What Is Prerenal Azotemia?

The traditional etiology classification divides acute renal failure into three categories: prerenal, parenchymal, and retrorenal:

Prerenal acute renal failure

Right!

Acute renal failure (ARF), referred to as acute renal failure, refers to the rapid decrease in glomerular filtration function within hours to weeks. According to clinical manifestations, ARF can be divided into oliguria type, non-oliguria type, and high resolution type. The incidence of acute renal failure in hospitalized patients is about 5%, and the mortality rate is still about 50%.

Western Medicine Name

The traditional etiology classification divides acute renal failure into three categories: prerenal, parenchymal, and retrorenal:

Prerenal Acute Renal Failure : Prerenal acute renal failure is also known as prerenal azotemia. Incidence accounts for 55% to 50% of acute renal failure. The root cause of prerenal acute renal failure is the decrease in effective circulating blood volume caused by various factors, which leads to a decrease in renal perfusion pressure, which prevents the glomeruli from maintaining a sufficient filtration rate, while the renal parenchymal tissue integrity is No damage.

Common causes of prerenal acute renal failure, the most common of which may be dehydration, bleeding, various shocks and heart failure. Prerenal azotemia due to dehydration or blood loss can be treated by simple expansion, and often under stress, when the extracellular fluid volume expands significantly, such as in liver failure, nephrotic syndrome, and heart failure, Prerenal azotemia may be caused by insufficient arterial filling. Prerenal acute renal failure related to heart failure requires attention to the amount of diuretics, reduction of heart load, and injection of vasoconstriction drugs to improve renal perfusion pressure. Prerenal acute renal failure associated with liver failure is particularly difficult to treat. If diuretics are used too aggressively, acute tubular necrosis (ATN) or hepatorenal syndrome (HRS) can easily occur. Hepatorenal syndrome is a particularly serious condition in prerenal azotemia. At this time, vasoconstriction of the kidney and heart filling caused by expansion cannot be reversed, but this vasoconstriction can be achieved by transplanting the kidney of a patient with hepatorenal syndrome It can be reversed in a patient with good liver function. Hepatorenal syndrome can also be reversed through liver transplantation, so its complexity can be imagined.

Acute renal failure : Renal acute renal failure is caused by renal parenchymal lesions, including glomeruli, tubulointerstitial, and renal vascular lesions. The incidence of acute renal failure accounts for 35% to 40% of acute renal failure.

According to the etiology and pathological changes, the causes of renal acute renal failure can be divided into two types: nephrotoxic and renal ischemic:

Renal poisoning : common causes: Exogenous toxins include heavy metals, X-ray contrast agents, antibiotics, sulfa drugs, insecticides, biological poisons, etc. Endogenous toxins include myoglobin and hemoglobin.

Renal ischemia type : Common causes are: blood circulation is reduced due to trauma, major bleeding, major surgery, burns, septic shock, and anaphylactic shock; renal blood vessels and renal tissue diseases such as glomerulonephritis, acute interstitial Nephritis, epidemic hemorrhagic fever, toxemia of pregnancy, renal artery embolism, etc.

These causes of renal acute renal failure can also be clinically divided into three categories secondary to systemic disease, primary glomerulonephropathy and primary tubular interstitial nephropathy:

Secondary to systemic diseases : Although a variety of systemic diseases can manifest in the kidneys, a relatively small proportion of them can cause acute renal failure. More commonly, acute renal failure can be secondary to systemic vasculitis, especially in patients with nodular polyarteritis, primary cryoglobulinemia, systemic lupus erythematosus, and multiple myeloma. in. Diabetes itself is not a typical cause of acute renal failure, but it is a powerful susceptible factor for other causes of acute renal failure, including acute renal failure caused by contrast agents. Acute renal failure may be accompanied by hemolytic uremia or thrombotic thrombocytopenic purpura. In particular, the prognosis of renal recovery from acute renal failure in pregnant patients is poor, which may be because it can cause necrosis of the renal cortex.

Primary glomerulonephropathy : Although other forms of primary glomerular disease such as membranous glomerulopathy or membranoproliferative glomerulonephritis may have an accelerated course, acute renal failure is the most common Primary glomerular disease is caused by an anti-glomerular basement membrane (anti-GMB) antibody, which may be accompanied by or without pulmonary hemorrhage (Goodpasture syndrome).

Primary tubular interstitial nephropathy : Of all the tubular interstitial diseases that cause acute renal failure, the most important is acute tubular necrosis. Acute tubular necrosis can be caused by a variety of damage. There are often multiple underlying causes.

Crush injury : Acute tubular necrosis was originally thought to be secondary to crush injury. This injury usually has a period of oliguria of 10 to 14 days, followed by a period of polyuria recovery of 10 to 14 days. It is now clear that the probability of acute tubular necrosis of non-oliguria type is about the same as that of acute tubular necrosis of oliguria type, and both types of acute tubular necrosis may have different courses. However, the mortality of oliguria-type acute tubular necrosis with multiple organ failure is 60% to 80%, and the mortality of non-oliguria-type acute tubular necrosis is 20%.

