Opn stages. Acute kidney failure (acute kidney injury). Is hospitalization necessary

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- Potentially reversible, sudden onset of severe impairment or cessation of renal function. Characterized by a violation of all renal functions (secretory, excretory and filtration), marked changes in water and electrolyte balance, rapidly increasing azotemia. In the development of acute renal failure, 4 consecutive phases are distinguished: initial, oligoanuric, diuretic and the recovery period. Diagnosis is carried out according to clinical and biochemical blood and urine tests, as well as instrumental studies of the urinary system. Treatment depends on the stage of acute renal failure. It includes symptomatic therapy, methods of extracorporeal hemocorrection, maintenance of optimal blood pressure and diuresis.

Acute renal failure is a potentially reversible, sudden onset severe impairment or cessation of kidney function. Characterized by a violation of all renal functions (secretory, excretory and filtration), marked changes in water and electrolyte balance, rapidly increasing azotemia.

Allocate the following forms OPN:

Hemodynamic(prerenal). Occurs due to acute violation hemodynamics.
Parenchymal(renal). The cause is a toxic or ischemic lesion of the renal parenchyma, less often an acute inflammatory process in the kidneys.
Obstructive(postrenal). It develops as a result of acute obstruction of the urinary tract.

Etiology of prerenal acute renal failure

Prerenal acute renal failure can develop in conditions that are accompanied by a decrease in cardiac output (with pulmonary embolism, heart failure, arrhythmia, cardiac tamponade, cardiogenic shock). Often the cause is a decrease in the amount of extracellular fluid (with diarrhea, dehydration, acute blood loss, burns, ascites caused by liver cirrhosis). May occur due to severe vasodilation that occurs with bacteriotoxic or anaphylactic shock.

Etiology of renal acute renal failure

Occurs with toxic effects on the renal parenchyma of fertilizers, poisonous fungi, salts of copper, cadmium, uranium and mercury. It develops with uncontrolled intake of nephrotoxic drugs (anticancer drugs, a number of antibiotics and sulfonamides). X-ray contrast agents and the listed drugs, prescribed in the usual dosage, can cause renal acute renal failure in patients with impaired renal function.

In addition, this form of acute renal failure occurs when circulating in the blood a large number myoglobin and hemoglobin (with severe macrohemagglobinuria, transfusion of incompatible blood, prolonged tissue compression in trauma, drug and alcohol coma). Less often, the development of renal acute renal failure is due to inflammatory disease kidneys.

Etiology of postrenal acute renal failure

It develops with a mechanical violation of the passage of urine with bilateral obstruction of the urinary tract by stones. Rarely occurs with tumors prostate, Bladder and ureters, tuberculous lesions, urethritis and periurethritis, dystrophic lesions of the retroperitoneal tissue.

In severe concomitant injuries and extensive surgical interventions acute renal failure is caused by several factors (shock, sepsis, blood transfusion, treatment with nephrotoxic drugs).

Symptoms of acute renal failure

There are four phases of acute renal failure:

The patient's condition is determined by the underlying disease causing acute renal failure. Clinically, the initial phase is usually not detected due to the lack of characteristic symptoms. The circulatory collapse that occurs in this phase has a very short duration, so it goes unnoticed. Nonspecific symptoms of acute renal failure (drowsiness, nausea, lack of appetite, weakness) are masked by manifestations of the underlying disease, injury or poisoning.

Anuria is rare. The amount of urine separated is less than 500 ml per day. Severe proteinuria, azotemia, hyperphosphatemia, hyperkalemia, hypernatemia, and metabolic acidosis are characteristic. Diarrhea, nausea, vomiting are noted. At pulmonary edema due to hyperhydration, shortness of breath and moist rales appear. The patient is lethargic, drowsy, may fall into a coma. Often develops pericarditis, uremic gastroenterocolitis, complicated by bleeding. The patient is susceptible to infection due to reduced immunity. Possible pancreatitis, stomatitis parotitis, pneumonia, sepsis.

