**1. Introduction**

Chronic kidney disease (CKD)-mineral and bone disorder (CKD-MBD) becomes an important issue in CKD management [1]. CKD patients show a bone and mineral disor‐ der as follows: (i) laboratory abnormal metabolisms of calcium, phosphate, and vitamin D; (ii) evidence of calcified tissue disturbance; (iii) and arterial calcification. Arterial calcifica‐ tion is known to be related to numerous worse symptomatic outcomes, such as ischemic cardiovascular attacks and death [2]. The pathogenesis of vascular calcification in CKD is complex, and instead of occurring by a simple process of calcium and phosphate precipita‐ tion, it is produced by an active process in which vascular smooth muscle cells (VSMCs) undergo apoptosis and vesicle formation and are transformed into osteoblast-like cells that induce matrix formation and attract local factors that are involved in the mineralization process [3] (Fig. 1).

The pathogenesis of the multifactorial interactions between aging and progression of vascular calcification remains uncertain. However, there is no doubt that end-stage renal disease (ESRD) patients are at high risk of and have a common finding of vascular calcification due to multiple confounders that promote the differentiation of VSMCs to osteoblast-like cells, which are able to enhance the tissue calcium deposition process [4]. Vascular calcification has recently reported to be associated with many traditional risk factors, aging, high blood pressure, diabetes, and hyperlipidemia, and with nontraditional risk factors, including elevated serum phosphate level, hyperparathyroidism, and high-dose prescription of calcium [5]. Vascular calcification causes a decrease in vascular elasticity, an increase in pulse wave velocity [6], an induction of cardiomyopathy [7], a decrease in coronary artery flow, and an ischemic change (Fig. 2).

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**Figure 1.** Relationship between calcium and phosphorus and vascular calcification.

**Figure 2.** Schematic representation of the clinical effects of arterial intimal and medial calcification.

Recent therapeutic regimens that are performed to suppress vascular calcification are concen‐ trated on the control of metabolic markers of skeletal disorder, including phosphate, and vitamin D. The antiosteoporosis drugs such as bisphosphonates [8] have shown therapeutic possibility, but more additional clinical trials are needed. The ADVANCE study has recently shown that cinacalcet and low-dose vitamin D reduce vascular and cardiac valve calcification in hemodialysis (HD) patients with secondary hyperparathyroidism (SHPT) [9]. This review article describes recent progress in terms of the pathogenic mechanisms and methods of assessing and managing vascular calcification in ESRD patients.
