acute renal failure
Introduction
Introduction to acute renal failure Acute renal failure (acuterenalfailure, ARF) is referred to as acute kidney failure and is a clinically critical disease. The disease is an acute kidney damage caused by a variety of causes, which can make the nephron regulating function drastically decrease within a few hours to several days, so that the body fluid electrolyte balance and excretion of metabolites cannot be maintained, resulting in hyperkalemia and metabolic acid. Poisoning and acute uremia syndrome, this syndrome is clinically known as acute renal failure. Acute renal failure in the narrow sense refers to acute tubular necrosis. The generalized ARF can be divided into three types according to the cause: pre-renal, post-renal, and renal parenchymal acute renal failure. According to the clinical manifestations, ARF can be divided into oliguria and non-oliguric type and high decomposition type. The incidence of acute renal failure in hospitalized patients is about 5%, and the mortality rate is still as high as 50%. basic knowledge Sickness ratio: 0.05% Susceptible people: no specific population Mode of infection: non-infectious Complications: acute renal failure heart failure pericarditis hypertension headache headache coma epilepsy bloating blood in the stool stress ulcer anemia metabolic acidosis hyponatremia dehydration
Cause
Causes of acute renal failure
(1) Causes of the disease
The traditional etiology classification divides acute renal failure into pre-renal, renal and post-renal:
1. Prerenal acute renal failure Prerenal acute renal failure is also known as prerenal azotemia, which accounts for 55% to 50% of acute renal failure, producing prerenal acute renal failure. The underlying cause is the reduction in effective circulating blood volume due to various factors, resulting in a decrease in renal perfusion pressure, which prevents the glomerulus from maintaining adequate filtration rate, while the tissue integrity of the renal parenchyma is not impaired.
The most common causes of prerenal acute renal failure may be dehydration, hemorrhage, various shocks and heart failure, etc. Pre-renal azotemia due to dehydration or blood loss can be treated by simple expansion, and often Under stress, when the extracellular fluid volume expands a lot, such as in liver failure, nephrotic syndrome and heart failure, pre-renal azotemia may be caused by insufficient arterial filling, and pre-renality associated with heart failure. Acute renal failure requires attention to the amount of diuretics, the reduction of cardiac load and the injection of vasoconstrictor drugs, thereby improving renal perfusion pressure, especially when pre-renal acute renal failure associated with liver failure occurs, such as Excessive use of diuretics is very prone to acute tubular necrosis (ATN) or hepatorenal syndrome (HRS). Hepatorenal syndrome is a particularly serious condition in prerenal azotemia. And the expansion of the heart caused by the expansion can not be reversed, but this vasoconstriction can be transplanted to a liver function patient by transplanting the kidney of patients with hepatorenal syndrome With reversal, hepatorenal syndrome can also be reversed by liver transplantation, so the complexity can be imagined.
2. Renal acute renal failure: Renal acute renal failure is caused by renal parenchymal lesions, including glomeruli, tubulointerstitial and renal vascular lesions, accounting for 35% to 40% of acute renal failure. %.
According to the different causes and pathological changes, the causes of renal acute renal failure can be divided into two types: renal poisoning type and renal ischemia type:
(1) Kidney poisoning type: Common causes include heavy metals, X-ray contrast agents, antibiotics, sulfonamides, insecticides, and biotoxic drugs.
(2) Renal ischemic type: The common causes are: 1 The amount of blood circulation is reduced due to trauma, major bleeding, major surgery, burns, septic shock, and anaphylactic shock. 2 renal blood vessels, renal tissue lesions, such as glomerulonephritis, acute interstitial nephritis, epidemic hemorrhagic fever, pregnancy toxemia, renal artery embolism. 3 vasoconstrictive substances such as burns, crushed hemoglobin, myoglobin, etc. can directly cause blood vessels to contract.
(3) Clinically, these causes of renal acute renal failure can be divided into three types: secondary to systemic diseases, primary glomerular nephropathy and primary tubulointerstitial nephropathy:
1 secondary to systemic diseases: although a variety of systemic diseases will have kidney performance, but a relatively small part of them will cause acute renal failure, more commonly, acute renal failure can be secondary to systemic veins Tube inflammation, especially in patients with nodular polyarteritis, primary cryoglobulinemia, systemic lupus erythematosus and multiple myeloma, diabetes itself is not a typical cause of acute renal failure, but it It is a strong susceptibility factor for acute renal failure caused by other causes, including acute renal failure caused by contrast agents. Acute renal failure may be accompanied by hemolytic uremic or thrombotic thrombocytopenic purpura. It is suggested that the kidney with acute renal failure in pregnant patients has a poor prognosis, which may be due to renal cortical necrosis.
2 primary glomerular nephropathy: although other forms of primary glomerular disease such as membranous glomerular disease or membrane proliferative glomerulonephritis may have accelerated disease, but acute renal failure is the most common The primary glomerular disease is caused by an anti-GMB antibody that is not associated with or associated with pulmonary hemorrhage (Goodpasture syndrome).
3 primary tubulointerstitial nephropathy: in all tubulointerstitial diseases causing acute renal failure, the most important is acute tubular necrosis, acute tubular necrosis may be caused by a variety of damage, often more a potential cause.
