Acute tubular necrosis

　　I. Acute renal ischemia

　　Acute renal ischemia is the most common type of ATN, which is partly due to the persistent action and development of the aforementioned pre-renal factors, causing prolonged renal ischemia and hypoxia and leading to ATN. Massive bleeding or blood transfusion during or after major thoracic and abdominal surgery, various reasons for shock and post-shock correction, extracorporeal circulation cardiac restart, allogeneic renal transplantation to restore renal blood circulation and cardiac resuscitation, etc., all belong to the condition of renal ischemia-reperfusion, so generally speaking, ischemic acute renal failure is more serious than other types of ATN, and the time required for renal function recovery is also longer.

　　II. Acute nephrotoxicity

　　Nephrotoxic damage is mainly exogenous nephrotoxicity, such as drugs, heavy metals, chemical toxins, and biological toxins, etc.

　　1. Nephrotoxic damage from drugs

　　The incidence rate is on the rise at present, accounting for 11% of the total incidence rate of acute renal failure and 17.1% of acute renal failure caused by internal medicine etiology.

　　2. Nephrotoxic damage from toxins

　　(1) Heavy metal nephrotoxins: such as mercury, cadmium, arsenic, uranium, chromium, lithium, bismuth, lead, and platinum, etc.;

　　(2) Industrial toxins: such as cyanides, carbon tetrachloride, methanol, toluene, ethylene glycol, and chloroform, etc.;

　　(3) Disinfectants and sterilizing agents: such as cresol, resorcinol, formaldehyde, etc.;

　　(4) Pesticides and herbicides: such as organophosphorus, grassicide, etc., poisoning by these toxins should pay attention to taking early measures to remove toxins from the body.

　　3. Biological toxins

　　There are such as mylopharyngodon piceus bile, snake bite, poisonous mushrooms, bee venom, and other toxins. These toxins are often easy to cause multiple organ failure, often simultaneously damaging lung, kidney, liver, and heart function, and attention should be paid to maintaining the function of the main organs during emergency treatment.

　　4. Contrast agent nephropathy

　　Acute renal dysfunction is prone to occur in the presence of pre-existing renal dysfunction, diabetes, elderly patients, insufficient blood volume, hyperuricemia, and multiple myeloma.

　　III. Infectious diseases

　　ATN caused by diseases such as epidemic hemorrhagic fever and leptospirosis. Among them, epidemic hemorrhagic fever is the most common, accounting for 18.6% of the total incidence rate of acute renal failure and 29% of the causes of internal medicine. The pathological basis of hemorrhagic fever is the hemorrhagic damage of small blood vessels throughout the body, and the mortality of severe cases is very high. Early diagnosis and early dialysis treatment should be emphasized.

　　IV. Acute hemolysis and intravascular hemolysis

　　Incompatible blood transfusions, red blood cell damage caused by various extracorporeal circulation, hemolytic crisis caused by immune diseases, various hemoglobinuria due to various reasons, black urine fever in the malaria-endemic areas, severe malaria, and antimalarial drugs such as primaquine and quinine, etc., all cause hemolysis. Crush, trauma, and non-traumatic rhabdomyolysis cause a large amount of myoglobin to deposit in the renal tubules, causing kidney damage similar to hemolysis.

　　V. Pathogenesis

　　The pathogenesis of acute tubular necrosis is multi-faceted. Renal hemodynamic changes and acute tubular damage are the main factors. The key points of various theories are described as follows:

　　1. Renal hemodynamics

　　Changes in renal hemodynamics play a leading role in the early stage of ATN and are often the initiating factor. In cases of hemorrhagic shock or severe hypovolemia, due to neural and humoral regulation, the blood in the whole body is redistributed, the renal artery constricts, and renal blood flow can be significantly reduced, leading to a decrease in renal perfusion pressure and marked constriction of the renal glomerular arterioles, causing renal cortical ischemia and the occurrence of ATN. Sometimes, in the early stage of acute ischemic ATN caused by massive hemorrhage, although blood volume is rapidly restored, the glomerular filtration rate and GFR do not recover, indicating that in the early stage of ATN, there are changes in renal hemodynamics and abnormal distribution of renal blood flow. The pathological and physiological basis of these renal hemodynamic abnormalities is considered to be related to the following factors.

