Vascular calcification is a very common event in patients affected by diabetes and chronic kidney disease (CKD). Recently, it has been well documented that abnormalities in mineral and bone metabolism in CKD patients associate with increased morbidity and mortality. Elevated serum phosphate and calcium-phosphate product levels play an important role in the pathogenesis of vascular mineralization in uremic patients and also appear to be associated with increased cardiovascular mortality. Together with classical passive precipitation of calcium-phosphate in soft tissues, during the last decade it has been demonstrated that inorganic phosphate may cause extraskeletal calcification directly through a real “ossification” of the tunica media in the vasculature of CKD patients. Therefore, control of phosphate retention is now an even more crucial target of treatment in patients affected by chronic kidney disease. 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 “old generation” therapy is not free of complications.Patents are also reported discussing the role of derivatives of Lanthanum carbonate hydrates are also used for the treatment of hyperphosphataemia in patients with renal failure. New calcium- and aluminium-free phosphate binders, such as sevelamer hydrochloride and lanthanum carbonate, can be used to treat hyperphosphatemia and secondary hyperparathyroidism, reduce atherosclerotic process, and prevent vascular calcification in CKD patients.