A. crush injury: Initially considered acute tubular necrosis is secondary to crush injury, this injury usually has 10 to 14 days of oliguria, followed by 10 to 14 days of polyuria recovery, now clear The probability of non-oliguric acute tubular necrosis is about the same as that of oliguric acute tubular necrosis, and both acute tubular necrosis may have multiple different courses, but the mortality of oliguric acute tubular necrosis is 60% to 80%, but not urinary acute tubular necrosis, the mortality rate is 20%.
B. Renal ischemia: Renal ischemia is the most common cause of acute tubular necrosis. Acute tubular necrosis can actually be the result of any factor that causes prerenal azotemia, and For example, congestive heart failure rarely causes acute tubular necrosis, and most of the renal ischemia leading to acute tubular necrosis is related to long-term hypotension or surgical blockage of renal blood flow. Some drugs such as non-steroidal anti-inflammatory drugs ( NSAIA), angiotensin-converting enzyme inhibitor (ACEI) or cyclosporine may cause acute renal failure through hemodynamic effects, especially in the case of reduced renal perfusion pressure, in most cases, These drugs cause only pre-renal azotemia, but in some cases they may cause significant acute tubular necrosis.
C. Application of nephrotoxic antibiotics: Among the antibiotics with nephrotoxicity, aminoglycosides are a common and important cause of acute tubular necrosis. Typical acute tubular necrosis caused by aminoglycosides is non-oliguric, usually in medication. After 5 to 7 days, it is most common in patients who have already had chronic renal insufficiency and who have recently added aminoglycoside antibiotics, or who have other kidney damage, especially renal ischemia, with aminoglycoside antibiotics.
D. Contrast agent: Acute tubular necrosis caused by contrast agent is not uncommon, and it is more likely to affect patients with chronic renal insufficiency, especially those caused by diabetes or multiple myeloma, but with aminoglycosides. Nephrotoxicity is opposite. Its nature is usually oliguria. Although it is oliguria, the course of nephropathy caused by contrast agents is often a short-term and benign process. This nephrotoxicity is reversible in most cases. Severe renal failure, which necessitates dialysis treatment, is rare. Low osmolality contrast agents (LOM) are safer than high osmolality contrast agents, and therefore, in patients with advanced renal insufficiency, especially those with diabetes The use of LOM may be relatively appropriate in these patients. In these patients, a small reduction in glomerular filtration rate is likely to cause problems. It is not yet determined which serum creatinine level should be used.
E. Other drugs: Other drugs that may cause acute tubular necrosis include cisplatin, amphotericin and acyclovir. Drug poisoning, especially ethylene glycol or acetaminophen, may cause acute tubular necrosis.
F. Acute interstitial nephritis (AIN): is a relatively rare but very important cause of acute renal failure. Acute interstitial nephritis is first known to be caused by penicillin, but actually can be caused by many species. Drug-induced, the most important of which are shown in Table 3, typical symptoms of acute interstitial nephritis include fever, eosinophilia, rash and eosinophilic urine, more particularly, caused by non-steroidal anti-inflammatory drugs Acute interstitial nephritis has severe proteinuria, but no fever, eosinophilic urine, eosinophilia or rash. It may be possible to find eosinophils in the urine of patients with acute interstitial nephritis. Difficulties, Nolan and his colleagues confirmed that looking for eosinophils in the urine, Hansel staining is superior to the typical Wright staining. These researchers also pointed out that other causes of renal failure may also appear eosinophils in the urine. Especially in acute glomerulonephritis, although acute interstitial nephritis and acute glomerulonephritis may have macroscopic and microscopic hematuria, the appearance of red blood cell cast is strongly mentioned. Show the latter.
G. Acute pyelonephritis: Acute pyelonephritis usually does not cause acute renal failure, because most patients have unilateral onset, while the other kidney has normal function, but for those with only one isolated kidney or transplanted kidney Acute pyelonephritis is a potential cause of acute renal failure. Therefore, for kidney transplant patients, the main causes of acute renal failure include cyclosporine nephrotoxicity, transplant rejection and ischemic acute Renal failure, but acute pyelonephritis occasionally causes acute renal failure, and performance is very similar to transplant rejection.
3. Post-renal acute renal failure obstruction of urinary flow may occur in any part of the way from the kidney to the urethra, and should be a bilateral obstruction of the urinary flow, including renal pelvis, ureter, bladder, urethral obstruction, such as Bilateral ureteral stones, benign prostatic hyperplasia, bladder dysfunction, etc., will eventually lead to a decrease in glomerular filtration rate, which accounts for about 5% of acute renal failure, because normal single kidney can meet the function of removing metabolic waste. Therefore, acute renal failure is mostly caused by bilateral obstruction. Bladder neck obstruction caused by prostate (including hyperplasia, tumor) is the most common cause. Other causes are neurogenic bladder and lower urinary tract obstruction (such as blood clot). Blockage, stones and external compression, etc., when a single kidney or one of the kidneys has previously lost function in patients with post-renal acute renal failure, malignant tumor metastasis or infiltration of the ureter or renal pelvis accounted for about 60%; by ureteral stones Caused by about 30%; ureteral inflammatory stenosis is about 10%, it should be emphasized here that all patients with acute renal failure should think The possibility of obstruction, especially in patients with abnormal urine tests, is that most patients can recover completely if the obstruction is relieved.
