The annual mortality rate in uremic patientscorrected for agesexand raceis significantly higher than in the general population. This is primarily due to cardiovascular events. Vascular calcifications play a vital role in the development of cardiovascular morbidity and subsequent increased mortality. Vascular calcification affects both vascular intima and media layers and its mechanism remains poorly understood. Over the last few years it has been shown thatin addition to traditional cardiovascular risk factorsdisturbances in mineral metabolism in the uremic milieucalcium-containing phosphate bindersand vitamin D treatment of secondary hyperparathyroidism may contribute to the pathogenesis of vascular calcifications. Other uremia-related risk factors (e.g.increased oxidized low-density lipoprotein cholesteroluremic toxinsincreased oxidative stressdialysis and dialysate-related factorshemodynamic overloadhyperhomocysteinemia) may also play a role. In uremic patientsapart from these facilitating factorsdecreased levels of endogenous calcification inhibitors such as fetuin-Amatrix Gla proteinosteoprotegerinand osteopontin have also been associated with increased calcium-phosphate precipitation in extraskeletal tissues. Finallyvascular calcification is the outcome of the active and dynamic balance of procalcifying and anticalcifying influences. For the prevention and treatment of vascular calcificationsit is essential to avoid treatment modalities that lead to calcium overloadachieve good metabolic controland optimize dialysis.