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. 1. oliguric phase A daily urine output of less than 400 ml is called oliguria. absolute anuria rarely occurs in ATN. If absolute anuria occurs, it is mostly complete urinary tract obstruction, acute glomerulonephritis and acute renal cortical necrosis. The duration of the oliguric period varies from 2 to 3 days to 2 to 4 weeks. The duration of oliguria usually does not exceed 1 month; if it exceeds 1 month, it mostly indicates that the ATN is extremely serious and the renal function is difficult to recover, or the cause of ATN is more complicated. Water and electrolyte disturbances and metabolic acidosis are prominent. Water retention is mainly due to the inability of the kidneys to excrete water and the high amount of fluid intake, which manifests as generalized edema, cerebral edema, hypertension, congestive heart failure and pulmonary edema. Congestive heart failure and pulmonary edema are among the leading causes of death in patients with oliguria. Hyponatremia (blood sodium <135mEq/L) is more common in ARF and is divided into dilutional hyponatremia and sodium deficiency hyponatremia, which mostly manifests as dilutional hyponatremia; while sodium deficiency hyponatremia is an absolute lack of sodium in the body, mostly due to vomiting and diarrhea in patients, and may be associated with low blood pressure, dehydrated appearance and weight loss. Most ATN patients can develop hyperkalemia (blood potassium >5,5 mEq/L), which is one of the important causes of death in the oliguric phase. Other conditions such as hyperphosphatemia, hypocalcemia and metabolic acidosis are also more common. Another major manifestation of the oliguric phase of ATN is azotemia and its associated damage to various systems. impaired excretion of protein metabolites occurs in the body during ATN and accumulates in the body, leading to azotemia or uremia. Creatinine (Cr) and urea nitrogen (BUN) are not major uremic toxins per se, but they are the main indicators of toxin accumulation in the body, and their blood concentrations generally correspond to the severity of uremia. In patients with high catabolism blood urea nitrogen rises at a rate of 30 mg/dl/day or more. When uremia occurs in severe ATN, the clinical manifestations and complications of the systemic systems mainly involve the digestive system, cardiovascular system, respiratory system and nervous system. 2.Polyuric phase When the urine volume continues to increase and exceeds 400ml/day, it marks the beginning of recovery of renal function and enters the polyuric phase. In the early stage of polyuria, although the urine volume increases, the glomerular filtration rate is still very low, so the serum creatinine and urea nitrogen can still be significantly increased, and the symptoms of metabolic acidosis and uremia can still be heavy. In the late stage of polyuria, the urine volume is above 2000ml/24 hours, and in many cases, it can be 4000-6000ml/24 hours. At this time, the edema of the patient disappears, the blood creatinine and urea nitrogen decrease, and the symptoms of metabolic acidosis and uremia are gradually reduced. However, due to the large amount of water and electrolyte excretion, the patient may develop dehydration, hyponatremia, hypokalemia and other water-electrolyte disorders. Severe hypokalemia can appear as mild paralysis, arrhythmia and other manifestations. 3.Recovery period The glomerular filtration rate is gradually restored, urine volume is normal, blood creatinine and urea nitrogen are reduced to normal range. It takes about six months to one year for the kidney function to recover completely, and a few patients may remain with different degrees of kidney function damage and develop into chronic renal failure.