(two) pathogenesis
The pathogenesis of acute renal failure is very complicated, and it has not yet been fully elucidated. Most of the traditional understandings remain at the cellular level, that is, renal tubular obstruction due to various renal ischemia (or poisoning) factors, renal tubule fluid leakage, kidney Changes in vascular hemodynamics and changes in glomerular permeability, but are difficult to fully explain the cause of renal dysfunction after acute poisoning. In the past 10 years, the pathogenesis of acute renal failure in cell biology and molecular level The morphological changes of acute tubular necrosis (ATN), cell biology, ischemia-reperfusion injury, apoptosis to vasoactive peptides, cytokines, adhesion molecules, etc. have been studied in depth. It plays an important role in the pathogenesis of acute renal failure.
Acute tubular necrosis is a major form of acute renal failure, and its pathogenesis is multi-link. Renal hemodynamic changes and acute tubular damage are caused by decreased glomerular filtration rate, which leads to various ARF The main factors of pathophysiological changes and clinical manifestations are now described as follows:
1. Renal hemodynamic changes: Renal hemodynamic changes play 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 re- Distribution, 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 with rapid blood volume, renal blood flow increased However, glomerular filtration rate, GFR still does not recover, indicating that in the early stage of ATN, there are intrarenal hemodynamic changes and renal blood flow distribution abnormalities, the pathophysiological basis of these renal hemodynamic abnormalities and the following Related factors.
(1) Role of renal nerve: Renal sympathetic nerve fibers are widely distributed in renal blood vessels and glomerular bodies. Adrenergic activity increases renal vasoconstriction, resulting in decreased renal blood flow and GFR, and stimulates kidney in ischemic ATN The degree of renal vasoconstriction caused by nerves far exceeds 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 renal nerve stimulation appears. Renal vasoconstriction is associated with changes in renal vascular smooth muscle calcium activity, but ischemic ATN can be up to 30% after allogeneic kidney transplantation without neurological dominance in clinically recovered renal blood supply, which does not support the occurrence of renal nerves in ATN The leading role in the.
(2) The role of renin-angiotensin in renal tissue: There is a complete renin-angiotensin system in renal tissue. In ischemic ATN, changes in renal blood circulation path are considered to be related to renin-angiotensinus in renal tissue. The activation of the prime system is related to the 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 prostaglandin PGI2 is synthesized in the renal cortex, which has a significant dilating effect on blood vessels, which can increase renal blood flow and GFR, and is beneficial to sodium and anti-diuretic hormone on the collecting tube to water. Reabsorption, a diuretic effect, has been shown to significantly reduce PGI2 in blood and kidney tissue at ATN; prostaglandin antagonist indomethacin can accelerate ischemic renal damage, in addition to renal ischemia, kidney Increased cortical synthesis of thromboxane also promotes renal vasoconstriction, but there is currently no evidence that prostaglandins play a leading role in ATN.
(4) Role of endothelial cell-derived contractile and relaxing factor in ATN: increased pathological secretion of vascular endothelial-derived contractile factor and vascular endothelial-derived relaxing factor such as nitric oxide (NO) release disorder on ATN hemodynamic changes Important role, ATN early renal blood flow reduction, renal ischemia, hypoxia, vascular endothelial cells release more endothelin (experimental found that low concentration of endothelin can make the renal blood vessels strong and sustained contraction, renal small blood vessel resistance increased, leading to GFR declines or stops, glomerular capillaries and mesangial cells, high-dense endothelin receptors in the small blood vessels, and continuous intravascular injection of endothelin can also cause significant contraction of renal blood vessels), which causes renal entry The ball and the small arterioles have increased contraction resistance, and the resistance of the small arteries increases more obviously. Therefore, the renal blood flow and GFR decrease in parallel, but sometimes the patient's serum endothelin concentration increases by more than 10 times, and ATN does not occur clinically. The normal vascular endothelium can release the relaxing factor, synergistically regulate blood flow to maintain blood circulation, increase blood flow to the kidney, and reduce the resistance of the ball into the ball and the small artery. ATN Release of vascular relaxing factor that is impaired, increased oxygen free radicals after reperfusion also affect the release of relaxing factor, endothelial cell contraction and relaxation factors regulate imbalances are likely to occur and the development of certain types of ATN play an important role.
(5) Renal medullary congestion: In the ischemic ATN model, the renal medulla and the intracortical region were most damaged, and the degree of renal medullary congestion was significantly correlated with the degree of ATN damage. The medullary congestion and oxygen deficiency first affected The blood supply of the tubular segment of the ascending branch is a high energy-consuming area, which is sensitive to hypoxia. The hypoxic tubular cells have a reduced ability to actively reabsorb sodium chloride, and the ascending branch is damaged. It is easy to deposit TH glycoprotein in the thick segment, causing obstruction of the distal small lumen and leakage of luminal fluid. Therefore, it is considered that medullary congestion is also an important factor in ischemic ATN.
