In patients with chronic renal failure, due to reduced glomerular rate filtration, phosphorus excretion is impaired at endogenous creatinine clearance less than 60 ml/min.1.73 m2 and blood phosphorus begins to rise. After uremic patients start hemodialysis, the occurrence of hyperphosphatemia becomes more pronounced due to reduced urine volume and increased protein diet intake. Epidemiological surveys show that the prevalence of hyperphosphatemia in uremic hemodialysis patients in China is 57.4%, and in peritoneal dialysis patients the prevalence is 47.4%, while the blood phosphorus control rate is only 38.5%. The current recommendation for dialysis patients is to maintain blood phosphorus levels at 1.13-1.78 mmol/L. High blood phosphorus can cause a range of uremic complications such as uremic bone disease, cardiac valve and vascular calcification, and skin pruritus. Large meta-analyses have shown that elevated blood phosphorus (>1.78 mmol/L) in uremic patients leads to an increased risk of death, with each 1 mg/dL increase in serum phosphorus associated with an 18% increase in all-cause mortality and a 10% increase in the risk of cardiovascular death. With the popularity of dialysis treatment, it is urgent to prevent hyperphosphatemia to avoid complications, a clinical challenge. For hyperphosphatemia in uremic patients, there are three clinical treatment strategies. 1, control the dietary phosphorus intake (limit to 800-1000mg/d). Since organic phosphorus is mainly distributed in cells with protein-binding disease, protein-rich foods also have high blood phosphorus levels. Since protein intake has to be increased after dialysis in uremic patients, it can easily lead to high phosphorus occurrence. Secondly, the absorption of phosphorus from plant-based proteins is lower than that of phosphorus from animal-based proteins. Studies have found that excessive restriction of phosphorus intake can lead to malnutrition disease increasing mortality, protein and phosphorus intake must be balanced, so it is more appropriate to use the phosphorus (mg)/protein (g) ratio to measure the phosphorus load in the diet. Foods low in phosphorus but rich in protein, such as egg proteins, should be consumed as much as possible, while foods high in phosphorus but low in protein should be consumed as little as possible. In addition, phosphorus is one of the main components of food additives, uremic patients should limit the intake of phosphorus-containing additives. 2. Increasing the number of dialysis sessions or extending the duration of dialysis helps phosphorus removal. Because phosphorus is mainly distributed in cells and tissues, the transfer rate from intracellular to extracellular is very slow, and often requires a long time of dialysis to achieve phosphorus reduction. 3, the use of phosphorus binding agents, mainly by reducing the absorption of phosphorus from the gastrointestinal tract to reduce blood phosphorus levels. The current clinical application of phosphorus binding agents are mainly calcium-containing phosphorus binding agents, aluminum-containing phosphorus binding agents and non-calcium non-aluminum phosphorus binding agents. In uremic dialysis patients, if the phosphorus level cannot be controlled by dietary restriction and adequate dialysis, and the calcium level is in the normal range or lower, it is recommended to use calcium-containing phosphorus conjugates, and if hypercalcemia persists or recurs, non-calcium and non-aluminum phosphorus conjugates are recommended. In conclusion, the incidence of hyperphosphatemia in uremic dialysis patients is extremely high. In addition, hyperphosphatemia can be caused or aggravated by the intake of a high-protein diet, inadequate doses or methods of phosphorus-binding agent administration, and/or inadequate dialysis. Therefore, the treatment of hyperphosphatemia must be an organic combination of limiting phosphorus intake, ensuring adequate dialysis, and applying phosphorus binding agents in order to achieve the best therapeutic effect.