The diagnosis and treatment of chronic kidney disease-associated metabolic bone disease (CKD-MBD) caused by disorders of calcium and phosphorus metabolism is a worldwide challenge. First, the incidence is high and the disease progresses rapidly. When the glomerular filtration rate (GFR) of CKD patients decreases to 50 ml/min.1.732, abnormal calcium and phosphorus metabolism can appear, and with the decline of residual renal function, the lesions show continuous progression and lead to damage of bones, heart, blood vessels and a series of other important organs, which is one of the important factors leading to the death of patients with end-stage renal failure (ESRD). Secondly, the lack of sensitive diagnostic methods for CKD-MBD today makes it difficult to take individualized interventions for ESRD patients. Third, most of the drugs currently used clinically to correct disorders of calcium and phosphorus metabolism vary greatly among individuals, and their improper use is highly likely to cause serious complications. This article focuses on the clinical issues that should be concerned in the treatment of calcium and phosphorus metabolism disorders in PD patients. 1, pay attention to the danger of calcium and phosphorus metabolism disorders to CKD patients Calcium and phosphorus metabolism disorders are one of the most common comorbidities in patients with chronic renal failure (CRF). Its effect on the body is not limited to the skeletal system, but hyperphosphatemia can also mediate ectopic calcium deposits and stimulate vascular and cardiac valve calcification. There is also substantial evidence that hyperphosphatemia can be involved in cardiovascular disease through other mechanisms. (1) direct increase in reactive oxygen species causing vascular damage, leading to oxidative stress and impairment of vascular endothelial function; (2) increase in parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), both of which can directly contribute to cardiovascular disease; (3) elevated phosphorus inhibits the synthesis of 1,25 dihydroxyvitamin D3 [1,25(OH)2D3], causing vascular calcification and myocardial disease. Studies have shown that for every 1 mg/dl increase in blood phosphorus levels, the risk of death in CKD patients increases by 18%. Therefore, adequate reduction of blood phosphorus without causing hypercalcemia is also the key to prevent vascular calcification and cardiovascular disease in CRF patients. A large number of clinical observations have proved that cardiovascular events have become one of the important causes of death in patients with PD, and a significant proportion of them are closely related to disorders of calcium and phosphorus metabolism. However, there is not enough attention to the local and systemic damage caused by hyperphosphatemia, especially the indirect lethality of calcium and phosphorus metabolism disorders in PD patients, which is highlighted by the low clinical awareness of these diseases, not to mention early intervention and active and effective treatment.