2. Mechanism of renal ischemia-reperfusion injury: The renal tissue recovers blood supply after acute ischemia and hypoxia. For example, after shock correction, blood transfusion after hemorrhage, after cardiopulmonary bypass or recovery of cardiac resuscitation, after recovery of renal blood circulation, A large number of oxygen free radicals, energy decomposation is more than synthesis in the absence of oxygen, and the adenosine triphosphate decomposed product aggregates under the action of xanthine oxidase, which produces a large amount of xanthine, which in turn increases the production of oxygen free radicals. a substance, such as a polyunsaturated fatty acid, which has a high affinity with free radicals to produce a variety of lipid peroxides, which can distort the ratio of polyunsaturated fatty acids to proteins on the cell membrane, resulting in cell membrane fluid flow. Sexual and permeability changes, resulting in dysfunction, decreased activity of various enzymes, increased capillary permeability, increased exudation leading to cell and interstitial edema, etc. Free radicals and other damaged cell membranes make a large number of extracellular calcium ions Entering the cells, the intracellular calcium ions increase, the cells die, in addition, the renal mitochondrial function is significantly reduced during renal ischemia, and the adenosine triphosphate Reduced, the ion transport function on the cell membrane dependent on the adenosine triphosphate energy is reduced, intracellular calcium ion accumulation, the latter stimulates the increase of calcium ion uptake by mitochondria, and the calcium content in the mitochondria is too high, leading to cell death, using calcium ions Antagonists can prevent the increase of intracellular calcium concentration, thereby preventing the occurrence of ATN.
3. Acute tubular damage theory: severe crush injury and acute toxic poisoning, such as mercury chloride, arsenic and other causes of ATN pathological changes in renal tubular cell shedding, acute damage such as necrosis and renal interstitial edema as the main changes, and Glomerular and renal vascular changes are relatively mild or absent, indicating that the main pathogenesis of ATN is due to primary lesions of the renal tubules caused by GFR decreased or stopped, Thurau et al believe that acute tubular damage can cause tubule-small ball feedback mechanism, near 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) 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, etc. block the renal tubules, resulting in an increase in the proximal tubule pressure in 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 glomerulus In the capillary internal pressure, sputum caused glomerular filtration to stop, the experiment proved that renal ischemic or nephrotoxicity caused sublethal renal tubular injury, mainly in the proximal tubule brush margin shedding, cell swelling and vacuolar degeneration, etc. Renal tubular epithelial cells (TEC) detached from the basement membrane, causing a defect in the basement membrane of the renal tubule, but most of the detached TECs were intact and viable, and the number of TEC in the urine was also significantly increased, and there was a considerable amount. The TEC did not die. Studies have shown that TEC is detached from the basement membrane due to changes in renal cell adhesion. It is known that integrin has the greatest influence on ATN in the family of renal tubular epithelial adhesion molecules. Avidin can mediate cell-cell and cell adhesion to the matrix and maintain the integrity of the tubular structure, changes in TEC damage of cell adhesion in:
1 changes in the cytoskeleton: especially actin microfilament components play 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 Matrix protein changes: 30-40 min after the experimental animal clamped the renal pedicle, semi-quantitative analysis of immunofluorescence showed a one-degree decrease in laminin, and laminin at the junction of cortex and cortex at 3 to 4 days after ischemic injury. Increased, 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 significant changes in matrix components in early ischemic injury. These changes will affect the adhesion of the TEC.
(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, causing reflux of primary urine in the small lumen to the kidney Interstitial, causing renal interstitial edema, oppressing the nephron, aggravating renal ischemia, and reducing GFR, but experimental observation only in the case of severe tubular necrosis, the renal tubule stock solution has a leakage phenomenon, renal blood flow and GFR decreased It can be leaked before the renal tubule fluid, 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 the development of the disease.
(3) tube-ball feedback mechanism: ischemia, nephrotoxicity and other factors cause acute tubular damage, resulting in the re-absorption of sodium and chlorine in the renal tubules, the concentration of sodium and chlorine in the lumen increases, and the distal tubules The dense plaque induces the increase of renin secretion in 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. In the kidney, the release of prostacyclin into the cortex is reduced, and the 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, etc. cause ATN, often diffuse microvascular damage, platelet and fibrin deposition in injury Renal 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 When prostacyclin is reduced, 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 progress in the course of ATN. It can cause or aggravate bilateral renal cortical necrosis, and DIC is rare in uncomplicated ATN, so DIC can not be used as a general pathogenesis of ATN.
The site of ATN histopathological damage, nature and extent vary with the etiology and severity of the disease. The main pathological changes of the kidney are kidney enlargement, paleness and weight increase; the cut cortex is pale, the medulla is dark red, and the light is examined by kidney. Tubuloblastic cell degeneration, shedding and necrosis changes, the lumen is filled with detached tubular epithelial cells, casts and exudates, nephrotoxic substances, renal tubular lesions are mainly distributed in proximal convoluted tubules, such as mercury, gentamicin The nephrotoxicity is located in the proximal part of the proximal convoluted tubule, while in the middle and posterior segments, the arsenide causes the entire proximal convoluted tubule, the degeneration of the epithelial cells, the necrosis and the cell itself, evenly distributed, the renal tubule The surface of the basement membrane is intact or defective, renal interstitial edema, etc., and there is obvious inflammatory cell infiltration in time. Generally, about 1 week, the necrotic tubular epithelial cells begin to regenerate and quickly re-cover on the basement membrane, kidney. The shape of the tubules gradually returned to normal.
