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. (a) Blood tests to understand the presence and degree of anemia, to determine the presence of cavernous bleeding and signs of hemolytic anemia, and to observe the morphology of red blood cells for deformation, broken red blood cells, nucleated red blood cells, reticulocytosis and/or hemoglobinemia and other laboratory changes suggestive of hemolytic anemia, which are useful for etiologic diagnosis. (ii) Urine examination of ATN patients is very important for diagnosis and differential diagnosis, but the results must be judged in combination with the clinical: ① Urine volume change: daily urine volume is below 400ml in oliguric phase, and the urine volume can be normal or increased in non-oliguric type. ②Urinary routine examination: the appearance of more cloudy, dark urine, sometimes soy sauce color; urine protein is mostly (+) to (++), sometimes up to (+++) to (++++), often in the middle, small molecule protein, the degree of proteinuria is not helpful to the diagnosis of the cause, urine sediment examination often appear in different degrees of hematuria, to microscopic hematuria is more common, but in heavy metal poisoning often have a large amount of proteinuria and carnal hematuria, in addition In addition, there are detached renal tubular epithelial cells, epithelial cell tubular and granular tubular and different degrees of leukocytes, etc. Sometimes there is no pigmented tubular or leukocytic tubular. The specific gravity of urine is lower and more fixed, mostly below 1.015, because the renal tubular reabsorption function is damaged and the urine cannot be concentrated. ④The urine osmotic concentration is lower than 350mOsm/kg, and the ratio of urine to blood osmotic concentration is lower than 1.1. ⑤The urine sodium content is increased, mostly in the range of 40-60mmol/L, due to reduced sodium reabsorption by the renal tubules. (6) The ratio of urinary urea to blood urea is decreased, often below 10, because urinary urea excretion is decreased and blood urea is increased. (7) The ratio of urinary creatinine to blood creatinine decreases, often below 10. (8) The renal failure index is often greater than 2, which is the ratio of urinary sodium concentration to urinary creatinine and blood creatinine ratio, and the index increases because of more urinary sodium excretion and less urinary creatinine excretion and higher blood creatinine. ⑨ Filtration sodium excretion fraction (FeNa), which represents the ability of the kidney to remove sodium, is expressed as a percentage of glomerular filtration rate, i.e. (ratio of urinary sodium, blood sodium / ratio of urinary creatinine, blood creatinine) × 100, i.e.: FeNa (%) = UNaV ÷ GRF × 100 PNa = UNa-V ÷ UCr-V × 100 PNa PCr = UNa × PCr × 100 PNa UCr UNa is urine sodium, PNa is blood sodium, V is urine volume, UCr is urine creatinine, PCr is blood creatinine, GFR is glomerular filtration rate, which is often >1 in patients with ATN and <1 in those with pre-renal oliguria. The above-mentioned ⑤ to ⑨ urine diagnostic indices are often used to differentiate pre-renal oliguria from ATN, but in practice these indices are unreliable and contradictory when patients are treated with diuretics and hypertonic drugs. Therefore, it is only used as an auxiliary diagnostic reference. (C) Glomerular filtration function examination of blood creatinine (Scr) and blood urea nitrogen (BUN) concentration and daily rise to understand the degree of functional impairment and the presence of hypercatabolism, generally in uncomplicated medical cause of ATN, the daily Scr concentration rose 40.2 ~ 88.4?mol/L (0.5 ~ 1.0mg/dl), most of the oliguric period in 353.6 ~ 884 BUN increased about 3.6-10.7 mmol/L (10-30 mg/dl) per day, mostly in the range of 21.4-35.7 mmol/L (60-100 mg/dl); if the disease is severe and the oliguric period is prolonged with hypercatabolic state, daily Scr can rise 176.8?mol/L (2 mg/dl) or more. (dl) or more, BUN can rise more than 7mmol/L per day; in crush injury or muscle injury, the rise of Scr can not be parallel to the rise of BUN. (d) Blood gas analysis is mainly to understand whether there is acidosis and its degree and nature, as well as hypoxemia, blood pH, alkali storage and bicarbonate is often lower than normal, suggesting metabolic acidosis, arterial partial pressure of oxygen is very important, below 8.0kPa (60mmHg), especially oxygen can not be corrected, the lungs should be checked to exclude lung inflammation and the presence of adult respiratory distress syndrome (ARDS), for serious cases It is important to check the blood gas analysis dynamically. (E) Blood electrolyte examination should be closely followed up during oliguria and polyuria, including blood potassium, sodium, calcium, magnesium, chloride and phosphorus concentration, etc. Be especially alert to hyperkalemia, hypocalcemia, hyperphosphatemia and hypomagnesemia during oliguria; pay attention to hyperkalemia or hypokalemia, hyponatremia and hypochlorhydria and hypokalemic and hypochlorhydria alkalosis during polyuria. (F) liver function tests in addition to coagulation function to understand the presence of hepatocyte necrosis and other dysfunctions, including transcarbital, blood bilirubin, blood albumin, etc., in addition to understanding the degree of impaired liver function, but also to understand the presence of primary liver failure caused by acute renal failure. (G) bleeding tendency examination: ① dynamic platelet count reduction and its degree, for patients with bleeding tendency or serious risk should be related to DIC laboratory examination, platelet function examination to understand the platelet agglutination increased or reduced; ② normal or prolonged prothrombin time; ③ thrombin generation or no adverse; ④ blood fibrinogen reduction or elevation; ⑤ blood fibrin cleavage products (FDP) increased If bleeding tendency occurs during the oliguric phase of ATN, the occurrence of DIC should be suspected. At this time, reduced platelet count and dysfunction and coagulation disorders are seen, manifesting as in vivo depletion hypocoagulation, the latter being due to diffuse intravascular coagulation consuming a large amount of coagulation factors and secondary fibrinolysis, manifesting as hypofibrinogenemia and significantly increased blood FDP concentration.