acute tubular necrosis
Introduction
Introduction to acute tubular necrosis 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. basic knowledge The proportion of sickness: 0.01% Susceptible people: no specific population Mode of infection: non-infectious Complications: congestive heart failure, hyperkalemia, hypertension
Cause
Acute tubular necrosis
Etiology
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 renal ischemia and nephrotoxicity can exist simultaneously. .
(1) Acute renal ischemia Acute renal ischemia is the most common type of ATN. It is partly due to the sustained action and development of the aforementioned pre-renal factors, resulting in long-term renal ischemia, hypoxia and ATN, chest and abdomen. A large amount of bleeding or blood transfusion during or after surgery, various causes of shock and shock correction, cardiopulmonary bypass, allogeneic renal transplantation to restore renal blood circulation and cardiac resuscitation are renal ischemia-reperfusion conditions, so generally speaking The ischemic acute renal failure is more severe than other types of ATN, and the time required for renal function recovery is also longer.
(B) acute nephrotoxicity damage nephrotoxicity is mainly exogenous nephrotoxicity, such as drugs, heavy metals and chemical poisons and biological toxicity.
1. The current incidence of drug nephrotoxicity has an increasing trend, accounting for 11% of the total acute renal failure rate and 17.1% of the cause of acute renal failure, and the common drug causing ATN is the aminoglycoside antibiotic such as Qingdamycin. , kana and amikacin, polymyxin B, tobramycin, sulfonamides, amphotericin, cyclosporin A and cispa.
2. Toxic nephrotoxicity
(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, herbs, etc., such poison poisoning should pay attention to early measures to remove poisons in the body.
3. Biotoxins include blue fish gall, snake bites, poisonous mites, bee venom, etc. These toxin poisonings often cause multiple organ failure, often impairing lung, kidney, liver and heart function, etc. Each major organ function.
4. Contrast agent kidney damage original renal function damage, diabetes, elderly patients, blood volume deficiency, hyperuricemia and multiple myeloma, etc. are prone to acute renal injury.
(3) Infectious diseases such as epidemic hemorrhagic fever, leptospirosis, etc. cause ATN, of which 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, severe mortality rate is very high, should emphasize early diagnosis and early implementation of dialysis treatment.
(4) Heterotypic transfusion with acute hemolysis and intravascular hemolysis, red blood cell destruction caused by various extracorporeal circulation, hemolytic anemia crisis caused by immune diseases, hemoglobinuria for various reasons, black urine fever in malaria endemic areas, falciparum malaria Hemolysis, squeezing, trauma, and non-traumatic striated muscle lysis caused by antimalarial drugs such as primaquine and quinine cause a large amount of myoglobin to deposit renal tubules, causing kidney damage similar to hemolysis.
[Pathogenesis]
The pathogenesis of acute tubular necrosis is multi-link, renal hemodynamic changes and acute tubular damage are the main factors, and the various points of the theory are described as follows:
(1) Renal hemodynamic changes Renal hemodynamic changes have played a leading role in the early stage of ATN, and are often the initiating factors. In hemorrhagic shock or severe hypovolemia, due to the regulation of nerves and body fluids, systemic blood Redistribution, renal artery contraction, renal blood flow can be significantly reduced, renal perfusion pressure decreased and glomerular small arteries contracted significantly, causing renal cortical ischemia and ATN, sometimes in the early stage of acute ischemic ATN caused by major bleeding Although the blood volume was restored quickly and the renal blood flow was restored, the glomerular filtration rate and GFR did not recover, indicating that there was an abnormality of intrarenal hemodynamics and abnormal renal blood flow distribution in the early stage of ATN. The pathophysiological basis of rheological abnormalities is related to the following factors.
1. The role of renal nerves The renal sympathetic nerve fibers are widely distributed in the renal blood vessels and the juxtaglomerular body. The adrenergic activity is enhanced to cause renal vasoconstriction, resulting in a decrease in renal blood flow and GFR, and stimulation of the renal nerves in ischemic ATN. The degree of renal vasoconstriction is much higher than that of normal animals, indicating that the sensitivity of blood vessels to renal nerve stimulation is increased at ATN, but this enhanced response can be inhibited by calcium channel blockers, suggesting that kidneys are present in renal nerve stimulation. Vasoconstriction is associated with changes in renal vascular smooth muscle calcium activity, but clinically observed in non-nervous kidneys, the incidence of ischemic ATN can be as high as 30% after the recovery of renal blood supply by allogeneic kidney transplantation, and does not support The leading role of renal nerves in the development of ATN.
