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Vascular calcification is a common complication of end-stage renal disease (ESRD). The mechanisms responsible are complex and have so far been considered to be mainly the result of a passive mechanism due to elevated PO(4) levels and high Ca x PO(4) ion product resulting in saturated plasma. However, recent results suggest that also other features, commonly observed in the uremic milieu, such as chronic inflammation, hyperleptinemia and a dysregulation of various mineral-regulating proteins might also contribute to an enhanced calcification process. Moreover, as an inverse relationship between vascular calcification and bone density has been documented in ESRD, it could be speculated that pathologically low bone remodelling (adynamic bone disease) associated with active vitamin D treatment and low parathyroid hormone (PTH) levels may predispose to ectopic calcification of vessels, valves and heart. As patients with vascular calcification have a higher intake of calcium-containing PO(4) binders, novel, non-calcium containing PO(4) binders may diminish the risk of progressive vascular calcification in this patient group. Further studies are needed to elucidate the respective role of chronic inflammation, hyperleptinemia and PTH-lowering therapies in this fatal complication of ESRD.

Why Do Dialysis Patients Develop a Heart of Stone and Bone of China?