Vascular calcification in chronic kidney disease

Abstract

The aim of this review is to present current knowledge of vascular calcification in chronic kidney disease. Recent investigations point mainly at the disturbed balance between factors facilitating and protecting extraosseous mineralization as crucial in the creation of calcification of vessels. Chronic kidney disease is associated with multiple abnormalities potentially accelerating calcification, such as hypercalcemia, hyperphosphatemia, dyslipidemia, and inflammation. Their impact triggers the change of vascular smooth muscle cells into osteoblast- or chondrocyte-like cells expressing bone-associated proteins. This differentiation induces the production of apoptotic bodies that become nuclei of mineralization. The decreased capacity of calcification inhibitors, such as fetuin-A, osteoprotegerin, and osteopontin, additionally weakens the protection against excessive mineralization. These disturbances are of paramount importance in CKD patients because of the close connection between pathomorphology and clinical outcome. Both medial and intimal calcification affect the cardiovascular system due to the increased vascular stiffness and calcified atherosclerotic lesions, creating a vast clinical panorama of symptoms from stroke to heart failure. Therefore, clarifying the mechanisms responsible for vascular calcification in CKD patients seems to be a key target for effective future prevention. © Copyright by Silesian Piasts University of Medicine in Wroclaw.