Renal ischemia : Renal ischemia is the most common susceptible cause of acute tubular necrosis. Acute tubular necrosis can be the result of virtually any factor that causes prerenal azotemia, and congestive heart failure rarely causes acute tubular necrosis directly. Renal ischemia leading to acute tubular necrosis is mostly related to prolonged hypotension or surgical block of renal blood flow. Some drugs such as non-steroidal anti-inflammatory drugs (NSAIA), angiotensin-converting enzyme inhibitors (ACEI) or cyclosporine may cause acute renal failure through hemodynamic effects, especially in renal perfusion pressure Reduced case. In most cases, these drugs only cause prerenal azotemia, but in some cases they may cause significant acute tubular necrosis.

Application of nephrotoxic antibiotics : Among nephrotoxic antibiotics, aminoglycosides are a common and important cause of acute tubular necrosis. The typical acute tubular necrosis caused by aminoglycosides is non-oliguria. It usually appears 5 to 7 days after medication. It is most common in patients who have potential chronic renal insufficiency and recently received aminoglycoside antibiotics. Renal damage, especially in patients with renal ischemia, when aminoglycoside antibiotics are added.

Contrast : Acute tubular necrosis caused by contrast is also not uncommon, and tends to affect patients with chronic renal insufficiency, especially caused by diabetes or multiple myeloma, but nephrotoxicity with aminoglycoside Instead, it is usually oliguria in nature. Although the oliguria type, the course of nephropathy caused by contrast agents is often a short-term and benign process. This nephrotoxicity is reversible in most cases, and severe renal failure that requires dialysis treatment is rare. Low osmotic contrast agents (LOM) are safer than high osmotic contrast agents. Therefore, the use of LOM in patients with advanced renal insufficiency, especially with diabetes, may be relatively appropriate. In these patients, a small reduction in glomerular filtration rate is likely to cause problems. It has not yet been determined which serum creatinine levels should be used for LOM.

Other drugs : Other drugs that can cause acute tubular necrosis include cisplatin, amphotericin, and acyclovir. Drug poisoning, especially ethylene glycol or acetaminophen, can cause acute tubular necrosis.

Acute interstitial nephritis (AIN): It is a relatively rare but very important cause of acute renal failure. Acute interstitial nephritis was first known to be caused by penicillin, but it can actually be caused by many drugs. Typical symptoms of acute interstitial nephritis include fever, eosinophilia, rash, and eosinophilic urine. More specifically, acute interstitial nephritis caused by non-steroidal anti-inflammatory drugs has severe proteinuria, but no fever, eosinophilia, eosinophilia, or rash. Finding eosinophils in the urine of patients with acute interstitial nephritis can be difficult. Nolan and his colleagues confirmed that Hansel staining is superior to typical Wright staining when looking for eosinophils in urine. These researchers also point out that renal failure caused by other causes may also show eosinophils in the urine, especially acute glomerulonephritis. Although acute interstitial nephritis and acute glomerulonephritis may have gross and microscopic hematuria, the appearance of red blood cell casts strongly suggests the latter.

Acute pyelonephritis : Acute pyelonephritis usually does not cause acute renal failure. This is because most patients develop unilateral disease while the other side has normal kidney function.

Postrenal acute renal failure : Obstruction of the urinary flow may occur anywhere from the kidney to the urethra, and it should be a sudden block of bilateral urinary flow, which includes obstruction of the renal pelvis, ureter, bladder, and urethra, such as double Lateral ureteral stones, benign prostatic hyperplasia, and bladder dysfunction will eventually lead to a reduction in glomerular filtration rate, which accounts for about 5% of acute renal failure. Because a normal single kidney can meet the function of removing metabolic waste, acute renal failure is mostly caused by bilateral obstruction. Bladder and neck obstruction caused by prostate (including hyperplasia, tumor) is the most common cause. Other causes are neurogenic bladder, lower urinary tract obstruction (such as clot clogging, stones and external compression, etc.). Malignant tumor metastasis compresses or infiltrates the ureter or renal pelvis when a single kidney or one of the kidneys has previously lost function. About 30% are caused by ureteral stones; inflammatory stenosis at the end of the ureter is about 10%. It should be emphasized here that the possibility of obstruction should be thought of for all patients with acute renal failure, especially those who have no abnormal findings in routine urine tests, because most patients can recover completely once the obstruction is removed. ^[1]

The pathogenesis of acute renal failure is very complex and has not yet been fully elucidated. Traditional understanding mostly stays at the cellular level, that is, renal tubular obstruction, renal tubular fluid leakage, renal vascular hemodynamic changes, and glomerular permeability changes due to various renal ischemia (or poisoning) factors. However, it is difficult to satisfactorily explain the cause of sudden renal failure after acute poisoning. In the past 10 years, the pathogenesis of acute renal failure has been morphologically altered in acute tubular necrosis (ATN) at the cellular and molecular levels, cell biology, ischemia-reperfusion injury, apoptosis to vasoactive peptides Intensive research has been carried out on cytokines, cytokines, and adhesion molecules. At present, many factors are considered to play an important role in the pathogenesis of acute renal failure.