　　(1) The role of renal nerves: The sympathetic nerve fibers of the adrenal gland are widely distributed in renal vessels and glomerular extra-cellular bodies. The enhancement of adrenaline activity leads to renal vessel constriction, resulting in a decrease in renal blood flow and GFR. In ischemic ATN, the degree of renal vessel constriction induced by stimulation of the renal nerves is much greater than that in normal animals, indicating that the sensitivity of blood vessels to renal nerve stimulation increases in ATN, but this enhanced response can be inhibited by calcium channel blockers, suggesting that the renal vessel constriction caused by renal nerve stimulation is related to the change in calcium activity of renal vascular smooth muscle. However, it is observed clinically that in kidneys without innervation, such as in allogeneic renal transplantation, the incidence of ischemic ATN after the recovery of renal blood supply can be as high as 30%, which does not support the dominant role of renal nerves in the occurrence of ATN.

　　(2) The role of renin-angiotensin system in renal tissue There is a complete renin-angiotensin system in the renal tissue. It is widely believed that the changes in renal blood circulation pathways in ischemic ATN are related to the activation of the renin-angiotensin system in the renal tissue, leading to a strong contraction of the glomerular arterioles. However, even if the activity of renin is inhibited and angiotensin II is antagonized, ATN can still occur, indicating that the renin-angiotensin system is not the decisive factor for ATN.

　　(3) The role of renal prostaglandins The renal prostaglandins, especially prostacyclin PGI2, are synthesized in the renal cortex and have a significant vasodilatory effect. They can increase renal blood flow and GFR, and have natriuretic and antidiuretic hormone-inhibitory effects on the reabsorption of water by the collecting ducts, thus exerting a diuretic effect. It has been confirmed that in ATN, PGI2 in the blood and renal tissue is significantly reduced; it has now been proven that renal PGI2 can prevent the occurrence of ischemic ATN, and the prostaglandin antagonist indomethacin can accelerate ischemic renal damage. In addition, when renal ischemia occurs, the synthesis of thromboxane in the renal cortex increases, which also promotes renal vasoconstriction. However, there is currently no evidence to show that prostaglandins play a leading role in ATN.

　　(4) The role of endothelial-derived contractile and dilatory factors in ATN has been emphasized by many scholars over the years. Pathological over-secretion of endothelial-derived contractile factors and the release disorder of endothelial-derived dilatory factors such as nitric oxide (NO) play an important role in the hemodynamic changes of ATN. They found that in the early stage of ATN, the renal blood flow decreases, not due to the action of renin-angiotensin, but rather due to renal ischemia and hypoxia, when a large amount of endothelin is released by vascular endothelial cells (it was found in the experiment that low concentration of endothelin can cause a strong and sustained contraction of renal arteries, increase renal arteriolar resistance, leading to a decrease or cessation of GFR. There are high-density endothelin receptors in the glomerular capillaries and mesangial cells, and true small vessels. Continuous intravascular injection of endothelin in experimental animals can also cause significant vasoconstriction of renal arteries), which leads to increased resistance of the renal arterioles entering and exiting the glomerulus, and the resistance of the entering arterioles increases more significantly, so the renal blood flow and GFR decrease in parallel. However, sometimes the concentration of endothelin in the patient's serum increases by ten or more times, but clinically, ATN does not occur. Normal vascular endothelium can still release dilatory factors to coordinate blood flow to maintain blood circulation, and it has the effect of increasing blood flow and reducing the resistance of the entering and exiting arterioles in the kidneys. The release of dilatory factors by vascular endothelium in the early stage of ATN is already impaired, and the increase in oxygen free radicals after ischemia-reperfusion also affects the release of dilatory factors. In this situation, the hemodynamic changes of the kidney may be more prominent. It is currently believed that the imbalance of endothelial cell contraction and dilatory factor regulation may play an important role in the occurrence and development of certain types of ATN.