In patients with renal ischemia, the peripheral part of the interlobular artery is the earliest and severely affected. Therefore, the cortical tubules, especially the tubules and the distal tubules, are most obvious. The focal necrosis of the epithelial cells is aggravated with the degree of ischemia. The development of lesions affects various segments of the renal tubules and collecting ducts, so the lesions are distributed unevenly, often in a segmental distribution, from the proximal convoluted tubules to the collecting ducts, there may be scattered distribution, tubular epithelial cell necrosis, shedding and steatosis, The basement membrane of the damaged tube can also be broken and collapsed, so that the contents of the lumen enter the stroma, causing interstitial edema, hyperemia and inflammatory cell infiltration. In addition, cortical vasoconstriction and medullary vasodilation are seen. Congestion, if the lesion involves adjacent venules, can cause thrombosis or interstitial hemorrhage, hematuria, severe damage to the basement membrane of renal tubular epithelial cells, cells often can not be regenerated, this part is replaced by connective tissue hyperplasia, so ischemic damage Long recovery time, electron microscopy can detect microvilli rupture and shedding of renal tubular epithelial cells, mitochondrial swelling of TEC, mitochondrial mitigation Mitochondrial membrane rupture, primary and secondary lysosomes increased, phagocytic vacuoles also showed an increase, TEC severely damaged mitochondria, Golgi and other organelles disintegration, dissolution, and even complete necrosis, thrombotic microvascular disease ATN, Renal microvessels are deposited with transparent substances such as platelets and fibrin, which block the microvascular lumen. The damaged blood vessel wall often has focal necrosis and inflammation. The glomerulus may have mild mesangial cell proliferation, ischemic changes, and even kidney. Small ball hardening, glomerular and tubular necrosis of the bilateral renal cortex in both cases.
Prevention
Acute renal failure prevention
The prevention of acute renal failure is mainly to actively prevent and treat the primary disease. Avoiding and eliminating the predisposing factors is the basis of prevention. Therefore, pay attention to the following three points:
First, nursed the five internal organs: normal living, diet, health, and avoid foreign invasion, especially in the seasons and areas where infectious diseases are prevalent, preventive measures should be strengthened. However, the food is spicy and savory, so as to avoid the growth of damp heat, to adjust the emotions, to maintain a happy spirit, to make the blood flow smooth and avoid qi stagnation and blood stasis, strengthen physical exercise and improve the body's defense ability.
Second, to prevent poisoning: the relevant information shows that 20% - 50% of acute renal failure is caused by drugs, and some are caused by exposure to harmful substances, therefore, should try to avoid the use of drugs and poisons that are toxic to the kidneys In case of accidental taking or contact, it should be discovered and treated early.
Third, prevention and timely: once the primary disease of acute renal failure occurs, should be treated early, pay attention to expand blood volume, correct water, electrolyte imbalance and acid-base imbalance, restore circulation function, if the disease is about to occur, should be early Take measures to supplement blood volume, increase cardiac output, restore renal perfusion flow and glomerular filtration rate, exclude renal tubular obstruction, prevent infection, prevent DIC, renal parenchymal damage caused by renal ischemia, and as soon as possible The application of blood circulation and phlegm drugs has a positive effect on preventing the occurrence of this disease.
Complication
Acute renal failure complications Complications acute renal failure heart failure pericarditis hypertension headache coma epilepsy abdominal distension blood stasis ulcer anemia metabolic acidosis hyponatremia dehydration
Acute renal failure mostly passes through three stages of oliguria (or anuria), polyuria and recovery. The complications that may occur during oliguria of acute renal failure are:
First, infection is one of the most common and serious complications, and it is more common in severely decomposed acute renal failure caused by severe trauma and burns;
Second, cardiovascular system complications, including heart rhythm disorders, heart failure, pericarditis, high blood pressure, etc.;
Third, the nervous system complications include headache, lethargy, muscle twitching, coma, epilepsy, etc., neurological complications and toxins in the body retention and water poisoning, electrolyte imbalance and acid-base balance disorders;
Fourth, digestive system complications manifested as anorexia, nausea, vomiting, abdominal distension, hematemesis or blood in the stool, etc., bleeding is mostly caused by gastrointestinal mucosal erosion or stress ulcer;
V. Complications of the blood system Due to the sharp decline of renal function, erythropoietin can be reduced, causing anemia, but most of them are not serious. In a few cases, there may be bleeding tendency due to the decrease of coagulation factors;
Sixth, electrolyte imbalance, metabolic acidosis, hyperkalemia, hyponatremia and severe acidosis, is one of the most dangerous complications of acute renal failure.
In the polyuria period, the daily urine volume of the patient can reach 3000-5000ml. Dehydration, hypokalemia, hyponatremia, etc. may occur due to the discharge of a large amount of water and electrolytes. If not replenished in time, the patient may die from severe dehydration. And electrolyte imbalance.
Entering the recovery period of serum urea nitrogen, creatinine level returned to normal, uremia symptoms subsided, renal tubular epithelial cells were regenerated and repaired, most patients with renal function can be fully restored, a small number of patients may leave varying degrees of renal dysfunction.