Acute tubular necrosis is a major form of acute renal failure. Its pathogenesis is multi-stage. The decrease in glomerular filtration rate caused by changes in renal hemodynamics and acute tubular damage has led to various types of ARF. The main factors of pathophysiological changes and clinical manifestations. The main points of various doctrines are as follows:

1. Renal hemodynamic changes Renal hemodynamic changes play a leading role in early ATN and are often the initiating factor. In hemorrhagic shock or severe hypovolemia, due to the regulation of nerves and body fluids, blood is redistributed throughout the body and renal arteries contract. Sometimes renal blood flow increased after rapid blood volume replenishment, but the glomerular filtration rate and GFR did not recover, suggesting that in the early stage of ATN, there were changes in renal hemodynamics and abnormal renal blood flow distribution. The pathophysiological considerations of these renal hemodynamic abnormalities are related to the following factors.

(1) The role of renal nerves: Renal sympathetic nerve fibers are widely distributed in renal blood vessels and glomeruli. Increased adrenergic activity causes renal vasoconstriction, leading to decreased renal blood flow and GFR. The degree of renal vasoconstriction induced by renal nerve stimulation in ischemic ATN far exceeds that of normal animals, indicating that the sensitivity of blood vessels to renal nerve stimulation is increased during ATN, but this enhanced response can be affected by calcium channel blockers. Inhibition, suggesting that renal vasoconstriction due to renal nerve stimulation is related to changes in renal vascular smooth muscle calcium activity. However, ischemic ATN can occur in up to 30% of allograft renal allografts after clinical recovery of renal blood supply, which does not seem to support the leading role of renal nerves in the occurrence of ATN.

(2) The role of renin-angiotensin in renal tissue: There is a complete renin-angiotensin system in renal tissue. In ischemic ATN, changes in the renal blood circulation pathway are mostly thought to be related to the activation of the renin-angiotensin system in renal tissue, which leads to the strong contraction of the arterioles. However, ATN can still occur by inhibiting renin activity and antagonizing angiotensin II, indicating that the renin-angiotensin system is not a decisive factor for ATN.

(3) The role of prostaglandins in the kidney: PGI2 in the kidney is synthesized in the renal cortex and has a significant vasodilator effect. It can increase renal blood flow and GFR, and favor sodium and anti-diuretic hormones on the collecting tube against water Reabsorption and diuretic effect. It has been confirmed that PGI2 is significantly reduced in blood and kidney tissues at ATN; indomethacin, a prostaglandin antagonist, can accelerate ischemic renal damage. In addition, during renal ischemia, the increased thromboxane synthesis in the renal cortex also promotes renal vasoconstriction. However, there is no evidence that prostaglandins play a leading role in ATN.

(4) Endothelial-derived contraction and the role of diastolic factor in ATN: Pathologically increased secretion of vascular endothelial-derived contraction factor and vascular endothelial-derived diastolic factor such as nitrogen oxide (NO) release disorder affect the hemodynamic changes of ATN Important role. In the early stage of ATN, renal blood flow is reduced. When renal ischemia and hypoxia, vascular endothelial cells release more endothelin. (Experiments found that low concentrations of endothelin can cause strong and continuous contraction of renal blood vessels, increase renal small blood vessel resistance, and reduce GFR. Discontinued. Glomerular capillaries, mesangial cells, and straight small blood vessels have high density of endothelin receptors. Continuous injection of endothelin in experimental renal blood vessels can also cause significant contraction of renal blood vessels), which causes the kidneys to enter and exit The arteriolar arteriolar resistance increased, and the resistance of the arteriolar arterioles increased more significantly, so renal blood flow and GFR decreased in parallel. But sometimes patients with serum endothelin concentration increased more than 10 times did not occur ATN clinically. Normal vascular endothelium can still release diastolic factors and synergistically regulate blood flow to maintain blood circulation. It has an effect on the kidneys to increase blood flow and reduce the resistance of the arterioles into and out of the ball. In the early stage of ATN, there is an obstacle to the release of vascular endothelial relaxing factor. The increase of oxygen free radicals after ischemia-reperfusion also affects the release of relaxing factor. 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 medulla congestion: In the ischemic ATN model, the damage to the extramedullary and intracortical areas is most obvious, and the degree of renal medulla congestion is significantly related to the degree of ATN damage. Hypoxic medullary congestion first affects the blood supply of renal tubular cells in the thick segment of the ascending branch. Because the thick segment of the ascending branch is a high energy-consuming region, it is sensitive to hypoxia, and the capacity of hypoxic tubule cells to actively reabsorb sodium chloride reduce. Thick segment injury of the ascension branch can easily deposit TH glycoprotein in the thick segment, causing distal small lumen obstruction and luminal fluid overflow. Therefore, it is thought that medullary congestion in ischemic ATN is also an important factor.