The oligoanuric phase of acute renal failure develops during the first three days after exposure. Late development of the oligoanuric phase is considered a prognostically unfavorable sign. The average duration of this stage is 10-14 days. The period of oliguria can be shortened to a few hours or extended to 6-8 weeks. Prolonged oliguria occurs more often in elderly patients with concomitant vascular pathology. With the oliguric stage of acute renal failure, lasting more than a month, it is necessary to conduct an additional differential diagnosis to exclude progressive glomerulonephritis, renal vasculitis, renal artery occlusion, diffuse necrosis of the renal cortex.

The duration of the diuretic phase is about two weeks. Daily diuresis gradually increases and reaches 2-5 liters. There is a gradual restoration of water and electrolyte balance. Possible hypokalemia due to significant loss of potassium in the urine.

There is a further recovery of renal function, which takes from 6 months to 1 year.

Complications of acute renal failure

The severity of disorders characteristic of renal failure (fluid retention, azotemia, impaired water and electrolyte balance) depends on the state of catabolism and the presence of oliguria. With severe oliguria, there is a decrease in the level of glomerular filtration, the release of electrolytes, water and nitrogen metabolism products is significantly reduced, which leads to more pronounced changes in the composition of the blood.

With oliguria, the risk of developing water and salt overload increases. Hyperkalemia in acute renal failure is caused by insufficient excretion of potassium with a continuing level of its release from the tissues. In patients who do not suffer from oliguria, the potassium level is 0.3-0.5 mmol / day. More pronounced hyperkalemia in such patients may indicate exogenous (blood transfusion, medications, the presence in the diet of foods rich in potassium) or endogenous (hemolysis, tissue destruction) potassium load.

The first symptoms of hyperkalemia appear when the potassium level exceeds 6.0-6.5 mmol/L. Patients complain of muscle weakness. In some cases, flaccid tetraparesis develops. Are celebrated ECG changes. The amplitude of the P waves decreases, the PR interval increases, and bradycardia develops. A significant increase in potassium concentration can cause cardiac arrest.

In the first two stages of acute renal failure, hypocalcemia, hyperphosphatemia, and mild hypermagnesemia are observed.

The consequence of severe azotemia is the inhibition of erythropoiesis. The lifespan of red blood cells is shortened. Normochromic anemia develops.

Immune suppression leads to infectious diseases in 30-70% of patients with acute renal failure. Accession of infection aggravates the course of the disease and often becomes the cause of death of the patient. Inflammation develops in the area of postoperative wounds, the oral cavity suffers, respiratory system, urinary tract. A frequent complication of acute renal failure is sepsis, which can be caused by both gram-positive and gram-negative flora.

There is drowsiness, confusion, disorientation, lethargy, alternating with periods of excitement. Peripheral neuropathy is more common in older patients.

Complications from the cardiovascular system

With acute renal failure, congestive heart failure, arrhythmia, pericarditis, and arterial hypertension may develop.

Patients are concerned about the feeling of discomfort in the abdominal cavity, nausea, vomiting, loss of appetite. In severe cases, uremic gastroenterocolitis develops, often complicated by bleeding.

OPN diagnostics

The main marker of acute renal failure is an increase in potassium and nitrogenous compounds in the blood against the background of a significant decrease in the amount of urine excreted by the body up to the state of anuria. The amount of daily urine and the concentration ability of the kidneys are evaluated according to the results of the Zimnitsky test. It is important to monitor such indicators of blood biochemistry as urea, creatinine and electrolytes. It is these indicators that make it possible to judge the severity of acute renal failure and the effectiveness of ongoing therapeutic measures.

The main task in the diagnosis of acute renal failure is to determine its form. To do this, ultrasound of the kidneys and bladder is performed, which allows you to identify or exclude obstruction of the urinary tract. In some cases, bilateral catheterization of the pelvis is performed. If at the same time both catheters freely passed into the pelvis, but no urine output is observed through them, it is safe to exclude the postrenal form of acute renal failure.