　　(5) In the ischemic ATN model, it has been observed that the outer zone of the renal medulla and the inner zone of the cortex are most severely damaged, and the degree of renal medullary congestion is significantly correlated with the degree of ATN damage. The first to be affected by medullary congestion and hypoxia is the blood supply of the ascending limb of the loop of Henle renal tubular cells, as the ascending limb is a high-energy-consuming area, which is abnormally sensitive to hypoxia. The hypoxic tubular cells have a reduced ability to actively reabsorb sodium chloride. Damage to the ascending limb can cause T-H glycoprotein to deposit easily in the thick segment, causing obstruction of the distal tubule lumen and leakage of tubular fluid. Therefore, it is believed that medullary congestion in ischemic ATN is also an important pathogenic factor.

　　2. The Mechanism of Renal Ischemia and Protoporphyrin Cell Damage

　　After the renal tissue recovers blood supply after acute ischemia and hypoxia, such as after correcting shock, after blood transfusion after massive hemorrhage, after extracorporeal circulation or cardiac resuscitation, and after the recovery of blood circulation in the transplanted kidney, a large amount of oxygen free radicals are produced. Under hypoxia, energy decomposition is more than synthesis, and the inosine monophosphate breakdown product hypoxanthine accumulates, which, under the action of xanthine oxidase, produces a large amount of xanthine, followed by an increase in the production of oxygen free radicals. The cell membrane of renal tissue cells is rich in lipids, such as polyunsaturated fatty acids, which have a high affinity for free radicals, producing various lipid peroxides. These lipid peroxides can cause the ratio of polyunsaturated fatty acids to proteins on the cell membrane to be out of balance, resulting in changes in the fluidity and permeability of the cell membrane, leading to dysfunction, a decrease in enzyme activity, a significant increase in capillary permeability, and an increase in exudation, leading to edema of cells and interstitium. The damage to the cell membrane by free radicals also causes a large amount of extracellular calcium ions to enter the cell, increasing the intracellular calcium ions, leading to cell death. In addition, when the kidney is ischemic, the function of the cortical mitochondria is significantly reduced, which also reduces the synthesis of adenosine triphosphate, leading to a decrease in the ion transport function on the cell membrane that depends on adenosine triphosphate energy, causing the accumulation of calcium ions in the cell. The latter stimulates the mitochondria to increase the uptake of calcium ions, leading to an excessive amount of calcium in the mitochondria and cell death. Calcium ion antagonists can prevent an increase in intracellular calcium concentration, thereby preventing the occurrence of ATN.

　　3. The Theory of Acute Renal Tubular Damage

　　Severe crush injuries and acute poisoning by toxic substances such as mercury chloride and arsenic mainly cause acute changes in ATN pathology, including the shedding and necrosis of renal tubular cells, and interstitial edema of the kidneys, while changes in glomeruli and renal blood vessels are relatively mild or absent, indicating that the main pathogenesis of ATN is due to primary damage to renal tubules, leading to a decrease or cessation of GFR. In 1975, Thurar et al. believed that the decrease in GFR during ATN was caused by the tubular-glomerular feedback mechanism induced by acute tubular damage. In recent years, many scholars have also proposed that renal tubular epithelial cell adhesion factors and polypeptide growth factors play an important role in the occurrence, development, and repair of ATN.