2. Renal ischemia-reperfusion cell injury mechanism Renal tissue recovers blood supply after acute ischemia and hypoxia, such as after shock correction, major hemorrhagic blood transfusion, recovery from cardiopulmonary bypass or cardiac resuscitation, and recovery of renal blood circulation after transplantation. Oxygen free radicals. The energy decomposition is more than the synthesis during hypoxia. Hypoxanthine, the decomposition product of adenosine triphosphate, aggregates and produces a large amount of xanthine under the action of xanthine oxidase, and then the generation of oxygen free radicals increases. Kidney tissue cell membranes are rich in lipids, such as polyvalent unsaturated fatty acids, which have a high affinity for free radicals and produce a variety of lipid peroxides. The latter can make the ratio of polyvalent unsaturated fatty acids to proteins on the cell membrane dysregulated, resulting in changes in the fluidity and permeability of the cell membrane fluid, which can cause dysfunction, reduce various enzyme activities, significantly increase capillary permeability, and increase exudation. Causes cell and interstitial edema. Free radicals and other damage to the cell membrane will cause a large amount of extracellular calcium ions to enter the cell, which will increase the intracellular calcium ions and cause the cell to die. In addition, the cortical mitochondrial function is significantly reduced during renal ischemia, which also reduces the synthesis of adenosine triphosphate, reduces the ion transport function of the cell membrane dependent on adenosine triphosphate energy, and accumulates intracellular calcium ions, which in turn stimulates mitochondria to react with calcium ions. Increased intake of calcium, excessive levels of calcium in the mitochondria and cell death. The use of calcium antagonists can prevent the increase of intracellular calcium concentration, thereby preventing the occurrence of ATN.

3. Acute tubular injury theory Severe crush injury and acute poisoning, such as mercury chloride, arsenic and other causes of ATN pathological changes in renal tubular cells shed, necrosis and other acute damage and renal interstitial edema as the main changes, and kidney Glomerular and renal vascular changes are relatively mild or absent, indicating that the main pathogenesis of ATN is the reduction or cessation of GFR due to primary tubular damage. Thurau et al. Believe that acute tubular damage can cause tubule-globule feedback mechanism. In recent years, many scholars have also proposed the important role of renal tubular epithelial cell adhesion factor and peptide growth factor in the occurrence, development and repair of renal tubules.

(1) Renal tubular obstruction theory: Toxins can directly damage renal tubular epithelial cells, and the lesions are evenly distributed, mainly in proximal tubules. Necrotic tubular epithelial cells and exfoliated epithelial cells and microvilli debris, cell casts or hemoglobin, myoglobin, etc., obstruct the renal tubules, leading to an increase in the pressure in the proximal tubules of the obstruction, which in turn leads to the glomerulus. The pressure rises, and when the sum of the latter pressure and the osmotic pressure of the colloid is close to or equal to the internal pressure of the glomerular capillary, the glomerular filtration stops. Experiments have proved that in sublethal renal tubular injury caused by renal ischemia or nephrotoxicity, the proximal tubular tubules are detached from the brush border, cell swelling, and vacuole degeneration. Tubular epithelial cells (TEC) detached from the basement membrane, causing a defect brushing area on the basement membrane of the renal tubule. However, most of the shed TECs are intact and viable. The number of TECs in the urine also increased significantly, and a significant number of TECs 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 in renal tubular epithelial cell adhesion molecule family has the greatest influence on the occurrence of ATN. Integrins can mediate cell-to-cell and cell-to-matrix adhesions and maintain the integrity of renal tubular structures. The changes in cell adhesion during TEC injury are:

Changes in the cytoskeleton: In particular, the actin microfilament components play an important role in the adhesion between TEC and cells, cells and matrix. When renal tubular epithelium is damaged, the cytoskeleton components change, causing TEC to fall off from the basement membrane.

Changes of integrin: Ischemia-reperfusion injury can cause obvious abnormal integrin redistribution, especially in the area without damage to the tubular structure, and the tubular epithelium loses the polar distribution of integrin, suggesting that reperfusion can cause changes in cell adhesion. The overexpression of integrin on the surface of injured cells may increase the cell-to-cell adhesion in the small lumen, and promote the formation of cell clumps that block the small lumen.

Matrix protein changes: 30-40 minutes after the renal pedicle was clamped in experimental animals, semi-quantitative analysis of immunofluorescence showed a decrease in laminin, and 3 to 4 days after ischemic injury, laminin at the junction of cortex and cortex and medulla. Increased, tenasein and fibronectin began to increase 1 to 2 days after ischemia, reached a peak on the 5th day, and there was no change in type IV collagen staining. These studies indicate that there are significant changes in matrix components in the early stages of ischemic injury.