If necessary, to assess the renal blood flow, ultrasound of the vessels of the kidneys is performed. Suspicion of tubular necrosis, acute glomerulonephritis, or systemic disease is an indication for a kidney biopsy.

Treatment of acute renal failure

Treatment in the initial phase

Therapy is aimed primarily at eliminating the cause that caused the kidney dysfunction. In shock, it is necessary to replenish the volume of circulating blood and normalize arterial pressure. In case of poisoning with nephrotoxins, patients are washed with the stomach and intestines. The use in urology of such modern methods of treatment as extracorporeal hemocorrection allows you to quickly cleanse the body of toxins that have caused the development of acute renal failure. For this purpose, hemosorption and plasmapheresis are carried out. In the presence of obstruction, normal urine passage is restored. To do this, stones are removed from the kidneys and ureters, surgical removal of ureteral strictures and removal of tumors.

Treatment in the phase of oliguria

To stimulate diuresis, the patient is prescribed furosemide and osmotic diuretics. Dopamine is administered to reduce renal vasoconstriction. When determining the volume of fluid to be administered, in addition to losses during urination, vomiting and bowel movements, it is necessary to take into account losses during sweating and breathing. The patient is transferred to a protein-free diet, limit the intake of potassium from food. Drainage of wounds, removal of areas of necrosis is carried out. When choosing a dose of antibiotics, the severity of kidney damage should be taken into account.

Indications for hemodialysis

Hemodialysis is carried out with an increase in the level of urea to 24 mmol / l, potassium - up to 7 mmol / l. Indications for hemodialysis are symptoms of uremia, acidosis and hyperhydration. Currently, to prevent complications arising from metabolic disorders, nephrologists increasingly perform early and preventive hemodialysis.

Mortality primarily depends on the severity of the pathological condition that caused the development of acute renal failure. The outcome of the disease is affected by the age of the patient, the degree of impaired renal function, the presence of complications. In surviving patients, renal function is restored completely in 35-40% of cases, partially - in 10-15% of cases. 1-3% of patients require permanent hemodialysis.

Acute renal failure (ARF) develops as a complication of many diseases and pathological processes. Acute renal failure is a syndrome that develops as a result of impaired renal processes (renal blood flow, glomerular filtration, tubular secretion, tubular reabsorption, renal concentrating ability) and is characterized by azotemia, disturbances in water and electrolyte balance and acid-base state.

Acute renal failure may be due to prerenal, renal, and postrenal disorders. Prerenal acute renal failure develops due to a violation of the renal blood flow, renal acute renal failure - with damage to the renal parenchyma, postrenal acute renal failure is associated with a violation of the outflow of urine.

The morphological substrate of ARF is acute tubulonecrosis, manifested by a decrease in the height of the brush border, a decrease in the folding of the basolateral membranes, and necrosis of the epithelium.

Prerenal acute renal failure is characterized by a decrease in renal blood flow as a result of vasoconstriction of afferent arterioles in conditions of impaired systemic hemodynamics and a decrease in circulating blood volume, while kidney function is preserved.

long-term or short-term (less often) decrease in blood pressure below 80 mm Hg. (shock due to various reasons: post-hemorrhagic, traumatic, cardiogenic, septic, anaphylactic, etc., extensive surgical interventions);

decrease in the volume of circulating blood (blood loss, plasma loss, indomitable vomiting, diarrhea);

an increase in intravascular capacity, accompanied by a decrease in peripheral resistance (septicemia, endotoxemia, anaphylaxis);

decrease in cardiac output (myocardial infarction, heart failure, pulmonary embolism).

