Introduction of new imaging techniques (i.e. electron beam computed tomography, EBCT; multi-slice spiral computed tomography, MSCT) has enabled detection and quantification of the calcium deposit burden within arterial walls. The results of the abovementioned evaluations, expressed as calcification score, indicate extremely high prevalence of calcifications within coronary arteries and aorta in patients with advanced renal failure (end-stage renal disease; ESRD), including those treated with dialysis. Furthermore, in most patients follow-up assessment (usually repeated after one - two years) reveals dynamic and significant progression of calcification as compared to baseline measurement. Several traditional and novel factors that promote excess and accelerated deposition of calcium within soft tissues were identified. Among traditional risk factors, age and calcium - phosphate balance abnormalities seem to play the most important role. Recent research and clinical observations have highlighted the crucial role of regulatory proteins, such as fetuin and osteoprotegerin in the formation and progression of pathologic calcification in uremia. The treatment with calcium- containing phosphate binders and possibly - with active preparations of vitamin D appear to have an adverse impact on calcium deposit formation within arterial walls. Novel treatment strategies, including the calcium-free phosphate binder sevelamer seem to slow down or even stop this process. Kidney transplantation, the treatment of choice in advanced uremia has also been shown to slow down the rate of calcification.