Abstract: In patients with chronic kidney disease(CKD), progressive deterioration of renal function leads to mineral metabolism disorders, acidosis, malnutrition, inflammation and accumulation of uremic toxins, which can cause secondary hyperparathyroidism and elevated serum calcium. Increased phosphate levels and elevated serum fibroblast growth factor-23 (FGF-23), resulting in CKD-related mineral and bone metabolism disorders, excess calcium and phosphate in the circulation can also promote protein-mineral complex called calpain particles(CPPs). In CKD, these CPPs contain little calcification inhibitors, induce inflammation, and promote calcification of vascular smooth muscle cells, thereby promoting the occurrence of vascular calcification. Many cross-sectional observation studies have shown that blood FGF-23 levels begin to increase in the early stage of CKD(stage 1-2) and are negatively correlated with glomerular filtration rate, promoting vascular calcification. The latest research indicates high levels of adiponectin plays a role in the effect of FGF23 on coronary artery calcification. This article reviews the research progress in the mechanism of vascular calcification in patients with CKD, and points out the direction for further search for potential new therapeutic goals.