Vascular calcification of chronic kidney disease: A brief review

Abstract

Vascular calcification (VC) is highly prevalent among patients with chronic kidney disease (CKD). There is growing evidence that there is more underlying this condition than the histological presentation of atherosclerotic plaque and arteriosclerosis and that the risk of cardiovascular disease in the context of CKD might be explained by the presence of VC. While VC has been observed in the absence of overt abnormal mineral metabolism, this association is coupled to abnormal homeostasis of minerals in patients with CKD, due to hyperphosphatemia and hypercalcemia. Furthermore, recent studies have shown that the differentiation of vascular smooth muscle cells into an osteogenic phenotype is highly regulated by pro-calcifying and anti-calcifying factors. There are several imaging modalities currently used in clinical practice to evaluate the extent and severity of VC; each has different advantages and limitations. Although there is no universally accepted method for the treatment of VC, there is growing evidence of the beneficial effects of medical therapy for the condition. This study discusses the mechanism underlying VC, imaging modalities used for evaluation of the condition, and possible treatments.

Keywords: Cardiovascular disease; Chronic kidney disease; Image; Treatment; Vascular calcification.

Figure 1

Pathophysiology of vascular calcification. After stimulation by pro-calcific diseases such as hyperlipidemia, DM, HTN, MetS or CKD, decreased anti.calcify and increased pro.calcify factors stimulated differentiation of VSMC into osteoblast-like SMC and then vascular calcification by the generation of mineralization-competent extracellular matrix vesicles. (↓↑ indicated increased and decreased expression). B-P.2: Bone morphogenic protein 2, Ca: Calcium, FGF-23: Fibroblast growth factor 23, IP: Inorganic phosphate, MGP: Matrix Gla protein, VSMC: Vascular smooth muscle cell, SMC: Smooth muscle cell, CKD: Chronic kidney disease, HTN: Hypertension, DM: Diabetes mellitus

Figure 2

Mechanism and treatments of hyperphosphatemia and secondary hyperparathyroidism. As renal function worsened, renal phosphate excretion decreased and resulted in hyperphosphatemia, elevation of FGF-23 and then secondary hyperparathyroidism. Solid lines indicated abnormal regulation of mineral and hormones in CKD patients. Dashed lines indicate potential treatments against these harmful pathways. Ca: Calcium, FGF-23: Fibroblast growth factor 23, IP: Inorganic phosphate, GI: Gastrointestinal, CKD: Chronic kidney disease