　　(1) The obstruction theory of renal tubular blockage states that toxins can directly damage renal tubular epithelial cells, with the lesions evenly distributed, mainly in the proximal tubules. Necrotic renal tubular epithelial cells, shed epithelial cells and microvillus debris, cell casts, or hemoglobin, myoglobin, and other substances can block the renal tubules, leading to an increase in intraluminal pressure in the proximal tubules of the blocked section. Subsequently, this causes an increase in intraglomerular pressure, and when the sum of this pressure and colloidal osmotic pressure is close to or equal to the intraglomerular capillary pressure, renal glomerular filtration stops. Experimental evidence shows that in sublethal renal tubular injury caused by renal ischemia or toxicity, the main manifestations are the shedding of the brush border of the proximal tubules, cell swelling, and vacuolar变性. Renal tubular epithelial cells (TEC) can shed from the basement membrane, causing defects or stripping areas on the renal tubular basement membrane. However, most of the shed TEC are morphologically intact and have viability. Similarly, in rabbit models of ischemic and toxic renal injury, the number of TEC in urine also significantly increases. This indicates that during ATN, TEC can shed, and a considerable number of TEC have not died. Studies have shown that the shedding of TEC from the basement membrane is due to a change in the adhesion force of renal tubular cells. It is known that among the renal tubular epithelial cell adhesion molecule families, integrins have the greatest impact on the occurrence of ATN. Integrins can mediate cell-cell and cell-matrix adhesion and maintain the integrity of renal tubular structure. In TEC injury, changes in cell adhesion are manifested as: ① Changes in the cytoskeleton, especially the actin microfilament component, which plays an important role in the adhesion of TEC to cells and the matrix, and in the adhesion between cells and the matrix. When renal tubular epithelial injury occurs, the components of the cytoskeleton change, leading to the shedding of TEC from the basement membrane. ② Changes in integrins, ischemia-reperfusion injury can cause significant abnormalities in integrin redistribution, especially in areas where the tubular structure has not been damaged, the tubular epithelium loses the polar distribution of integrins, suggesting that reperfusion can cause changes in cell adhesion, and the overexpression of integrins on the surface of damaged cells may increase cell-cell adhesion in the tubular lumen, promoting the formation of cell clusters blocking the tubular lumen. ③ Changes in matrix proteins, in 1991, Lin and Walker reported that after 30 to 40 minutes of clamping the renal hilum in experimental animals, immunofluorescence semi-quantitative analysis showed a transient decrease in laminin. After 3 to 4 days of ischemic injury, laminin increases at the junction of the cortex and medulla, and tenascin and fibronectin begin to increase 1 to 2 days after ischemia, reaching a peak on the fifth day, and there is no change in type IV collagen staining. These studies indicate that there are significant changes in matrix components in the early stage of ischemic injury, which can affect the adhesion of TEC and may be related to the shedding and repair of TEC after injury. In summary, the study of the adhesion mechanism of TEC and the changes in TEC adhesion in disease states is currently in the primary stage. Once these processes are elucidated, they will have a significant impact on the study of the pathogenesis of ATN. Understanding the mechanism of epithelial cell shedding helps to fundamentally explore methods to prevent shedding and enhance repair, maintain the integrity of the epithelial system function, and alleviate pathological injury.

　　(2) The back leak theory suggests that after the epithelial injury and necrosis of the renal tubules, there are defects and peeled areas in the tubular wall, and the lumen of the tubules can directly communicate with the renal interstitium. This causes the original urine in the tubular lumen to reflux and diffuse into the renal interstitium, leading to interstitial edema, compressing the renal units, exacerbating renal ischemia, and further reducing GFR. However, Donohoe et al. observed in experimental ATN that the back leak phenomenon of the original renal tubular fluid was only encountered when severe tubular necrosis occurred. Other experiments also prove that the decrease in renal blood flow and GFR can occur before the back leak of renal tubular fluid, indicating that the latter is not the initiating factor of ATN. However, the severity of interstitial edema in ATN is an important factor in the development of the disease.

　　(3) The ischemia, nephrotoxic factors, and tubulointerstitial injury caused by the tubulointerstitial feedback mechanism significantly reduce the reabsorption of sodium and chloride in the renal tubules, resulting in increased concentrations of sodium and chloride in the lumen. When passing through the distal tubules, the dense patch responds to the increased secretion of renin in the glomerular arterioles, followed by increased levels of angiotensin I and II, causing vasoconstriction of the glomerular arterioles and renal vessels, increased renal vascular resistance, and a significant decrease in GFR. In addition, the significantly reduced blood supply to the renal tubules leads to a decrease in the release of prostacyclin into the cortex, further reducing renal blood flow and GFR.

