Con: vascular calcification is a surrogate marker, but not the cause of ongoing vascular disease, and it is not a treatment target in chronic kidney disease.

In this narrative review, we discuss the dynamics and pathobiology of calcium accumulation in the arterial system and then appraise the validity of vascular calcification as a surrogate end point in cardiovascular (CV) diseases and in chronic kidney disease (CKD) in particular. Calcification follows inflammation in human atherosclerosis and therefore most likely represents a secondary phenomenon. This phenomenon is proportional to the severity of antecedent inflammation and is perhaps a healing process. As such, vascular calcification is a disease marker and a prognostic factor but not a relevant aetiological factor in arterial disease in CKD patients. Therefore, targeting vascular calcifications per se is unlikely to improve clinical outcomes. To maximize health benefits, the approach to vascular disease in CKD patients should focus on the prevention of arterial lesions by correcting the several, traditional and non-traditional, pro-atherogenic risk factors responsible for arterial injury, hyperphoshataemia and CKD-mineral and bone disorder disorders included. Interventions aiming at modifying late arterial lesions like calcifications are unlikely to produce tangible health benefits in these patients.