2. The role of renin-angiotensin in renal tissue There is a complete renin-angiotensin system in the kidney tissue. In ischemic ATN, the renal blood circulation path is thought to be related to the renin-angiotensin system in the kidney tissue. Activation, which leads to strong contraction of the small arteries into the ball, but inhibition of renin activity and antagonism of angiotensin II can still occur ATN, indicating that the renin-angiotensin system is not a decisive factor for ATN.
3. The role of prostaglandins in the kidney Intrarenal prostaglandins, especially prostacyclin PGI2, are synthesized in the renal cortex, which has a significant dilation of blood vessels, which can increase renal blood flow and GFR, and is beneficial to sodium and anti-diuretic hormone pairs. The reabsorption of water plays a role in diuresis. It has been confirmed that PGI2 is significantly reduced in blood and kidney tissue at ATN; it has been proven that PGI2 in the kidney prevents the development of ischemic ATN, and prostaglandin antagonist indomethacin can be used. Accelerated ischemic renal damage, in addition to renal ischemia, increased thromboxane synthesis in the renal cortex, also promote renal vasoconstriction, but there is no evidence that prostaglandins play a leading role in ATN.
4. The role of endothelial cell-derived contractile and relaxing factor in ATN Many scholars have emphasized the pathological secretion of vascular endothelial-derived contractile factor and the release of vascular endothelial-derived relaxing factors such as nitric oxide (NO) to ATN blood flow. Kinetic changes play an important role, they found that ATN early renal blood flow reduction, not due to the role of renin-angiotensin, but renal ischemia, hypoxia, vascular endothelial cells release more endothelin (in the experiment) It was found that low concentrations of endothelin can cause strong and sustained contraction of renal blood vessels, increased renal vascular resistance, leading to a decrease or stop of GFR, glomerular capillaries and mesangial cells, and highly dense endothelin receptors in experimental small blood vessels. Continuous intravascular renal injection of endothelin can also cause significant contraction of renal blood vessels, which causes increased resistance to contraction of the glomerular and ectocervical arteries, and increased resistance to arteriolar arteries, so renal blood flow and GFR Parallel decline, but sometimes the patient's serum endothelin concentration increased by more than ten times, clinically no ATN, normal vascular endothelium can release release factor, synergistically regulate blood flow to maintain Blood circulation, the increase of blood flow in the kidney, reduce the resistance of the ball into the ball and the small artery, the release of early vascular endothelium factor in ATN is disordered, and the increase of oxygen free radicals after ischemia-reperfusion also affects the release of relaxing factor. In this case, renal hemodynamic changes may be prominent. It is currently believed that imbalance of endothelial cell contraction and relaxation factor regulation may play an important role in the occurrence and development of certain types of ATN.
5. Renal medullary hemorrhage In the ischemic ATN model, the renal medulla and the intracortical region were most obviously damaged, and the degree of renal medullary blood stasis was significantly correlated with the degree of ATN damage. Oxygen firstly affects the blood supply of renal tubular cells in the ascending branch, and the thick segment of the ascending branch is a high-energy-consumption area, which is sensitive to hypoxia, and the ability of hypoxic tubular cells to actively reabsorb sodium chloride is reduced. The thick segmental injury can make TH glycoprotein easy to deposit in the thick segment, causing distal small lumen obstruction and luminal fluid spillover. Therefore, it is considered that medullary hemorrhage is also an important factor in ischemic ATN.
(II) Renal ischemia-C-perfusion cell injury mechanism Renal tissue recovers blood supply after acute ischemia and hypoxia. If shock is corrected, blood transfusion after big blood transfusion, after cardiopulmonary bypass or recovery of cardiac resuscitation, after recovery of blood circulation of transplanted kidney, A large number of oxygen free radicals, energy decomposation is more than synthesis in the absence of oxygen, adenosine triphosphate decomposition product hypoxanthine aggregation, a large amount of xanthine is produced under the action of xanthine oxidase, and then oxygen free radicals are increased, and the renal cell membrane is rich in lipid substances. Such as polyunsaturated fatty acids, the latter has a high affinity with free radicals, producing a variety of lipid peroxides, the latter can make the ratio of polyunsaturated fatty acids to protein on the cell membrane, resulting in multi-valent unsaturated cell membrane The imbalance of fatty acid and protein causes changes in fluidity and permeability of cell membranes, resulting in dysfunction, decreased activity of various enzymes, marked increase in capillary permeability, increased exudation leading to cell and interstitial edema, and free radicals. The damage of the cell membrane causes a large amount of extracellular calcium ions to enter the cell, causing the intracellular calcium ions to increase and the cells to die. In addition, the mitochondrial function of the cortex is significantly reduced during renal ischemia, which also reduces the synthesis of adenosine triphosphate, which reduces the ion transport function of the adenosine triphosphate-dependent energy on the cell membrane, and accumulate intracellular calcium ions, which in turn stimulates the increase of calcium ion uptake by mitochondria, mitochondria. Excessive calcium levels lead to cell death, and calcium ion antagonists can prevent an increase in intracellular calcium concentration, thereby preventing the occurrence of ATN.
