The Main Causes of the Heightened Risk of Cardiovascular Events in Individuals with Chronic Kidney Disease (CKD) are Vascular Calcification (VC) and Calcification of the Cardiac Valves (CVC)


In chronic kidney disease (CKD) patients, vascular calcification (VC) and cardiac valve calcification (CVC) are the major reasons of increased risk of cardiovascular events. Originally thought to be a passive kind of dead or dying cells, VC and CVC have since been identified as a disease caused by an active and highly controlled cellular process. Several of the processes implicated in VC have recently been identified, and many of them may be exacerbated in CKD patients. FGF-23/Klotho axis, Wnt pathways, PI3K/Akt signalling, P38MAPK signalling pathway, and microRNAs, in particular, have been demonstrated to be disturbed in CKD patients and may have a role in vascular calcification. Moreover, multiple researches confirmed the hazards of CVC in CKD patients as well as the molecular processes behind it. The purpose of this review is to describe the risk variables and pathophysiological processes that may be implicated in the relationship among CKD and VC and CVC development.