Vascular calcification in patients with renal failure: culprit or innocent bystander?

The mortality from cardiovascular events in CKD and dialysis patients is substantially higher than in the general population. VC is ubiquitous and progresses rapidly in this patient population. Although there has been progress in the understanding of the pathogenesis and correlates of VC, much work needs to be done in this area. The role of calcium and, probably, phosphate (obligatory participants) is unquestionable, but the understanding of the paracrine and molecular determinants of VC in renal failure is continuously evolving. VC is probably a dynamic process resulting from the imbalance between molecules that promote and those that inhibit VC. The understanding of latter area has recently evolved with identification of new signaling pathways with molecules such as osteoprotegerin, fetuin-A, and MPG. From a clinical perspective, new modalities such as EBCT and MDCT allow noninvasive detection and quantification of VC. VC may represent a potential useful index for prognostic stratification and treatment planning in patients who have renal failure. At present, however, the data on the prognostic value of VC are available only in populations of patients who have normal renal function. Large-scale, prospective, observational studies should be designed to identify the determinants of VC and to define the prognostic role of calcium scoring in cohorts of patients who have predialysis CKD and with ESRD.