Patients with chronic renal failure have higher cardiovascular morbidity and mortality rates compared to general population. Vascular calcification plays an important role for accelerated atherosclerosis of these patients and becomes more evident as the stage of renal failure increases. Although intimal calcification clinically occurs with atherosclerosis; medial calcification is more commonly seen in diabetics and patients with renal failure. It is also known that both intimal and medial calification can be present in at dialysis patients. It is known that the incidence of cardiac valve calcification is higher and valve stenosis progresses more rapidly in end stage renal failure patients compared to healthy population. Besides classical risk factors as age, smoking and diabetes mellitus, some uremia-associated risk factors as prolonged dialysis time, hypercalcemia and hyperphosphatemia play important roles for the progression of vascular and valvular calcifications. Lately more appreciated proteins as protein matrix Gla, fetuin-A, osteoprotegerin and osteopontin lead to inhibition of calcification when their blood levels increase. Among calcification inhibitors, most widely investigated protein is fetuin-A and studies until today revealed the decreased fetuin-a concentration as a non-conventional risk factor in dialysis patients. They may be used for treatment in the future after understanding active roles of fetuin-A and other calcification inhibitors in chronic renal failure patients.