Abstract
Chronic kidney disease (CKD) is associated with a higher prevalence of vascular calcification (VC) and cardiovascular disease. VC in CKD patients showed different pathophysiological features from those of the general population. The pathogenesis of VC in CKD is a highly organized process, and prior studies have suggested that patients with CKD have their own specific contributors to the phenotypic change of vascular smooth muscle cells (VSMCs), including uremic toxins, CKD-mineral and bone disease (CKD-MBD), inflammation, and oxidative stress. For the diagnosis and monitoring of VC in CKD, several imaging modalities, including plain radiography, ultrasound, and computed tomography have been utilized. VC in CKD patients has distinct clinical features and implications. CKD patients revealed a more intense and more prevalent calcification on the intimal and medial layers, whereas intimal calcification is predominantly observed in the general population. While a higher VC score is clearly associated with a higher risk of all-cause mortality and cardiovascular events, a greater VC score in CKD patients does not fully reflect the burden of atherosclerosis, because they have more calcification at equal volumes of atheromatous plaques. The primary goal of VC treatment in CKD is the prevention of VC progression, and the main management is to control the biochemical components of CKD-MBD. Cinacalcet and non-calcium-containing phosphate binders are the mainstay of VC prevention in CKD-MBD management. VC in patients with CKD is an ongoing area of research and is expected to advance soon.