　　(4) Disseminated intravascular coagulation (DIC) caused by reasons such as sepsis, severe infection, epidemic hemorrhagic fever, shock, postpartum hemorrhage, pancreatitis, and burns often leads to diffuse microvascular damage. Platelet and fibrin deposition in the damaged renal vascular endothelium can cause vascular obstruction or poor blood flow. When red blood cells pass through the damaged vessels, they are prone to deformation, fragmentation, and dissolution, leading to hemolysis within the microvasculature. The increased aggregation of platelets and the vasoconstriction and contraction may be related to a decrease in prostacyclin when renal ischemia occurs. The above causes often easily activate the coagulation pathway and inhibit fibrinolysis, causing microvascular thrombosis. It is generally believed that DIC is a serious condition. It can be a cause of ATN, but it can also appear during the progression of ATN, causing or aggravating bilateral renal cortical necrosis. DIC is rare in ATN without complications, so DIC cannot be considered as the general pathogenesis of ATN.

　　Since the 1980s, significant progress has been made in the study of the pathogenesis of ATN, but it is still difficult to explain all the phenomena of ATN with a single theory. Different etiologies and different types of tubular pathological damage may have common initiating mechanisms and factors for continuous development, and the various theories are interrelated and occur in an intertwined manner. Currently, a deep understanding and understanding of the various links of the pathogenesis of ATN has a positive guiding significance for early prevention and treatment.

　　常可出现体液潴留、充血性心力衰竭、高钾血症、高血压等并发症。

　　1、充血性心力衰竭系指在有适量静脉血回流的情况下，由于心脏收缩和(或)舒张功能障碍，心排血量不足以维持组织代谢需要的一种病理状态。

　　2、血钾高于5.5mmol/L称为高钾血症，>7.0mmol/L则为严重高钾血症。因高钾血症常常没有或很少症状而骤然致心脏停搏，应及早发现，及早防治。

　　3、在未用抗高血压药情况下，收缩压≥139mmHg和/或舒张压≥89mmHg，按血压水平将高血压分为1，2，3级。收缩压≥140mmHg和舒张压

　　一、少尿－无尿型急性肾衰

　　占大多数，少尿指每日尿量少于400ml，无尿指每日尿量少于50ml，完全无尿者应考虑有尿路梗阻，少尿型的病程可分为三期：少尿期，多尿期，功能恢复期。

　　1、少尿期

　　通常在原发病发生后一天内即可出现少尿，亦有尿量渐减者，少尿期平均每日尿量约在150ml，但在开始的1～2天，可能低于此值，这时由于肾小球滤过率骤然下降，体内水，电解质，有机酸和代谢废物排出障碍，其主要临床表现如下。

　　(1) Uremia: Patients may experience loss of appetite, nausea, vomiting, diarrhea, anemia, uremic encephalopathy such as drowsiness, coma, convulsions, and so on.

　　(2) Disturbance of electrolyte and acid-base balance.

　　(3) Imbalance of water and electrolyte balance.

　　2. Polyuria phase

　　After patients pass the oliguria phase, when urine output exceeds 400ml/d, they enter the polyuria phase, which is a sign of the beginning of renal function recovery. With the development of the disease, urine output can increase exponentially day by day, usually reaching 4000 to 6000ml/d. At the beginning of the polyuria phase, due to the still low glomerular filtration rate and the increased nitrogenous decomposition metabolism, blood creatinine and blood urea nitrogen in patients do not decrease and may even continue to increase. When the glomerular filtration rate increases, these indicators can rapidly decrease, but they do not recover to normal levels quickly. When blood urea nitrogen returns to normal, it only means that 30% of renal function has been restored.

　　3. Recovery period

　　Due to significant loss, patients are often weak and emaciated, with muscle atrophy, and physical strength usually recovers within half a year.

　　2. Non-oliguric acute renal failure

　　In this type of acute renal failure, the tubular reabsorption capacity is impaired, much more than the reduction in glomerular filtration rate, because the glomerular filtrate cannot be extensively reabsorbed by the tubules, resulting in increased or nearly normal urine output. However, due to the actual reduction in glomerular filtration rate, urea nitrogen and other metabolic products still accumulate in the body, leading to azotemia and uremia.