Symptom
Symptoms of acute renal failure Common symptoms Male abdominal pain, neonatal proteinuria, localized necrosis, head, dizziness, chest tightness, four limbs, numbness, nausea, apathy, anaerobic shock
Acute renal failure has two stages of renal tubular necrosis and repair in pathology. The most characteristic feature of ATN is that renal function can return to normal. This process includes the recovery of damaged cells, the removal of lumens of necrotic cells, cell regeneration, and finally The integrity of renal tubular epithelial cells is completely restored. According to the common law of clinical manifestations and disease course, acute renal failure is generally divided into three stages: oliguria, polyuria and recovery:
1. oliguria or anuria: The clinical manifestations of oliguria are mainly nausea, vomiting, headache, dizziness, irritability, fatigue, lethargy and coma. Due to the accumulation of water and sodium in the oliguria period, patients may develop hypertension. Pulmonary edema and heart failure, when protein metabolites can not be excreted by the kidneys, causing nitrogeny substances to accumulate in the body when azotemia occurs, such as accompanied by infection, injury, fever, protein catabolism is accelerated, blood urea nitrogen The creatinine rises rapidly, that is, uremia is formed. The main features of this period are:
(1) Decrease in urine output: sudden decrease or decrease in urine volume. Daily urine output is less than 400ml, which is called oliguria. Less than 50ml is called anuria. ATN patients are rarely completely urinary. Poor, and should exclude extrarenal obstruction and bilateral renal cortical necrosis, due to the cause of the disease and the severity of the disease, oliguria duration is inconsistent, usually 1 to 3 weeks, but a few cases of oliguria can last more than 3 months, It is generally believed that patients with nephrotoxicity have a short duration, while those with ischemic duration have a longer duration. If oliguria lasts for more than 12 weeks, the diagnosis of ATN should be reconsidered. There may be renal cortical necrosis or renal papillary necrosis, etc. Should pay attention to fluid retention, congestive heart failure, hyperkalemia, hypertension and various complications.
Non-oliguric ATN refers to the daily urine volume of patients in the progressive azotemia period of more than 500ml, or even 1000 ~ 2000ml, the incidence of non-oliguric type has increased in recent years, up to 30% to 60%, The reason is related to the improvement of people's understanding of this type, the widespread application of nephrotoxic antibiotics and the early application of diuretics such as furosemide, mannitol, etc. There are three reasons for the lack of urine volume:
1 The degree of damage of each nephron is different. The renal blood flow and glomerular filtration function of a small part of the nephron are present, and the corresponding renal tubular reabsorption function is significantly impaired.
2 The degree of damage to all nephrons is the same, but the degree of renal tubular reabsorption dysfunction is much lower than that of glomerular filtration function.
3 The ability of the deep medulla to form a hyperosmotic state is reduced, resulting in a decrease in water reabsorption in the myelin filtrate. The common disease of non-oliguric type is due to the long-term application of nephrotoxic drugs, major abdominal surgery and open heart surgery, etc. It is believed that although the non-oliguric type is less urinary, the hospital stay is short, the percentage of dialysis treatment is low, and the complications of upper gastrointestinal bleeding are few, but the incidence of hyperkalemia is similar to that caused by oliguria. The morbidity of the urinary type can still be as high as 26%, so it is still impossible to ignore any link in the treatment.
(2) progressive azotemia: oliguria or anuria caused by decreased glomerular filtration rate, resulting in decreased nitrogen excretion and other metabolic waste, elevated plasma creatinine and urea nitrogen, increased rate and protein in vivo According to the state of decomposition, in the case of no complications and correct treatment, the daily blood urea nitrogen rise rate is slow, about 3.6mmol / L (10mg / dl), plasma creatinine concentration is only 44.2 ~ 88.4mol / L (0.5 ~ 1.0mg/dl), but in high decomposition state, such as with extensive tissue trauma, sepsis, etc., daily urea nitrogen can be increased by 7.1mmol / L (20mg / dl) or more, plasma creatinine increased by 176.8mol / L per day ( 2mg/dl) or above, factors that promote hyperplasia of the protein include insufficient calorie supply, muscle necrosis, hematoma, gastrointestinal bleeding, infection and fever, and application of adrenal cortex hormones.
(3) Water, electrolyte imbalance and acid-base balance disorders:
1 too much water: seen in the water control is not strict, intake or rehydration is too much, the amount of water such as vomiting, sweating, wound penetration and other estimates are not accurate and the liquid amount is neglected to calculate endogenous water, with oliguria Prolonged, prone to excessive water, manifested as dilute hyponatremia, soft tissue edema, weight gain, high blood pressure, acute heart failure and cerebral edema.
