The causes of hyperphosphatemia include under-excretion of phosphorus by the kidney, over-giving of phosphorus by exogenous sources, over-production of endogenous phosphorus, and pseudohyperphosphatemia. 1. Low renal phosphorus excretion: the most common cause of renal damage is the reduction of glomerular filtration rate, resulting in high blood phosphorus. In addition to the reduction of glomerular filtration rate, the increase of proximal tubular phosphorus reabsorption will also lead to a decrease in phosphorus excretion, which can be seen in hypoparathyroidism, acromegaly, the application of bicarbonate phosphate compounds, and familial tuberculous calcium sedimentation disease. 2. Exogenous phosphorus oversupply: in some children given high-calcium milk, the application of phosphorus-containing laxatives or enemas (eg, sodium phosphate), vitamin D toxicity and transfusion of stored blood. 3. Excessive endogenous phosphorus production: seen in a large number of hemolysis, lymphoma or leukemia chemotherapy, rhabdomyolysis, lactic acidosis and diabetic ketoacidosis. 4. Pseudohyperphosphatemia: mainly seen in some patients with multiple myeloma. These patients often have a monoclonal protein in the blood can be tightly bound to phosphorus, and in the automatic biochemistry interferes with phosphorus detection, the application of sulfuric acid treatment or serum ultrafiltration can be exempted from this interference. In addition, hemolysis of the blood specimen may cause false hyperphosphatemia. If hyperphosphatemia occurs, it is important to go to the hospital in time to identify the cause of the disease and follow the doctor’s instructions to standardize the treatment.