　　1. Prevention

　　Active treatment of the primary disease causing acute tubular necrosis, such as timely correction of hypovolemia, insufficient renal blood flow, hypoxia, and infection, thorough removal of necrotic tissue, and close observation of renal function and urine output, early relief of renal vessel spasm, rational use of aminoglycoside antibiotics and diuretics, and performing intravenous urography in the elderly, those with pre-existing kidney diseases, and diabetic patients, especially when using high-dose contrast agents, should be done with caution.

　　2. Prognosis

　　Acute tubular necrosis is a severe and critical clinical disease. Its prognosis is related to the nature of the primary disease, age, pre-existing chronic diseases, the severity of renal function damage, early diagnosis and treatment, dialysis or not, the presence or absence of multiple organ failure and complications, and other factors. Currently, with the continuous improvement of dialysis therapy and the extensive implementation of early preventive dialysis, the number of cases directly dying from renal failure itself has significantly decreased, while the main causes of death are the primary disease and complications, especially multiple organ failure. According to statistics, the mortality rate of internal medicine and obstetrics causes has decreased significantly, but the mortality rate of acute tubular necrosis caused by severe trauma, large-area burns, major surgery, and sepsis remains above 70%, and a large part of them are complicated with multiple organ failure. Less than 3% of ATN develops into chronic renal insufficiency, mainly seen in severe primary diseases, pre-existing chronic kidney diseases, the elderly, severe conditions, or those with untimely diagnosis and treatment.

　　1. Blood examination

　　Understand the presence and degree of anemia to determine whether there is bleeding from the cavity and signs of hemolytic anemia, observe whether the morphology of red blood cells is deformed, there are破碎red blood cells, nucleated red blood cells, increased reticulocytes, and/or hemoglobinemia, etc., which suggest laboratory changes of hemolytic anemia, and are helpful for etiological diagnosis.

　　2. Urine examination

　　Urine examination for ATN patients is very important for diagnosis and differential diagnosis, but it must be combined with clinical comprehensive judgment of the results.

　　3. Renal glomerular filtration function examination

　　The concentration of blood creatinine (Scr) and blood urea nitrogen (BUN) and the daily increase in concentration are used to understand the degree of functional damage and whether there is a high catabolic metabolism. Generally, in the absence of complications from internal medicine causes of ATN, the daily Scr concentration increases by 40.2-88.4 μmol/L (0.5-1.0 mg/dl), and during the oliguria period, it is usually 353.6-884 μmol/L (4-10 mg/dl) or higher; BUN increases by about 3.6-10.7 mmol/L (10-30 mg/dl), and most of the time it is 21.4-35.7 mmol/L (60-100 mg/dl); if the condition is severe, the oliguria period is prolonged with a high catabolic state, and the daily Scr may increase by more than 176.8 μmol/L (2 mg/dl), and BUN may increase by more than 7 mmol/L; when there is crush injury or muscle injury, the increase in Scr may not be parallel to the increase in BUN.

　　4. Blood gas analysis

　　Mainly understand the presence and degree of acidosis, as well as the nature, and the blood pH, alkaline reserve, and bicarbonate are often lower than normal, indicating metabolic acidosis. The arterial blood oxygen partial pressure is very important, and if it is below 8.0 kPa (60 mmHg), especially if oxygen therapy cannot correct it, it is necessary to examine the lungs, exclude lung inflammation, and determine whether there is adult respiratory distress syndrome (ARDS). For critically ill cases, dynamic blood gas analysis is very important.

　　5. Blood electrolyte examination

　　During both oliguria and polyuria periods, close follow-up of blood electrolyte concentration measurements should be conducted, including blood potassium, sodium, calcium, magnesium, chloride, and phosphorus concentrations, especially being vigilant for hyperkalemia, hypocalcemia, hyperphosphatemia, and hypermagnesemia during the oliguria period; during the polyuria period, attention should be paid to hyperkalemia or hypokalemia, hyponatremia and hyponatremia, and hypokalemia and hypochloride alkalosis, etc.

　　6. Liver function examination

　　In addition to understanding the coagulation function, it is necessary to determine whether there is liver cell necrosis and other dysfunctions, including transaminase, blood bilirubin, blood albumin, etc. In addition to understanding the degree of liver function damage, it is also necessary to determine whether there is primary liver function failure leading to acute renal failure.

