Chronic renal failure is a well-known risk condition for cardiovascular disease and in particular vascular calcifications. In fact, with respect to the normal population, where only ''classic'' risk factors have been described, kidney patients also have non-classic risk conditions. Among these, alterations in divalent ions, parathyroid hormone and vitamin D are of utmost importance. Further, several substances are recognized to have inhibitory or inductive effects in the pathogenesis of vascular calcifications, affecting either the calcium salts precipitation phenomenon or the phenotypic transformation of vascular smooth muscle cells into osteoblast-like cells (the latter phenomenon being regarded as a determinant of calcification of the tunica media). Given that vascular calcifications are irreversible, therapeutic strategies are aimed at preventing their formation or at blunting their progression (which is especially accelerated in renal patients). For this purpose it is essential to pursue optimal biochemical control of secondary hyperparathyroidism, but we must consider that in the individual patient the choice of drugs and their dosage can be essential for the development of calcifications. Given the physiological importance of inhibitory substances, we can hypothesize their future use in this setting. Finally, we must consider that by administering drugs known to interfere with inhibitors (like warfarin) or with the normal process of mineralization (like bisphosphonates), we can hypothetically favor or respectively prevent vascular calcifications.