(2) Leakage doctrine: refers to necrosis and shedding after renal tubular epithelial injury, and defect and exfoliation areas appear in the tubular wall. The tubule lumen can directly communicate with the renal interstitial, causing the primary urine in the tubule to diffuse back to the kidney. Interstitial, causing renal interstitial edema, oppressing nephrons, aggravating renal ischemia, and lowering GFR. However, the experimental observation only encountered the renal tubules in the case of severe necrosis of renal tubules. The decrease in renal blood flow and GFR can precede the leakage of renal tubule fluid, indicating that the latter is not the initiating factor for the onset of ATN. However, the severity of renal interstitial edema at ATN is an important factor in disease development.

(3) Tubular-globular feedback mechanism: ischemia, nephrotoxicity and other factors cause acute tubular injury, resulting in a significant decrease in sodium reabsorption of sodium and chlorine in this section of the renal tubule, and increased sodium and chlorine concentrations in the lumen. Dense plaque induction increases the renin secretion of the arterioles, followed by angiotensin , , which causes the arterioles and renal vessels to contract, renal vascular resistance increases, and GFR decreases significantly. In addition, the renal tubular blood supply was significantly reduced, which reduced the release of prostacyclin into the cortex, and renal blood flow and GFR were further reduced.

(4) Disseminated intravascular coagulation (DIC): sepsis, severe infection, epidemic hemorrhagic fever, shock, postpartum hemorrhage, pancreatitis, and burns cause ATN, and often diffuse microvascular damage. Platelets and fibrin are deposited on the intima of damaged renal blood vessels, causing vascular occlusion or poor blood flow. Red blood cells are liable to deform, break, and dissolve when flowing through damaged blood vessels, leading to microvascular hemolysis.

The location, nature, and extent of ATN pathological lesions vary with the cause and severity of the disease. The main pathological changes of the kidney are kidney enlargement, paleness, and weight gain; the cut cortex is pale, and the medulla is dark red. Light microscopy revealed degeneration, shedding, and necrosis of renal tubular epithelial cells. The lumen is filled with exfoliated tubular epithelial cells, casts, and exudates. For those who are caused by nephrotoxic substances, renal tubular lesions are mainly distributed in the proximal tubules. The sites of nephrotoxicity such as mercury and gentamicin are near the proximal tubules, while those caused by chlorate are in the middle and posterior segments. Can affect the entire proximal tubule. Degeneration and necrosis of epithelial cells often affect the cells themselves, and they are evenly distributed. The surface of renal tubule basement membrane is intact or defective, and renal interstitial edema. There is time and quality with obvious infiltration of inflammatory cells. Usually until about 1 week, the necrotic renal tubular epithelial cells begin to regenerate and soon cover the basement membrane. The renal tubular shape gradually returns to normal. For renal ischemia, the peripheral part of the interlobular artery is the earliest affected and serious, so the lesions in the cortex, especially the ascending segment of the tubule and the distal tubules, are the most obvious. The focal necrosis of the epithelial cells increases with the degree of ischemia The development of the lesions spread to various sections of the renal tubules and collecting ducts, so the distribution of the lesions was very uneven. It is often distributed in segments, ranging from near curved tubules to collecting ducts. Tubular epithelial cells are necrotic, shed, and steatosis. The tubule basement membrane in severely damaged parts can also rupture and rupture, resulting in lumen The contents enter the stroma, causing interstitial edema, congestion, and inflammatory cell infiltration. In addition, cortical vasoconstriction, medulla vasodilation, and congestion were also seen. If the lesion involves adjacent small veins, it can cause thrombosis or interstitial hemorrhage and hematuria. In patients with severe damage to the basement membrane of renal tubular epithelial cells, the cells are often unable to regenerate. This part is replaced by connective tissue hyperplasia, so the recovery time of ischemic damage is longer. Electron microscopy showed that the microvilli of the renal tubular epithelial cells were broken and shed, TEC's mitochondria swelled, mitochondrial ridges disappeared, and mitochondrial membranes were ruptured. Primary and secondary lysosomes increased, and phagocytosis increased. TEC serious damage can be seen in mitochondria, Golgi and other organelles disintegrate, dissolve, and even completely necrosis. Thrombotic microangiopathy ATN, kidney microvessels have platelets and fibrin deposits, blocking the microvascular cavity, damaged vessel walls often have focal necrosis and inflammation, glomeruli may have mild mesangial cell proliferation, and ischemia Sexual changes, and even glomerulosclerosis. Glomerular and tubular necrosis of bilateral extensive renal cortex can occur in individual cases. ^[1]

Acute renal failure has two stages of renal tubular necrosis and repair. The biggest feature of ATN is that the renal function can return to normal. This process includes the recovery of damaged cells, the removal of casts in the lumen of necrotic cells, and cell regeneration, and finally the integrity of renal tubular epithelial cells is fully restored. Acute renal failure is generally divided into three stages: oliguria, polyuria, and recovery according to the common law of clinical manifestations and disease course:

1. The clinical manifestations of oliguria or anemia are mainly nausea, vomiting, headache, dizziness, irritability, fatigue, lethargy, and coma. Due to the accumulation of water and sodium in the oliguria, patients may develop hypertension, pulmonary edema, and heart failure. Nitroemia occurs when protein metabolites cannot be excreted by the kidneys, causing nitrogenous substances to accumulate in the body. If it is accompanied by infection, injury, and fever, protein catabolism is accelerated, and urea nitrogen and creatinine in the blood increase rapidly, forming uremia. The main features of this issue are:

(1) Decrease in urine output: A sudden decrease or gradual decrease in urine output. Those who continue to urinate less than 400ml per day are called oliguria, and those who are less than 100ml are called anuria. ATN patients rarely have complete anuria, and those with persistent anuria have a poor prognosis. Extrarenal obstruction and bilateral renal cortical necrosis should be excluded. Due to the cause and severity of the disease, the duration of oliguria is inconsistent, usually 1 to 3 weeks, but in a few cases, oliguria can last for more than 3 months. It is generally believed that the duration of nephrotoxicity is short, while the duration of ischemic is longer. If oliguria persists for more than 12 weeks, the diagnosis of ATN should be reconsidered. There may be necrosis of the kidney or necrosis of the kidney. People with prolonged oliguria should pay attention to fluid retention, congestive heart failure, hyperkalemia, hypertension, and various complications.

Non-oliguric ATN means that the patient's daily urine output during the progressive azotemia period is more than 500ml, or even 1000-2000ml. The incidence of non-oliguria type has increased in recent years, as high as 30% to 60%. The reason is related to the improvement of people's understanding of this type, the widespread use of nephrotoxic antibiotics and the early application of diuretics such as furosemide and mannitol. There are three reasons for the lack of urine output:

The degree of damage to each nephron varies, and renal blood flow and glomerular filtration function in a small number of nephrons are present, while the corresponding renal tubular reabsorption function is significantly impaired.

Although the degree of damage to all nephrons is the same, the proportion of renal tubular reabsorption dysfunction is far more severe than the reduction of glomerular filtration function.

The ability of the deep part of the renal medulla to form a hypertonic state is reduced, resulting in a decrease in water reabsorption in the pulp of the myelin. Common diseases of non-oliguria type are the long-term application of nephrotoxic drugs, major abdominal surgery and open heart surgery. It is generally believed that although the non-oliguric type is less urinary, the condition is shorter, the length of hospital stay is short, the percentage of dialysis treatment is low, and complications such as upper gastrointestinal bleeding are small, but the incidence of hyperkalemia is similar to that caused by oliguria. The mortality rate for oliguria can still be as high as 26%. Therefore, no link can be ignored in treatment.

(2) Progressive azotemia: decreased oliguria or anuria due to reduced glomerular filtration rate, resulting in reduced excretion of nitrogen and other metabolic wastes, increased plasma creatinine and urea nitrogen, the rate of increase and the protein in the body The decomposition status is related. In the case of no complications and correct treatment, the daily rise of blood urea nitrogen is slow, about 3.6mmol / L (10mg / dl), and the increase of plasma creatinine concentration is only 44.2 88.4mol / L (0.5 1.0mg / dl). ), But in a high decomposition state, such as with extensive tissue trauma, sepsis, etc., urea nitrogen can increase by 7.1mmol / L (20mg / dl) or more per day, and plasma creatinine increases by 176.8mol / L (2mg / dl) per day. or above. Factors that promote hyperproteolysis include insufficient heat supply, muscle necrosis, hematoma, gastrointestinal bleeding, fever with infection, and application of adrenal corticosteroids.

(3) Water, electrolyte disorders and acid-base balance disorders:

Excessive water: It is found that the water control is not strict, the intake or rehydration is too much, the output of water such as vomiting, sweating, wound penetration, etc. is not accurately estimated, and the calculation of endogenous water is ignored when the fluid is replenished. With the extension of oliguria, it is prone to hyperhydration, including dilute hyponatremia, soft tissue edema, weight gain, hypertension, acute heart failure, and cerebral edema.