2 hyperkalemia: 90% of normal people's intake of potassium salt is excreted from the kidneys, ATN oliguria due to reduced potassium excretion, if there is a high decomposition state in the body, such as muscle necrosis, hematoma and infection during crush injury, Insufficient calorie intake causes protein breakdown in the body, releasing potassium ions. When acidosis occurs, intracellular potassium is transferred to the outside of the cell, sometimes severe hyperkalemia can occur within a few hours. If the patient fails to be diagnosed in time, the intake contains Potassium-rich foods or beverages, intravenous infusion of large doses of penicillin potassium salt (1.6 mmol per 1 million U of penicillin potassium salt); large amount of blood in the case of large bleeding (stock 10 days of blood per liter of potassium up to 22mmol) ); can also cause or aggravate hyperkalemia, generally in the uncomplicated medical cause ATN daily blood potassium rise less than 0.5mmol / L, hyperkalemia can be no characteristic clinical manifestations, or nausea, vomiting, limb numbness Such as abnormalities, heart rate slowed down, severe neurological symptoms such as fear, irritability, apathy, until late sinus or atrioventricular block, sinus rest, indoor conduction block and even ventricular fibrillation, hyperkalemia Cardiac electrocardiogram The change of graph can be preceded by the clinical manifestation of high potassium. Therefore, the effect of electrocardiogram monitoring of hyperkalemia on myocardial is very important. When the potassium concentration is 6mmol/L, the electrocardiogram shows a tall T-wave with a narrow base and an increase in blood potassium. P wave disappeared, QRS widened, ST segment could not be identified, and finally merged with T wave, followed by severe arrhythmia until ventricular fibrillation. The effect of high potassium on myocardial toxicity was still in the receptor sodium, calcium concentration and acid-base balance. When there is low sodium, hypocalcemia or acidosis at the same time, the hyperkalemia electrocardiogram is more significant, and it is easy to induce various arrhythmias. It is worth mentioning that there may be inconsistencies between serum potassium concentration and ECG performance. Phenomenon, hyperkalemia is one of the common causes of death in patients with oliguria. Early dialysis can prevent it from occurring, but severe hyperkalemia often occurs in severe muscle tissue necrosis. Necrotic tissue should be completely removed in order to control hyperkalemia. disease.
3 Metabolic acidosis: Normally, the fixed acid metabolites per day are 50-100mmol, 20% of which are combined with bicarbonate ions, 80% are excreted by the kidneys, and when renal failure occurs, the renal tubules are secreted due to the decrease of acid metabolites. The ability and ability to preserve sodium bicarbonate decreased, resulting in a different degree of plasma bicarbonate concentration per day; more rapid and faster in the high decomposition state, most of the endogenous fixed acid from protein decomposition, a small part from sugar and fat Oxidation, phosphate and other organic anions are released and accumulated in the body fluid, resulting in an increase in anion gap in patients with this disease. If the metabolic dysfunction is not fully corrected in the case of oliguria, the muscle breakdown in the body is faster. In addition, acidosis is acceptable. Reduce the threshold of ventricular fibrillation, ectopic heart rhythm, hyperkalemia, severe acidosis and low calcium, hyponatremia is a serious condition of acute renal failure, although the cases that have been treated with dialysis have been rare, but some cases Drugs are still needed to correct metabolic acidosis during the dialysis period.
4 hypocalcemia, hyperphosphatemia: low calcium and hyperphosphatemia in ATN is not as prominent as chronic renal failure, but it has been reported that hypocalcemia can occur 2 days after oliguria, often accompanied by acid Poisoning, so that the extracellular calcium ion is increased, so there is no common clinical manifestation of low calcium. Hypocalcemia is caused by hyperphosphatemia. 60% to 80% of the phosphate ingested by normal people is excreted in the urine. ATN oliguria often has mild elevated blood phosphorus, but if there is significant metabolic acidosis, hyperphosphatemia is more prominent, but it is rarely elevated. After acidosis is corrected, blood phosphorus may decrease to some extent. If you continue to receive total intravenous nutrition, you should pay attention to hypophosphatemia.
5 hyponatremia and hypochloremia: both at the same time, hyponatremia may be due to excessive water caused by dilute hyponatremia, due to burns or vomiting, diarrhea, etc. lost from the skin or gastrointestinal tract Loss of hyponatremia caused by non-oliguric patients who are still responsive to high-dose furosemide. Severe hyponatremia can cause a decrease in blood osmotic concentration, resulting in permeation of water into cells and cell edema. Symptoms of acute cerebral edema, clinical manifestations of fatigue, weakness, lethargy or disturbance of consciousness, loss of orientation, and even hypotonic coma, hypochloremia is common in vomiting, diarrhea or non-oliguric use of large amounts of loop diuretics, bloating Or respiratory superficial, convulsions and other metabolic alkalosis.
6 hypermagnesemia: 60% of magnesium in normal people is excreted by feces, 40% is excreted from the urine. Since both magnesium and potassium ions are the main cations in the cell, the blood potassium and blood magnesium concentrations often rise in parallel at ATN. Hypermagnesemia is more prominent in muscle injury, magnesium ion has an inhibitory effect on the central nervous system, severe hypermagnesemia can cause respiratory depression and myocardial inhibition, should be alert, electrocardiogram changes of hypermagnesemia can also show PR Interval lengthening and QRS wave broadening. When hyperkalemia is corrected, the ECG is still prolonged in the PR interval and/or the QRS is broadened. The possibility of hypermagnesemia should be suspected. Hyponatremia, hyperkalemia Both acidosis and acidosis increase the toxicity of magnesium ions to the myocardium.