The key link in the pathogenesis of prerenal acute renal failure is a sharp decrease in the level of glomerular filtration due to spasm of afferent arterioles, shunting of blood in the juxtaglomerular layer and ischemia of the cortical layer under the influence of a damaging factor. Due to a decrease in the volume of blood perfused through the kidneys, the clearance of metabolites decreases and develops azotemia. Therefore, some authors call this type of OPN prerenal azotemia. With a prolonged decrease in renal blood flow (more than 3 days) prerenal acute renal failure turns into renal acute renal failure.

The degree of renal ischemia correlates with structural changes in the epithelium of the proximal tubules (decrease in the height of the brush border and the area of the basolateral membranes). Initial ischemia contributes to an increase in the permeability of tubular epithelium cell membranes for ions that enter the cytoplasm, are actively transported by a special carrier to the inner surface of mitochondrial membranes or to the sarcoplasmic reticulum. The energy deficit developing in the cells due to ischemia and energy consumption during the movement of ions leads to cell necrosis, and the resulting cellular debris obstructs the tubules, thereby aggravating anuria. The volume of tubular fluid in conditions of ischemia is reduced.

Damage to nephrocytes is accompanied by a violation of sodium reabsorption in the proximal tubules and an excessive intake of sodium in the distal regions. Sodium stimulates macula densa renin production; in patients with acute renal failure, its content is usually increased. Renin activates the renin-angiotensin-aldosterone system. The tone of the sympathetic nerves and the production of catecholamines are increased. Under the influence of the components of the renin-apgiotensin-aldosterone system and catecholamines, afferent vasoconstriction and renal ischemia are maintained. In the capillaries of the glomeruli, the pressure drops and, accordingly, the effective filtration pressure decreases.

With a sharp restriction of perfusion of the cortical layer, blood enters the capillaries of the juxtaglomerular zone ("Oxford shunt"), in which stasis occurs. An increase in pressure in the tubules is accompanied by a decrease in glomerular filtration. Hypoxia of the distal tubules most sensitive to it is manifested by necrosis of the tubular epithelium and basement membrane up to tubular necrosis. There is an obturation of the tubules by fragments of necrotic epithelial cells, cylinders, etc.

Under conditions of hypoxia in the medulla, a change in the activity of enzymes of the arachidonic cascade is accompanied by a decrease in the formation of prostaglandins that have a vasodilatory effect, and the release of biologically active substances(histamine, serotonin, bradykinin), which directly affect the vessels of the kidneys and disrupt renal hemodynamics. This, in turn, contributes to secondary damage to the renal tubules.

After the restoration of renal blood flow, the formation of reactive oxygen species, free radicals and activation of phospholipase occurs, which maintains impaired membrane permeability for ions and prolongs the oliguric phase of acute renal failure. In recent years, calcium channel blockers (nifedipine, verapamil) have been used to eliminate unwanted calcium transport into cells in the early stages of acute renal failure, even against the background of ischemia or immediately after its elimination. A synergistic effect is observed when calcium channel inhibitors are used in combination with substances that can trap free radicals, such as glutathione. Ions, adenine nucleotides protect mitochondria from damage.

The degree of renal ischemia correlates with structural changes in the epithelium of the tubules, the development of vacuolar degeneration or necrosis of individual nephrocytes is possible. Vacuolar degeneration is eliminated within 15 days after the termination of the damaging factor.

Renal acute renal failure develops due to ischemia of the kidney, that is, it occurs a second time with a primary impaired perfusion of the kidney or under the influence of the following reasons:

inflammatory process in the kidneys (glomerulonephritis, interstitial nephritis, vasculitis);

endo- and exotoxins (drugs, radiopaque substances, salts of heavy metals - compounds of mercury, lead, arsenic, cadmium, etc., organic solvents, ethylene glycol, carbon tetrachloride, poisons of animal and vegetable origin;

renovascular diseases (thrombosis and embolism of the renal artery, dissecting aortic aneurysm, bilateral thrombosis of the renal veins);

pigmentemia - hemoglobinemia (intravascular hemolysis) and myoglobinemia (traumatic and non-traumatic rhabdomyolysis);

This type of AKI is characterized by acute tubular necrosis caused by ischemia or nephrotoxins that are fixed on the cells of the renal tubules. First of all, the proximal tubules are damaged, dystrophy and necrosis of the epithelium occurs, followed by moderate changes in the interstitium of the kidneys. Glomerular lesions are usually minor.

