Acute tubular necrosis (ATN) is the most common type of acute renal failure, accounting for approximately 75% to 80% of cases. It is a clinical syndrome that occurs as a result of acute, progressive decompensation of renal function due to renal ischemia and/or nephrotoxic damage caused by various etiologies. The main manifestations are progressive azotemia due to a marked decrease in glomerular filtration rate, and imbalance of water, electrolyte and acid-base balance due to low renal tubular reabsorption and excretion function. The main etiologies of acute tubular necrosis are traditionally divided into two main categories, such as acute renal ischemia and acute nephrotoxic damage. However, intravascular hemolysis and certain infections are not uncommon. Sometimes renal ischemia and nephrotoxic factors can co-exist. (A) Acute renal ischemia: Acute renal ischemia is the most common type of ATN, which is partly caused by the continued action and development of the aforementioned prenephrotic factors, resulting in prolonged renal ischemia and hypoxia, etc. Large bleeding or blood transfusion during or after major thoracic or abdominal surgery, shock and shock correction for various reasons, cardioversion with extracorporeal circulation, restoration of renal circulation and cardiac resuscitation with homogeneous kidney transplantation are all renal ischemic reperfusion conditions. Ischemia-reperfusion conditions, so generally speaking, ischemic acute renal failure is more serious than other types of ATN and the time required to restore renal function is longer. (B) acute nephrotoxic damage: nephrotoxic damage is mainly exogenous nephrotoxicity, such as drugs, heavy metals and chemical toxins and biological toxicity. 1, drug nephrotoxic damage: the incidence rate has a tendency to increase, accounting for 11% of the total incidence of acute renal failure and 17.1% of the internal causes of acute renal failure, respectively. The common drugs that cause ATN are aminoglycoside antimicrobials such as gentamicin, kana and butamycin polymyxin B tobramycin, sulfonamides, dicloxacillin cyclosporine A and cisplatin, etc. 2, toxic nephrotoxic damage: (1) heavy metal nephrotoxic substances: such as mercury, cadmium, arsenic, uranium, chromium, lithium, bismuth, lead and platinum; (2) industrial toxins: such as cyanide, carbon tetrachloride, methanol, toluene, ethylene glycol and chloroform; (3) fungicidal disinfectants: such as cresol resorcinol, formaldehyde, etc.; (4) pesticides and herbicides: such as organophosphorus, bacillus, etc., such toxic poisoning should pay attention to early measures to remove toxic substances from the body. 3. Biotoxins: There are green fish bile, snake bite, poisonous mushrooms, bee venom, etc. This kind of toxin poisoning is often easy to cause multi-organ failure often while damaging lung, kidney, liver and heart function, etc. Attention should be paid to maintaining the function of each major organ during first aid. (4) Contrast agent kidney injury: Acute kidney injury is likely to occur in the presence of pre-existing renal impairment, diabetic elderly patients, hypovolemia, hyperuricemia and multiple myeloma. (iii) infectious diseases: such as epidemic hemorrhagic fever and leptospirosis cause ATN. among them, hemorrhagic fever is the most common, accounting for 18.6% of the total incidence of acute renal failure and 29% of the medical etiology. The pathological basis of hemorrhagic fever is hemorrhagic damage to small blood vessels throughout the body, and the mortality rate of heavy cases is very high. (D) Acute hemolysis and intravascular hemolysis: incompatible allogeneic transfusion, various extracorporeal circulation caused by the destruction of red blood cells immune diseases causing hemolysis anemia crisis various causes of hemoglobinuria malaria endemic areas of black urine fever, falciparum malaria and antimalarial drugs such as primaquine and quinine caused by hemolysis. Extrusion, trauma and non-traumatic rhabdomyolysis cause massive myoglobin deposition in the renal tubules, resulting in renal damage similar to hemolysis.