(C) acute tubular damage theory of severe crush injury and acute toxic poisoning, such as mercury chloride, arsenic and other causes of ATN pathological changes in renal tubular cell shedding, necrosis and other acute damage and renal interstitial edema as the main changes, The glomerular and renal vascular changes are relatively mild or absent, indicating that the main pathogenesis of ATN is due to the primary lesion of the renal tubules caused by the reduction or stop of GFR. In 1975, Thurar et al considered that the decrease of GFR during ATN was caused by acute damage of renal tubules. Due to the small tube-small ball feedback mechanism, in recent years, many scholars have proposed the important role of renal tubular epithelial cell adhesion factor and polypeptide growth factor in the development, development and renal tubular repair of ATN.
1. Renal tubular obstruction theory toxins can directly damage renal tubular epithelial cells, the lesions are evenly distributed, mainly proximal tubules, necrotic tubular epithelial cells and exfoliated epithelial cells and microvilli debris, cell cast or hemoglobin, Myoglobin blocks the renal tubules, causing an increase in the proximal small lumen pressure of the obstruction, which in turn increases the pressure in the glomerular capsule, when the sum of the latter pressure and the colloid osmotic pressure is close to or equal to the glomerular capillary When pressed, sputum caused glomerular filtration to stop, the experiment proved that renal ischemia or nephrotoxicity caused sublethal renal tubular injury, mainly manifested as proximal tubule brush margin shedding, cell swelling and vacuolar degeneration, etc. Epithelial cells (TEC) detached from the basement membrane, causing defect/exfoliation areas on the basement membrane of the renal tubules, but most of the detached TECs were intact and viable, as well as rabbit models of ischemic and toxic renal damage. The number of TEC in the liquid also increased significantly, indicating that TEC will fall off at ATN, and a considerable number of TECs did not die. Studies have shown that TEC is detached from the basement membrane due to changes in renal cell adhesion. Integrin has the greatest influence on the occurrence of ATN in the family of renal tubular epithelial cell adhesion molecules. Integrin can mediate cell-cell and cell-to-matrix adhesion, and maintain the structural integrity of the renal tubule. Cell adhesion in TEC injury The attached changes are manifested in:
1 The change of cytoskeleton, especially actin microfilament component plays an important role in the adhesion between TEC and cells, cells and matrix. When the renal tubular epithelium is damaged, the cytoskeletal composition changes, causing TEC to fall off the basement membrane. .
2 Integrin changes, ischemia-reperfusion injury can cause significant integrin redistribution abnormalities, especially in the uninjured area of tubule structure, the small tube epithelium loses the polar distribution of integrin, suggesting that reperfusion can cause cell adhesion changes Overexpression of integrin on the surface of damaged cells may increase the adhesion of cells to cells in the small lumen and promote the formation of cell clumps that block the small lumen.
3 Changes in matrix proteins. In 1991, Lin and Walker reported that the experimental animals were clamped for 30-40 minutes after clamping the renal pedicle. Semi-quantitative analysis of immunofluorescence showed a decrease in laminin, and cortex and skin were 3 to 4 days after ischemic injury. At the medullary junction, laminin increased, and tensein and fibronectin began to increase 1 to 2 days after ischemia, peaked on day 5, and there was no change in type IV collagen staining. These studies showed ischemic injury. Early changes in matrix components, these changes will affect the adhesion of TEC, may be related to TEC detachment and repair after injury, in summary, the TEC adhesion mechanism and TEC adhesion changes under disease conditions are still In the initial stage, once these processes are elucidated, it will have a major impact on the study of the pathogenesis of ATN. The understanding of the mechanism of epithelial cell shedding helps to fundamentally explore ways to prevent shedding and enhance repair, and to maintain the function of the epithelial system. Integrity, reducing pathological damage.