　　Bone Marrow Supplement Soup:

　　1 turtle (turtle), 200 grams of pork bone marrow, and appropriate amounts of scallion, ginger, and monosodium glutamate.

　　1. The turtle is boiled with hot water, the shell is peeled off, the internal organs and head are removed, and the pork bone marrow is cleaned and placed in a bowl.

　　2. Place the turtle meat in an aluminum pot, add seasonings, bring to a boil over high heat, then simmer over low heat to cook the turtle meat thoroughly. Add pork bone marrow and cook until done, then add monosodium glutamate to make it. It can be eaten as a side dish, and it can nourish the yin and kidney, fill the essence and nourish the骨髓.

　　1. Treatment of oliguria

　　Oliguria can often lead to death due to acute pulmonary edema, hyperkalemia, upper gastrointestinal bleeding, and concurrent infection. Therefore, the focus of treatment is to regulate fluid, electrolyte, and acid-base balance, control nitrogen retention, provide appropriate nutrition, prevent and treat complications, and treat the primary disease.

　　1. Bed rest All ATN patients should rest in bed.

　　2. For patients who can eat, try to use the gastrointestinal tract to supplement nutrition, mainly with light liquid or semi-liquid foods. Appropriately limit water, sodium, and potassium intake. Early on, protein intake should be limited (high biological value protein 0.5g/kg), as severe ATN patients often have obvious gastrointestinal symptoms. Supplementing part of the nutrition from the gastrointestinal tract should not be rushed. The first step is to allow the patient's gastrointestinal tract to adapt, with the aim of restoring gastrointestinal function, and avoiding bloating and diarrhea as a principle. Then, supplement part of the calories gradually, with a limit of 2.2-4.4kJ/d (500-1000 calories). Too fast or too much supplementation of food often cannot be absorbed, leading to diarrhea. According to the allowable fluid replacement volume, amino acid solution and glucose solution can be supplemented appropriately, with a heat of 6.6-8.7kJ/d (1500-2000 calories) to reduce protein catabolism in the body. If the patient must consume more than 6.6kJ/d (1500 calories), continuous venovenous hemofiltration should be considered to ensure the daily necessary fluid replacement volume.

　　3. Maintain fluid balance

　　Patients in oliguric phase should strictly calculate the water intake and output within 24 hours. The fluid replacement volume within 24 hours is the sum of the total amount of obvious fluid loss and insensible fluid loss minus the endogenous water volume. The obvious fluid loss refers to the total amount of lost fluids such as urine, feces, vomiting, sweating, drainage fluid, and wound exudate within the previous 24 hours; the insensible fluid loss refers to the daily water loss from exhalation (about 400-500ml) and evaporation from the skin (about 300-400ml). However, the estimation of insensible fluid loss is often difficult, so it can also be calculated at 12ml/kg, taking into account body temperature, ambient temperature, and humidity. It is generally believed that for every 1℃ increase in body temperature, the hourly water loss is 0.1ml/kg; when the room temperature exceeds 30℃, for every 1℃ increase, the insensible fluid loss increases by 13％; difficulty in breathing or tracheotomy will increase respiratory water loss. Endogenous water refers to the total amount of water generated by tissue metabolism, food oxidation, and glucose oxidation in the fluid replacement within 24 hours. The calculation of water generated by food oxidation is 0.43ml of water produced by 1 gram of protein, 1.07ml of water produced by 1 gram of fat, and 0.55ml of water produced by 1 gram of glucose. Since the calculation of endogenous water is often ignored, the calculation of insensible fluid loss is often an estimate, which affects the accuracy of fluid replacement during oliguria. Therefore, in the past, the principle of 'replacement of output with input, rather than more than necessary' was often adopted to prevent excessive fluid volume. However, attention must be paid to the presence of factors that may lead to insufficient blood volume, in order to avoid excessive restriction of fluid replacement, exacerbation of ischemic renal damage, and prolongation of the oliguric phase.

