Tubular necrosis

Introduction Acute tubular necrosis (ATN) is the most common type of acute renal failure, accounting for 75% to 80%. It is a clinical syndrome that occurs due to renal ischemia and/or nephrotoxicity caused by various causes of renal function and progressive decline. Mainly manifested as progressive azotemia caused by a significant decrease in glomerular filtration rate, as well as imbalance of water, electrolyte and acid-base balance caused by renal tubular reabsorption and excretion. According to the decrease in urine volume, it is divided into oliguria (no urine) type and non-oliguric type.

Cause

The main causes of acute tubular necrosis are traditionally divided into two categories: acute renal ischemia and acute nephrotoxicity. However, intravascular hemolysis and certain infections are not uncommon. Sometimes kidney ischemia and nephrotoxicity factors can coexist.

(A) acute renal ischemia: acute renal ischemia is the most common type of ATN, which is partly due to the sustained action and development of the aforementioned pre-renal factors, resulting in longer-term renal ischemia, hypoxia and cause ATN. A large amount of bleeding or blood transfusion in the chest or abdomen during or after surgery, various causes of shock and shock correction, cardiopulmonary bypass, and renal transplantation to restore renal blood circulation and cardiac resuscitation are renal ischemia-reperfusion conditions. Therefore, it is generally said that ischemic acute renal failure is longer than other types of ATN for the recovery of severe renal function.

(B) acute nephrotoxicity damage: nephrotoxic damage is mainly exogenous nephrotoxicity, such as drugs, heavy metals and chemical poisons and biological toxicity.

1, drug nephrotoxicity damage: the incidence rate has an increasing trend, accounting for 11% of the total acute renal failure rate and 17.1% of the cause of acute renal failure. Common drugs that cause ATN are aminoglycoside antibiotics such as gentamicin, kana and amikacin polymyxin B tobramycin, sulfonamides, amphotericin cyclosporin A and Pa and so on.

2. Toxic damage to poison:

(1) Heavy metal kidney poisons: such as mercury, cadmium, arsenic, uranium, chromium, lithium, antimony, lead and platinum;

(2) Industrial poisons: such as cyanide, carbon tetrachloride, methanol, toluene, ethylene glycol and chloroform;

(3) disinfectant: such as cresol resorcinol, formaldehyde, etc.;

(4) Insecticides and herbicides: such as organic phosphorus, paraquat, etc., such poison poisoning should pay attention to early measures to remove poisons in the body.

3, biological toxins: there are green fish gall, snake bites, poisonous cockroaches, bee venom and so on. This kind of toxin poisoning often causes multiple organ failure and often damages lung, kidney, liver and heart function. In the first aid, attention should be paid to maintaining the function of each major organ.

4, contrast agent kidney injury: the original renal dysfunction, elderly patients with diabetes, insufficient blood volume, hyperuricemia and multiple myeloma, etc. are prone to acute renal impairment.

(3) Infectious diseases: such as epidemic hemorrhagic fever, leptospirosis, etc. caused by ATN. Among them, hemorrhagic fever is the most common, accounting for 18.6% of the total incidence of acute kidney failure and 29% of the cause of internal medicine. The pathological basis of hemorrhagic fever is systemic small blood vessel hemorrhagic damage, and the high mortality rate in severe cases should emphasize early diagnosis and early dialysis treatment.

(4) Acute hemolysis and intravascular hemolysis: unsuitable heterotypic transfusion, various red blood cell destruction caused by extracorporeal circulation, immune diseases caused by hemolytic anemia crisis, various causes of hemoglobin, urinary malaria, black urine fever, falciparum malaria and resistance Hemolysis caused by malaria drugs such as primaquine and quinine. Squeezing, trauma, and non-traumatic striated muscle lysis cause a large amount of myoglobin to deposit renal tubules, causing kidney damage similar to hemolysis.

an examination

Related inspection

Renal function test kidney diagram

(1) Blood picture examination to understand the degree of anemia and its degree, to determine whether there are signs of channel bleeding and hemolytic anemia, to observe whether the red blood cell morphology is deformed, broken red blood cells, nucleated red blood cells, reticulocyte increase and/or hemoglobinemia, etc. A laboratory change suggesting hemolytic anemia is helpful for the diagnosis of the cause.