2. Back leakage theory refers to necrosis and exfoliation after renal tubular epithelial injury, defect and exfoliation area of renal tubular wall, tubule lumen can directly communicate with renal interstitial, resulting in the flow of primary urine in the small lumen to the renal interstitial Causes renal interstitial edema, oppresses the nephron, aggravates renal ischemia, and reduces GFR, but Donohoe et al observed in the experimental ATN that the tubular tubules were leaky only in the case of severe tubular necrosis. The experiment also proved that renal blood flow and GFR decreased before renal tubular fluid leakage, indicating that the latter is not the starting factor of ATN onset, but the severity of renal interstitial edema at ATN is an important factor in disease development.
3. Tube-ball feedback mechanism ischemic, nephrotoxicity and other factors cause acute tubular damage, resulting in the renal tubular reabsorption of sodium, chlorine and other significant reduction, intraluminal sodium, chlorine concentration increased, dense spots through the distal tubule Induction causes an increase in the secretion of renin from the small arteries, followed by an increase in angiotensin I and II, which causes the arteriolar and renal vasoconstriction, renal vascular resistance to increase, and GFR to decrease significantly. In addition, renal tubular blood supply is significantly reduced, Renal prostacyclin release into the cortex is reduced, renal blood flow and GFR are further reduced.
4. Disseminated intravascular coagulation (DIC) sepsis, severe infection, epidemic hemorrhagic fever, shock, postpartum hemorrhage, pancreatitis and burns cause ATN, often diffuse microvascular damage, platelet and fibrin deposition in injured kidney Endothelium, causing vascular occlusion or poor blood flow, red blood cells flowing through damaged blood vessels are prone to deformation, breakage, dissolution, resulting in microvascular hemolysis, increased platelet aggregation and vasospasm contraction may be due to renal ischemia Related to the reduction of cyclin, the above various causes are often easy to activate the blood coagulation pathway and inhibit fibrinolysis, resulting in microvascular thrombosis. It is generally considered that DIC is a critical condition, which can be used as a cause of ATN, but it can also appear in the progression of ATN. Can cause or aggravate bilateral renal cortical necrosis, DIC occurs in uncomplicated ATN, so DIC can not be used as a general pathogenesis of ATN.
Since the 1980s, the research on the pathogenesis of ATN has made great progress, but so far it is difficult to explain all the phenomena of ATN, possibly different causes, different types of renal tubular pathological damage, may have their common mechanism of initiation and sustainable development, and The various theories are interrelated and intertwined. At present, the in-depth understanding and understanding of the various aspects of the pathogenesis of ATN has positive guiding significance for early prevention and treatment.
Prevention
Acute tubular necrosis prevention
prevention
Active treatment of the primary disease causing acute tubular necrosis, such as timely correction of blood volume deficiency, insufficient renal blood flow, hypoxia and infection, completely remove the traumatic necrotic tissue, and closely observe renal function and urine output, early release of renal vasospasm Rational use of aminoglycoside antibiotics and diuretics to perform intravenous urography on elderly, pre-existing kidney disease, and diabetic patients, especially for large doses of contrast agents.
[prognosis]
Acute tubular necrosis is a clinically critical disease, its prognosis and primary disease nature, age, original chronic disease, severity of renal impairment, early diagnosis and early treatment dialysis or not, with or without multiple organ failure and concurrent Related factors such as the disease, at present, with the continuous improvement of dialysis therapy and the extensive development of early preventive dialysis, the number of cases directly dying from renal failure itself is significantly reduced, mainly due to primary disease and complications, especially more dirty According to statistics, the cause of internal medicine and the cause of obstetrics are significantly reduced, but the mortality of severe trauma, extensive burns, major surgery and acute renal tubular necrosis due to sepsis is still as high as 70% or more. A large proportion of patients with multiple organ failure, ATN developed into chronic renal insufficiency less than 3%, mainly seen in severe primary disease, the original chronic kidney disease, advanced age, serious illness or diagnosis and treatment is not timely.
Complication
Acute tubular necrosis complications Complications, congestive heart failure, hyperkalemia, hypertension
Frequent complications such as fluid retention, congestive heart failure, hyperkalemia, and hypertension may occur.
Symptom
Acute tubular necrosis symptoms Common symptoms Diarrhea convulsions coma, anuria, muscle atrophy, tubular necrosis, oliguria, sleepiness, polyuria, weakness
The symptoms of the pioneer can be typical of acute renal failure after hours or 1 to 2 days. According to the amount of urine, it can be divided into two types: oliguria - anuria - free and polyuria.
