The diagnosis and treatment of chronic kidney disease-related metabolic bone disease (CKD-MBD) caused by disorders of calcium and phosphorus metabolism is a worldwide challenge. 1. High incidence and rapid disease progression. When the glomerular filtration rate (GFR) of CKD patients decreases to 50ml/min.1.732, abnormal calcium and phosphorus metabolism can appear, and with the decline of residual renal function, the lesions show continuous progress and lead to a series of important organ damage such as bones, heart and blood vessels, which is one of the important factors leading to the death of patients with end-stage renal failure (ESRD). 2. The lack of sensitive diagnostic methods for CKD-MBD today makes it difficult to take individualized interventions for ESRD patients. 3. 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. The pathophysiological mechanisms of the effects of disorders of calcium and phosphorus metabolism on the parathyroid glands and bones are complex, and there are various types of pathological damage, but clinically they are usually divided into two major categories, namely, high-transport nephropathy and low-transport or power-deficient nephropathy. In addition to the pathological damage pattern, the major difference between the two types of CKD-MBD is the different parathyroid function status, with the former being relatively hyperactive and the latter being hypo-suppressed and hypofunctional. From a therapeutic point of view, high transit renal bone disease is effective with vitamin D receptor agonist (VDRA), while low transit renal bone disease is not only ineffective, but inappropriate use can further aggravate the bone disease by progressive suppression of parathyroid function, thus making such patients contraindicated to active Vit D3 drugs. After the 1980s, the widespread clinical use of calcium carbonate and active vitamin D3 (Vit D3) containing calcium and phosphorus binding agents has led to a significant change in the spectrum of CKD-MBD. This is highlighted by a significant decrease in the incidence of high-transport bone disease and a significant increase in the incidence of low-transport bone disease. In patients with CRF3-4, the incidence of fibrous osteitis characterized by high-transport bone disease is as high as 32%, while the incidence of power-deficient bone disease characterized by low-transport bone disease is only 18%; by the stage of PD treatment, the former is only 18%, while the latter is as high as 50%. The causes of these phenomena, although complex, are closely related to blind calcium supplementation and abuse of active VitD3 preparations. It should be noted that power-deficient bone disease is characterized by a lack of bone metabolic power due to the inhibition of PTH function, which is mainly caused by the overuse of active VitD3 and hypercalcemia. Such patients are not only ineffective to calcium- and phosphorus-containing binding agents, but their blind use can lead to increased accumulation of calcium and aluminum, promoting or increasing the risk of calcification of soft tissues, blood vessels and heart valves. Therefore, parathyroid function should be routinely evaluated in patients with ESRD before choosing an active VitD3 preparation. k/DOQI guidelines recommend that active VitD3 use be considered only in ESRD patients with iPTH levels above 300 pg/ml. this issue should be even more important in patients with long-term PD. Since a considerable number of units use normal calcium peritoneal dialysate (dialysate calcium level 1.5-1.75 mmol/L, 3.0-3.5 mEq/L), the calcium ion concentration in such dialysate is slightly higher than that in blood, and if calcium- and phosphorus-containing binding agents are also used, hypercalcemia and metastatic calcification of multiple organs of the body are highly likely to be induced. Therefore, patients with normal or high blood phosphorus should strictly grasp the indications for the use of calcium-phosphorus-containing binding agents and use them with caution in the following cases: 1. iPTH ≤ 150 pg/ml; 2. Blood calcium. ≥2.5 mmol/L.