(B) urine test ATN patients' calligraphic fluid examination is very important for diagnosis and differential diagnosis, but must be combined with clinical comprehensive judgment of the results: 1 urine volume change: daily urine volume in the oliguria period is below 400ml, non-oliguric The urine volume can be normal or increased, 2 urine routine examination: the appearance is turbid, the urine color is deep, sometimes it is soy sauce color; the urine protein is mostly (+) ~ (++), sometimes up to (+++) ~ (+++ +), often in the middle, small molecular proteins, proteinuria level is not helpful for the diagnosis of the cause, urine sediment examination often appears different degrees of hematuria, microscopic hematuria is more common, but in heavy metal poisoning often have a large amount of proteinuria and the naked eye Hematuria, in addition, there are detached renal tubular epithelial cells, epithelial cell casts and granules, and different degrees of white blood cells, etc., there are fashionable non-pigmented casts or white blood cell casts, 3 urine specific gravity is reduced and fixed, mostly below 1.015 Due to renal tubular reabsorption function damage, urine can not be concentrated, 4 urine osmotic concentration is lower than 350mOsm / kg, urine to blood osmotic concentration ratio is lower than 1.1, 5 urine sodium content increased, mostly in 40 ~ 60mmol / L, because Renal tubules reduce sodium reabsorption, 6 urine The ratio with blood urea is lower, often lower than 10, due to decreased urine urea excretion, and elevated blood urea, 7 ratio of urine creatinine to serum creatinine, often lower than 10,8 renal failure index is often greater than 2, the index is The ratio of urinary sodium concentration to urine creatinine and serum creatinine ratio, due to more urinary sodium excretion, less urinary creatinine excretion and increased serum creatinine, so the index increased, 9 filtered sodium excretion fraction (FeNa), representing the ability of the kidney to remove sodium, Expressed as a percentage of glomerular filtration rate, ie (urine sodium, blood sodium ratio / urine creatinine, serum creatinine ratio) × 100, namely:

FeNa(%) = UNaV ÷ GRF × 100 PNa = UNa·V ÷ UCr·V × 100 PNa PCr = UNa × PCr × 100PNaUCr

UNa is urinary sodium, PNa is blood sodium, V is urine volume, UCr is urine creatinine, PCr is serum creatinine, GFR is glomerular filtration rate, AT is often >1, and prerenal oliguria is often <1 .

The above 5 to 9 urinalysis index is often used as an identification of prerenal oliguria and ATN. However, in practical applications, these indexes are unreliable and contradictory after treatment with diuretics and hypertonic drugs, so they are only used as an aid. Diagnostic reference.

(C) glomerular filtration function check serum creatinine (Scr) and blood urea nitrogen (BUN) concentration and daily increase in order to understand the degree of functional damage and the presence or absence of high catabolism, generally in the uncomplicated medical cause ATN The daily Scr concentration increased by 40.2-88.4 mol/L (0.5-1.0 mg/dl), and the oliguria phase was mostly 353.6-884 mol/L (4-10 mg/dl) or higher; BUN increased daily by about 3.6~ 10.7mmol / L (10 ~ 30mg / dl), most of which are in 21.4 ~ 35.7mmol / L (60 ~ 100mg / dl); if the condition is heavy, prolonged oliguria with high decomposition state, the daily Scr can increase by 176.8mol / Above L (2mg/dl), BUN can increase by more than 7mmol/L per day; in crush injury or muscle injury, Scr rise can be parallel with BUN rise.

(4) Blood gas analysis mainly understands the presence or absence of acidosis and its degree and nature, as well as hypoxemia, blood pH, alkali storage and bicarbonate are often lower than normal, suggesting metabolic acidosis, arterial oxygen partial pressure is Important, below 8.0kPa (60mmHg), special oxygen can not be corrected, the lungs should be examined, lung inflammation and adult respiratory distress syndrome (ARDS) should be excluded. It is very important to check blood gas analysis in critically ill cases.

