally, recent observations suggest a direct association between phosphoremia and CKD. Undoubtedly, all these are powerful arguments in favor of increasingly strict control of P in CKD.