(4) Cardiovascular system performance:
1 Hypertension: In addition to renal ischemia, the role of neurohumoral factors promotes the secretion of active substances in contractile blood vessels. In addition, too much water can cause excessive load overload, which can aggravate hypertension. Early ATN is rare, but if it continues to be less In urine, about 1/3 of patients develop mild to moderate hypertension, usually at 18.62 to 23.94/11.97 to 14.63 kPa (140 to 180/90 to 110 mmHg), sometimes higher, or even hypertensive encephalopathy, accompanied by pregnancy. In particular, it should be closely observed.
2 acute pulmonary edema and heart failure: is the common cause of death in oliguria, it is mainly caused by fluid retention, but high blood pressure, severe infection, arrhythmia and acidosis are all influencing factors, the incidence rate in early years is high, take corrective The incidence of oxygen, controlled moisture, and early dialysis measures has decreased significantly, but it is still a common cause of death in severe ATN.
3 arrhythmia: in addition to hyperkalemia caused by sinus node suspension, sinus rest, sinus block, varying degrees of atrioventricular block and bundle branch block, ventricular tachycardia, ventricular fibrillation, still acceptable Heterotopic rhythm such as ventricular premature contraction and paroxysmal atrial fibrillation caused by viral infection and application of digitalis.
4 pericarditis: the annual incidence rate of 18%, after the early dialysis to 1%, mostly manifested as pericardial friction and chest pain, a rare large amount of pericardial effusion.
5 digestive system performance: is the earliest manifestation of ATN, common symptoms are loss of appetite, nausea, vomiting, bloating, hiccups or diarrhea, upper gastrointestinal bleeding is a common late complication, gastrointestinal symptoms are still associated with primary disease and water , electrolyte imbalance or acidosis and other related, persistent, severe gastrointestinal symptoms are often prone to obvious electrolyte imbalance, increase the complexity of treatment, early appearance of obvious gastrointestinal symptoms suggest early dialysis treatment.
6 patients with mild manifestations of the nervous system may have no neurological symptoms: some patients have early fatigue and poor spirit. If early consciousness is indifferent, lethargy or irritability or even coma, suggesting that the condition is heavy, it is not appropriate to delay dialysis time, nervous system performance and serious Infection, epidemic hemorrhagic fever, some heavy heavy metal poisoning, severe trauma, multiple organ failure and other causes.
7 blood system performance: ATN early rare anemia, the degree is closely related to the original cause, the length of the disease, the presence or absence of bleeding complications, severe trauma, blood loss after major surgery, hemolytic anemia, severe infection and emergency ATN, etc. Anemia can be more serious. If there is clinical bleeding tendency, thrombocytopenia, consumptive hypocoagulopathy and fibrinolytic signs, it is not early DIC.
2. Multi-urinary period: Daily urine volume is 2.5L, which means polyuria. In the early stage of ATN diuresis, the amount of urine gradually increases. If the amount of urine increases within 24 hours after oliguria or no urine, and it exceeds 400ml, it can be considered as polyuria. At the beginning, the polyuria lasts for about 2 weeks, and the daily urine volume can be multiplied. The diuretic period can reach 1000ml on the 3rd to 5th day, and then the daily urine volume can reach 3~5L. The progressive urine output is the beginning of renal function.GFR10ml/min;
3.ATN;361
Examine
Laboratory inspection
1.()()
(1)400ml
(2);(+)(++)(+++)(++++)
(3)1.015
(4)350mOsm/kg1.1
(5)4060mmol/L
(6)10
(7)10
(8)(RFI)2
(9)(Fe-Na)(/)×100
UNaPNaVUCrPcrGFRATN>1<1
(5)(9)ATN
2.
(1);()
(2)(Scr)(BUN)BUNScr>20ATNScr40.288.4mol/L(0.51.0mg/dl)353.6884mol/L(410mg/dl);BUN3.610.7mmol/L(1030mg/dl)21.435.7mmol/L(60100mg/dl);Scr176.8mol/L(2mg/dl)BUN7mmol/L;ScrBUN
(3)pH8.0kPa(60mmHg)(ARDS)
(4)
(5)
(6)DIC(FDP)
ATNDICFDP
(7)3
Miller(1978)(FENa)(RFI)<1ARFATNFENaRFI(>2)>500ml/dFENaRFI>2ATN
(FENa)(RFI)Anderson19841
Film degree exam
1.Ga
2.ARFARFB
3.CTMRICT(MRI)
4.ARF50%
Diagnosis
diagnosis
ARFARF
1.
(1)
(2)(<250ml/m2)(<50ml/m2)
(3)
(4)(Scr)>176mol/LBUN>15mmol/LScr>4488µmol/L BUN>3.577.5mmol/L()Ccr<30ml/(min·1.73m2)3.610.7mol/L88.4176.8mol/L
(5)B
(6)ARF
()()
(>2500ml/m2)
2.AFPAFP
(1)(ARF)(CRF)
1/2()
ARFARF
BARFCRFARF;CRF
3
(2)ARFARF3ARF
ARFA.B./C.D.1h5%1000ml2h40ml/hARF
ARF;
ARFA.B.C.
ARFARF
ARFARF4
A.ARF
B.ARF
C.ARFARF
D.ARF
Differential diagnosis
1.ARF
2.
3.
4.;ARF
5.
6.ARF130mmHg
(1)ARFB
(2)
7.ARF70%ARF30%IgE
8.ARF
(1)ARF
(2)ARF
(3)
(4)
(5)ARF
9.ARF