Hyperkalemia: Normal people ingest 90% of potassium and excrete it from the kidneys. ATN oliguria reduces potassium excretion due to urine. If there is a high decomposition state in the body at the same time, such as muscle necrosis, hematoma and infection during crush injury, Insufficient caloric intake results in the breakdown of protein in the body and release of potassium ions. Intracellular potassium is transferred to the outside of cells during acidosis, and sometimes severe hyperkalemia can occur within a few hours. If the patient is not diagnosed in time, ingest foods or beverages containing more potassium, intravenously inject a large amount of penicillin potassium salt (1.6 mmol potassium per 1 million U penicillin potassium salt); enter a large amount of stock blood when bleeding ( Inventory for 10 days blood can reach 22mmol per liter of potassium); can also cause or aggravate hyperkalemia. Generally, in uncomplicated medical causes, the daily potassium of ATN rises less than 0.5mmol / L. Hyperkalemia may have no characteristic clinical manifestations, or there may be nausea, vomiting, numbness in the limbs, slowed heart rate, and severe symptoms of neurological symptoms, such as fear, irritability, and indifferent consciousness, until the sinus or atrioventricular occurs later Conduction block, sinus rest, indoor block and even ventricular fibrillation. Electrocardiogram changes in hyperkalemia can precede clinical manifestations of hyperkalemia. Therefore, the monitoring of the effects of hyperkalemia on the myocardium by ECG is very important. When the blood potassium concentration is 6mmol / L, the ECG shows a high T wave with a narrow basal base. The P wave disappears with the increase of blood potassium, the QRS widens, the ST segment cannot be identified, and finally merges with the T wave, followed by severe arrhythmia. Until ventricular fibrillation. The effects of hyperkalemia on myocardial toxicity are the sodium and calcium concentrations and acid-base balance in the receptors. When hyponatremia, hypocalcemia, or acidosis are present at the same time, hyperkalemia has a significant ECG performance, and it is easy to induce various Arrhythmia. It is worth mentioning that there may be inconsistencies between serum potassium concentration and ECG performance. Hyperkalemia is one of the common causes of death in patients with oliguria, and early dialysis can prevent it. However, severe necrosis of muscle tissue often results in persistent hyperkalemia. Necrotic tissue should be completely removed during treatment in order to control hyperkalemia.

Metabolic acidosis: The fixed acid metabolites of normal people are 50-100 mmol per day, of which 20% are combined with bicarbonate ions, and 80% are excreted by the kidneys. In acute renal failure, due to decreased excretion of acidic metabolites, decreased renal tubular acid secretion capacity and ability to store sodium bicarbonate, etc., the daily plasma bicarbonate concentration decreases to varying degrees; in the high decomposition state, it decreases more and faster. Most of the endogenous fixed acids come from proteolysis, and a small part come from sugar and fat oxidation. Phosphate and other organic anions are released and accumulated in body fluids, leading to an increase in anion gap in patients with this disease. If metabolic acidosis is not adequately corrected in cases of persistent oliguria, muscles in the body disintegrate faster. In addition, acidosis can still lower the threshold of ventricular fibrillation and ectopic rhythm. Hyperkalemia, severe acidosis, hypocalcemia, and hyponatremia are serious conditions of acute renal failure. Although cases have been treated with dialysis, they are rare, but some cases still require drugs to correct metabolic symptoms during the dialysis interval. Acidosis.

Hypocalcemia and hyperphosphatemia: Hypocalcemia and hyperphosphatemia are not as prominent in chronic renal failure as ATN, but it has been reported that hypocalcemia can occur after 2 days of oliguria. Because often accompanied by acidosis, the extracellular calcium ions increase, so the common clinical manifestations of low calcium do not occur. Hypocalcemia is mostly caused by hyperphosphatemia, and 60% to 80% of the phosphate intake of normal people is excreted through the urine. ATN oliguria usually has a slight increase in blood phosphorus, but if there is significant metabolic acidosis, hyperphosphatemia is also prominent, but rarely significantly increased. After the acidosis is corrected, the blood phosphorus may be reduced to a certain extent. At this time, if patients receiving continuous intravenous nutrition treatment should pay attention to the occurrence of hypophosphatemia.

Hyponatremia and hypochloremia: Both of them exist at the same time. The cause of hyponatremia can be dilute hyponatremia due to excessive water, loss of skin or gastrointestinal tract due to burns or vomiting, diarrhea, or non-oliguric types that still respond to high-dose furosemide The patient developed hyponatremia. Severe hyponatremia can reduce blood osmotic concentration, cause water to penetrate into cells, appear cell edema, show 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-oliguria with a large amount of diarrhea, and manifestations of metabolic alkalosis such as abdominal distension or superficial breathing and convulsions.

Hypermagnesemia: 60% of the normal magnesium intake is excreted by feces and 40% is excreted from urine. Because magnesium and potassium ions are the main cations in the cell, blood potassium and blood magnesium concentrations often rise in parallel during ATN, and hypermagnesemia is more prominent during muscle injury. Magnesium ions have inhibitory effects on the central nervous system. Severe hypermagnesemia can cause respiratory depression and myocardial depression and should be vigilant. Electrocardiogram changes in hypermagnesemia can also show prolonged PR interval and QRS wave widening. When hyperkalemia is corrected, the possibility of hypermagnesemia should be suspected when the PR interval is extended and / or the QRS is widened on the ECG. Hyponatremia, hyperkalemia, and acidosis all increase the toxicity of magnesium to the heart muscle.

(4) Cardiovascular system performance:

Hypertension: In addition to the factors that promote the secretion of active substances that constrict blood vessels due to the role of neurohumoral factors during renal ischemia, excessive volume caused by excessive volume of water can increase hypertension. Early onset of hypertension in ATN is rare, but if oliguria persists, about one-third of patients develop mild to moderate hypertension, generally between 18.62 to 23.94 / 11.97 to 14.63 kPa (140 to 180/90 to 110 mmHg), sometimes Higher, and even hypertension.