(V) blood electrolyte examination oliguria and polyuria should be closely followed by blood electrolyte concentration determination, including serum potassium, sodium, calcium, magnesium, chloride and phosphorus concentrations, etc., oliguria period, special alert for hyperkalemia, low Calcemia, hyperphosphatemia and hypermagnesemia; during the polyuria period should pay attention to high potassium or hypokalemia, low sodium and hypochloremia and low potassium, low chloride alkalosis.

(6) Liver function test In addition to coagulation function, hepatic cell necrosis and other dysfunction, including transaminase, blood bilirubin, blood globulin, etc., in addition to understanding the degree of liver damage, Hepatic failure causes acute renal failure.

(7) bleeding tendency check 1 dynamic platelet count with or without reduction, for patients with bleeding tendency or critical risk should be related to DIC laboratory tests, platelet function test to understand the increase or decrease of platelet aggregation; 2 prothrombin time is normal Or prolonged; 3 thromboplastin production or no bad; 4 decreased or increased fibrinogen; 5 increased fibrin cleavage product (FDP), if there is bleeding tendency in ATN oliguria, DIC should be suspected, At this time, there can be a decrease in the number of platelets and dysfunction and coagulopathy, which is characterized by consumptive hypocoagulopathy in the body. The latter is caused by diffuse intravascular coagulation, which consumes a large amount of coagulation factors and secondary fibrinolysis, which is expressed as low fibrinogen. Blood, blood FDP concentration increased significantly.

Differential diagnosis

Differential diagnosis

In the differential diagnosis, pre-renal oliguria and post-renal urinary tract obstruction should be excluded. When it is determined that the kidney is substantial, it should be identified as glomerular, renal vascular or renal interstitial lesions caused by different causes and different pathological changes, and there are completely different treatment methods in the early stage. Such as allergic renal interstitial lesions and glomerulonephritis caused by more glucocorticoid treatment and renal tubular necrosis caused by no.

(1) Identification with pre-renal oliguria: The patient has a history of insufficient capacity or cardiovascular failure, and the degree of azotemia in simple pre-renal failure is not serious. After the blood volume is increased, the amount of urine increases, and blood Cr returns to normal. Urine routine changes were not obvious, urine specific gravity was above 1.020, urine osmotic concentration was greater than 550mOsm/kg, urine sodium concentration was below 15mmol/L, and urine, serum creatinine and urea nitrogen ratio were above 40:1 and 20:1, respectively. However, in elderly patients with pre-pregnancy failure, if there is already kidney damage, it also reflects changes in renal parenchymal failure.

(B) identification of post-renal urinary tract obstruction: urinary calculi pelvic organ tumor or surgical history, sudden complete anuria or intermittent anuria (one side of ureteral obstruction and contralateral renal insufficiency can be expressed as oliguria Or non-oliguric), renal colic and sputum pain in the kidney area, no significant changes in urine routine, B-type ultrasound urinary system examination and urography X-ray examination can often make a differential diagnosis.

(C) with severe acute glomerulonephritis or rapid glomerulonephritis identification: severe nephritis often have obvious edema, high blood pressure, large amount of proteinuria with obvious microscopic or gross hematuria and various types of tubular glomerulonephritis Changes to the diagnosis of difficulty, the use of immunosuppressive therapy should be done to confirm the diagnosis of renal biopsy.

(D) differentiation with acute renal interstitial lesions: mainly based on the cause of acute interstitial nephritis, such as drug allergy or infection history, obvious renal pain drugs caused by fever, rash, joint pain, blood eosinophils Increase and so on. Acute tubular necrosis and ATN identification are sometimes difficult. Kidney biopsy should also be performed first. Most acute renal interstitial nephritis should be treated with glucocorticoids. Renal biopsy is important for the identification of the cause of acute kidney failure. Sometimes, renal biopsy can reveal some diseases that are not considered for identification.

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