Abstract

Vascular calcification (VC) and cardiac valve calcification (CVC) are the important causes to increase the risk of cardiovascular events in terms of chronic kidney disease (CKD) patients. Once VC and CVC considered a passive form of dead or dying cells, it has now emerged as a pathology results from an active and highly regulated cellular process. Recently, mechanisms of VC have been further elucidated and many of the pathways involved could be amplified in CKD patients. In particular, FGF-23/Klotho axis, Wnt pathways, PI3K/Akt signaling, P38MAPK signaling pathway, and microRNAs have been shown to be impaired among patients with CKD and could play a role during vascular calcification. Furthermore, risks for CVC in CKD patients and molecular mechanisms related to it were verified by several researchers. The scope of the present review is to summarize the risk factors and pathophysiological mechanisms potentially involved in the link between CKD and the progression of VC and CVC.

Keywords: Chronic kidney disease; Vascular calcification; Cardiac valve calcification; Mechanisms