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. Acute renal failure is a common critical condition in pediatric clinics, manifested by rapid deterioration of renal function, retention of metabolites in the body, and disturbance of water, electrolyte and acid-base balance. 1992 discussions in nephrology in China stipulated that the serum creatinine (SCr) value should rise 44-88 μmol/L (0.5-1.0 mg/dl) daily in acute renal failure. Early diagnosis and early treatment are key to improving the prognosis and survival of children with acute renal failure. Diagnostic basis of tubular necrosis due to acute renal failure: 1. According to urine volume Anyone who meets the criteria of oliguria or anuria in the oliguric phase as described by clinical symptoms is considered to have acute renal failure after excluding urinary retention. Clinically, if oliguria or even increased urine output but blood urea nitrogen continues to rise and has other clinical manifestations and biochemical changes of renal failure, then it is non-oliguric acute renal failure. The longer the duration, the more serious the kidney damage is. If the duration of oliguria is more than 5 days or no urine is more than 10 days, the prognosis is not good. (2) Polyuric phase: When the urine volume of children with acute renal failure gradually increases, the general edema decreases, and the 24-hour urine volume reaches more than 250 ml/m2, it is the diuretic phase, which usually lasts 1-2 weeks (the longest can be up to 1 month). In the early stage, azotemia persists or even worsens, and in the later stage, renal function gradually recovers. (3) Recovery period: After the diuretic period, renal co-monitoring improves, urine volume returns to normal, blood urea nitrogen and creatinine gradually return to normal, while renal concentrated function takes several months to return to normal, and a few patients remain partially irreversible renal function damage. At this stage, the child may show weakness, wasting, malnutrition, anemia and immune deficiency. ATN due to nutrition is mostly non-oliguric acute renal failure, with milder clinical manifestations and fewer complications than oliguric acute renal failure, and lower morbidity and mortality rate. 3. Etiological diagnosis (1) Differentiation between pre-renal and renal parenchymal acute renal failure. (2) Post-renal acute renal failure: urological imaging can help detect the cause of urinary tract obstruction. 4.Blood biochemical changes Plasma urea nitrogen is elevated, blood creatinine is elevated, plasma carbon dioxide binding capacity is decreased, serum potassium is increased, and serum sodium is decreased (mostly dilutive).