Acute pulmonary edema and heart failure: common causes of death during oliguria. It is mainly caused by fluid retention, but hypertension, severe infection, arrhythmia, and acidosis are all influencing factors. The incidence was high in the early years, and the incidence has decreased significantly after taking measures to correct hypoxia, control water and early dialysis. But it is still a common cause of death in severe ATN.

Arrhythmia: Except for hyperkalemia caused by sinus node pause, sinus rest, sinus ventricular block, varying degrees of atrioventricular block and bundle branch block, ventricular tachycardia, ventricular fibrillation, Ectopic rhythms such as premature ventricular contractions and paroxysmal atrial fibrillation due to viral infection and digitalis application.

Pericarditis: The annual incidence rate is 18%, and it is reduced to 1% after taking early dialysis. Mostly manifested as pericardial fricatives and chest pain, and rarely a large amount of pericardial effusion.

Digestive system performance: It is the earliest performance of ATN. Common symptoms are decreased appetite, nausea, vomiting, bloating, hiccups, or diarrhea. Upper gastrointestinal bleeding is a common late complication. Gastrointestinal symptoms are still related to the primary disease and water, electrolyte disorders or acidosis. Persistent and severe gastrointestinal symptoms are often prone to obvious electrolyte disturbances, increasing the complexity of treatment. Early manifestation of gastrointestinal symptoms suggests early dialysis treatment.

Nervous system symptoms may be lack of neurological symptoms: some patients are tired early and have poor mental performance. If early indifference, drowsiness, irritability, or even coma appear, it indicates that the condition is severe, and the dialysis time should not be delayed. Nervous system manifestations are related to etiologies such as severe infection, epidemic hemorrhagic fever, certain heavy heavy metal poisoning, severe trauma, and multiple organ failure.

Blood system performance: ATN is rare in the early stage of anemia, and its degree is closely related to the primary etiology, duration of the disease, and the presence or absence of bleeding complications. Severe trauma, blood loss after major surgery, factors of hemolytic anemia, severe infection and acute ATN, etc., anemia can be more serious. If there are clinical signs of bleeding, thrombocytopenia, wasting hypocoagulation, and signs of fibrinolysis, it is no longer early DIC.

2.2.5LATN24h400ml2351000ml35L;GFR10ml/min;

3.ATN;361 ^[2]

ARFARF

1.

(1)

(2)(<250ml/m2)(<50ml/m2)

(3)

(4)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 ^[2]

Laboratory inspection

1.()()

Blood test

(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

(3)pH8.0kPa(60mmHg)(ARDS)

(4);

(5)

(6)DIC;;;;(FDP)

ATNDICFDP

(7)3

1.Ga

2.ARFARFB

3.CTMRICT(MRI)

4.ARF50% ^[3]

:

1.

2.

3-7

(30g)120m1

(1)120g60g

(2)30g

(3)

(4)2

(5) ^[4]

ARF40%50%;;;;;70% ATN3% ^[4]

1.

2.

3.

4.

5.

6.

7. ^[5]

1520

1/21/3

()()C

As various foods contain potassium, in addition to avoiding foods with high potassium content, methods such as freezing, soaking in water, or discarding soup can be used to reduce the potassium content. ^[6]

Acute renal failure mostly passes through three stages of development: oliguria (or anuria), polyuria, and recovery. The main complications that may occur during the oliguria of acute renal failure are:

I. Infection is one of the most common and serious complications. It is more common in high-resolution acute renal failure caused by severe trauma and burns;

Second, the cardiovascular system complications, including heart rhythm disorders, heart failure, pericarditis, hypertension, etc .;

Third, neurological complications include headache, drowsiness, muscle twitching, coma, epilepsy and so on. Neurological complications are related to the retention of toxins in the body and water poisoning, electrolyte disturbances and acid-base balance disorders;

Digestive system complications include anorexia, nausea, vomiting, abdominal distension, vomiting or blood in the stool, etc. Most of the bleeding is caused by gastrointestinal stress ulcers;

Fifth, hematological complications due to the rapid decline of renal function, can reduce erythropoietin, thereby causing anemia, but most are not serious. Few cases may have bleeding tendency due to reduced coagulation factors;

6. Electrolyte disorders, metabolic acidosis, hyperkalemia, hyponatremia, and severe acidosis can occur. It is one of the most dangerous complications of acute renal failure.

In the polyuria phase, the patient's daily urine output can reach 3000-5000ml. Dehydration, hypokalemia, and hyponatremia can occur due to the discharge of a large amount of water and electrolytes. If not replenished in time, the patient can die from severe dehydration. And electrolyte disorders.

In the recovery period, serum urea nitrogen and creatinine levels returned to normal, uremia symptoms subsided, and renal tubular epithelial cells were regenerated and repaired. Most patients could fully recover renal function, and a few patients could leave different degrees of renal impairment. ^[7]