(1) oliguria-free urinary acute renal failure, accounting for the majority, oliguria refers to daily urine volume less than 400ml, no urine refers to daily urine volume less than 50ml, completely urinary should consider urinary tract obstruction, The course of oliguria can be divided into three phases: oliguria, polyuria, and functional recovery.
1. Oliguria: usually oliguria can occur within one day after the onset of the primary disease, and there is also a decrease in urine output. The average daily urine output during oliguria is about 150ml, but it may be lower than the first 1-2 days. Value, at this time due to a sudden drop in glomerular filtration rate, body water, electrolytes, organic acids and metabolic waste discharge barrier, the main clinical manifestations are as follows.
(1) uremia: patients with loss of appetite, nausea, vomiting, diarrhea, anemia, uremia encephalopathy such as lethargy, coma, convulsions and so on.
(2) Electrolyte and acid-base balance disorders.
(3) Water balance imbalance.
2. Polyuria: After the patient has passed the oliguria period, the urine volume exceeds 400ml/d and enters the polyuria phase. This is a sign that the renal function begins to recover. As the disease progresses, the urine volume can be multiplied daily, usually Up to 4000 ~ 6000ml / d, at the beginning of the polyuria period, because the glomerular filtration rate is still low, and due to increased nitrogen catabolism, the patient's serum creatinine and urea nitrogen does not decrease, and can continue to increase, when the glomerulus When the filtration rate increases, these indicators can drop rapidly, but not quickly return to normal levels. When blood urea nitrogen drops to normal, it only means that 30% of kidney function is restored.
3. Recovery period: due to a large number of losses, the patient is weak, weak, muscle atrophy, more than half a year of physical recovery.
(2) Non-oliguric type acute renal failure, the renal tubular resorption ability of this type of acute renal failure patients is impaired, far less than the glomerular filtration rate, because the small ball filtration fluid can not be absorbed back by the small tube. As a result, the amount of urine is increased or nearly normal, but since the glomerular filtration rate is actually lowered, metabolites such as urea nitrogen are still stored in the body, causing azotemia and uremia.
Examine
Acute tubular necrosis
(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 for sodium reabsorption Reduced, 6 urine urea and blood urea ratio decreased, often less than 10, due to reduced urine urea excretion, and elevated blood urea, 7 ratio of urine creatinine to serum creatinine, often lower than 10,8 renal failure index often More than 2, the index is the ratio of urinary sodium concentration to urine creatinine, serum creatinine ratio, due to more urinary sodium excretion, less urinary creatinine excretion and increased serum creatinine, so the index increases, 9 filtered sodium excretion fraction (FeNa), representing The ability of the kidney to remove sodium is 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 × 100 PNa UCr
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.
Diagnosis
Diagnosis and diagnosis of acute tubular necrosis
Differential diagnosis
In the differential diagnosis, the pre-renal oliguria and post-renal urinary tract obstruction should be excluded first. When the kidney is substantive, it should be identified as glomerular, renal vascular or renal interstitial lesions, due to different causes. Pathological changes, in the early stages have different treatments, such as allergic renal interstitial lesions and glomerulonephritis caused by glucocorticoid treatment, but not caused by tubular necrosis.
(1) Patients with pre-renal oliguria have a history of insufficient capacity or cardiovascular failure. The degree of azotemia in simple prerenal failure is not serious. After the blood volume is increased, the amount of urine increases, and blood Cr returns to normal. The change is not obvious, the urine specific gravity is above 1.020, the urine osmotic concentration is greater than 550mOsm/kg, the urine sodium concentration is below 15mmol/L, and the urine, serum creatinine and urea nitrogen ratios are above 40:1 and 20:1, respectively. In cases with pre-pre-kidney failure, if there is already renal impairment, it also reflects changes in renal parenchymal failure.
(B) with post-renal urinary tract obstruction identified 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 differential severe nephritis early often have obvious edema, high blood pressure, a large number of proteinuria with obvious microscopic or gross hematuria and various types of tubular glomerulonephritis changes For the diagnosis, it is difficult to diagnose the kidney biopsy when it is planned to be treated with immunosuppressive agents.
(D) The identification of acute renal interstitial lesions is mainly based on the cause of acute interstitial nephritis, such as drug allergy or infection history, obvious renal pain, drug-induced fever, rash, joint pain, blood eosinophils Increase, etc., this disease and ATN identification is sometimes difficult, kidney biopsy should also be done first, most acute renal interstitial nephritis need to 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.
