The Role of Phosphate in the Pathogenesis of Secondary Hyperparathyroidism and Vascular Calcification in Chonic Kidney Disease

High serum phosphate is a major complication in chronic kidney disease (CKD) patients. Recent investigations have been well documented that abnormalities in mineral and bone metabolism in CKD patients associate with increased cardiovascular morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of secondary hyperparathyroidism and extra-skeletal calcification in dialysis patients. Furthermore, inorganic phosphate may cause vascular mineralization directly through a real ”ossification” of the tunica media in the vasculature of CKD patients. The ”classical” treatment of secondary hyperparathyroidism and hyperphosphatemia in CKD patients consists of either calcium or aluminium based phosphate-binders and calcitriol administration. Unfortunately, this ”first generation” therapy is not free of complications. New free-calcium and-aluminum phosphate binders, such as sevelamer hydrochloride, can be used to treat hyperphosphatemia and secondary hyperparathyroidism, reduce atherosclerotic process, and prevent vascular calcification in CKD patients.