　　4. Hyperkalemia

　　The most effective treatment method is hemodialysis or peritoneal dialysis. If there is severe hyperkalemia or a state of high metabolic catabolism, hemodialysis is preferred. Hyperkalemia is a clinical emergency and should be treated as an emergency before the dialysis treatment is prepared.

　　5. Metabolic Acidosis

　　For the oliguria period without high metabolic catabolism, sufficient calories should be supplemented to reduce tissue decomposition in the body, and generally metabolic acidosis is not severe. However, metabolic acidosis with high metabolic catabolism occurs early, is severe, and sometimes difficult to correct. Severe acidosis can exacerbate hyperkalemia and should be treated promptly. When the actual bicarbonate level in plasma is below 15mmol/L, 100-250ml of 5% sodium bicarbonate should be administered intravenously, the infusion rate should be controlled according to the cardiac function status, and blood gas analysis should be monitored dynamically. Sometimes 500ml (containing 60mmol/L sodium) needs to be supplemented daily, so severe metabolic acidosis should be corrected by hemodialysis as soon as possible for safety.

　　6. Application of Lasix and Mannitol

　　After ruling out the factors of insufficient blood volume, ATN oliguria cases can be treated with Lasix. Lasix can dilate blood vessels, reduce renal vascular resistance, increase renal blood flow and glomerular filtration rate, and regulate the distribution of renal blood flow, reducing tubular and interstitial edema. Early use has a preventive effect on acute renal failure, reducing the chance of acute tubular necrosis. For oliguria type acute renal failure, Lasix can also be used for the differential diagnosis of acute renal failure due to functional or organic causes. A dose of 4mg/kg of Lasix intravenous injection can significantly increase urine output within one hour, which may be due to functional causes. However, there is controversy about the standard dose, whether high-dose efficacy still belongs to functional, and the author advocates for a dose of 200-400mg intravenous infusion as a moderate dose, stopping the medication if it is ineffective once. There have been reports that daily doses exceeding 1g even up to 4g can achieve diuretic effects, but such high doses of Lasix can damage the renal parenchyma, prolong the recovery time of renal lesions. Currently, hemodialysis technology is widely used, and for those who do not respond to diuretics, early dialysis should be considered. Over-reliance on Lasix to increase urine output also increases the ototoxicity of Lasix.

　　Mannitol, as an osmotic diuretic, can be used for the prevention of various causes of ATN, such as forced diuresis in cases of shock corrected after crush injury and still without urine, and it is also used to differentiate between pre-renal factors or acute renal failure causing oliguria. The dosage is intravenous infusion of 100-200ml of 20% mannitol. If there is still no increase in urine output within one hour or if the oliguria (anuria) has been diagnosed as ATN, mannitol should be discontinued to avoid excessive blood volume, which may trigger heart failure and pulmonary edema.

　　Chapter 2: Polyuria Phase Treatment

　　During the polyuria phase, life-threatening complications still exist. The focus of treatment is still to maintain water, electrolyte, and acid-base balance, control azotemia, treat the primary disease, and prevent various complications. In some cases of acute tubular necrosis, the polyuria phase can last for a long time, with daily urine output often exceeding 4L. The fluid intake should be gradually reduced (less than 500-1000ml than output), and it is as far as possible to be supplemented through the gastrointestinal tract to shorten the polyuria phase. For patients who cannot get out of bed, special attention should be paid to the prevention and treatment of pulmonary infections and urinary tract infections.

　　During the polyuria phase, even if the urine output exceeds 2500ml/day, blood urea nitrogen can still continue to rise. Therefore, for those who have already undergone dialysis treatment, dialysis should still be continued at this time to ensure that blood urea nitrogen does not exceed 17.9mmol/L (50mg/dl), and blood creatinine gradually decreases to below 354μmol/L (4mg/dl) and stabilizes at this level. For patients whose clinical conditions have significantly improved, dialysis can be temporarily suspended for observation, and dialysis can be stopped after the condition stabilizes.

　　Chapter 3: Recovery Period Treatment

　　Generally, no special treatment is required. Regularly follow up on renal function and avoid using drugs that are harmful to the kidneys.