To date, more than 100 nephrotoxins have been described that have a direct damaging effect on the cells of the renal tubules (acute tubular necrosis, nephrosis of the lower nephron, vasomotor vasopathy). Acute renal failure caused by nephrotoxins accounts for about 10% of all admissions of patients to acute hemodialysis centers.

Nephrotoxins cause damage to tubuloepithelial structures of varying severity - from dystrophies (hydropic, vacuole, balloon, fatty, hyalinodroplet) to partial or massive coagulative necrosis of nephrocytes. These changes occur as a result of reabsorption and deposition of macro- and microparticles in the cytoplasm, as well as fixation on the cell membrane and in the cytoplasm of nephrotoxins filtered through the glomerular filter. The occurrence of a particular dystrophy is determined by the acting factor.

nephrotoxicity of poisons thiol group"(compounds of mercury, chromium, copper, gold, cobalt, zinc, lead, bismuth, lithium, uranium, cadmium and arsenic) is manifested by blockade of sulfhydryl (thiol) groups of enzymatic and structural proteins and a plasma coagulating effect, which causes massive coagulation necrosis of the tubules. Sublimate causes selective damage to the kidneys - " sublimate nephrosis". Other substances in this group do not differ in selectivity of action and damage the tissue of the kidneys, liver and red blood cells. For example, a feature of poisoning with copper sulphate, dichromates, arsenic hydrogen is the combination of coagulation necrosis of the epithelium of the proximal tubules with acute hemoglobinuric nephrosis. In case of poisoning with bichromates and arsenic hydrogen, centrilobular necrosis of the liver with cholemia and chelaturia is observed.

Poisoning ethylene glycol and its derivatives is characterized by irreversible destruction of intracellular structures, called balloon dystrophy. Ethylene glycol and its decay products are reabsorbed by the epithelial cells of the renal tubules, a large vacuole is formed in them, which displaces the cell organelles together with the nucleus to the basal regions. Such dystrophy, as a rule, ends with colliquat necrosis and complete loss of the function of the affected tubules. Sequestration of the damaged part of the cell together with the vacuole is also possible, and the preserved basal sections with the pushed out nucleus can be a source of regeneration.

Poisoning dichloroethane, less often chloroform, accompanied fatty degeneration nephrocytes (acute lipid nephrosis) of the proximal, distal tubules and the loop of Henle. These poisons have a direct toxic effect on the cytoplasm, changing the ratio of protein-lipid complexes in it, which is accompanied by inhibition of reabsorption in the tubules.

Reabsorption of protein pigment aggregates (hemoglobin, myoglobin) epithelial cells of the proximal and distal tubules causes hyalino-droplet dystrophy. Pigment proteins filtered through the glomerular filter move along the tubule and are gradually deposited on the brush border in the proximal tubules, partially reabsorbed by nephrocytes. The accumulation of pigment granules in epithelial cells is accompanied by partial destruction of the apical sections of the cytoplasm and their sequestration into the lumen of the tubules along with the brush border, where granular and lumpy pigment cylinders are formed. The process unfolds over 3-7 days. During this period, non-reabsorbed pigment masses in the lumen of the tubules become denser, move into the loop of Henle and the distal tubules. In the apical sections of epithelial cells overloaded with pigment granules, partial necrosis occurs. Separate pigment granules are converted into ferritin and remain in the cytoplasm for a long time.

Nephrotoxicity aminoglycosides(kanamycin, gentamicin, monomycin, neomycin, tobarmycin, etc.) is associated with the presence in their molecules of free amino groups in the side chains. Aminoglycosides are not metabolized in the body, and 99% of them are excreted unchanged in the urine. Filtered aminoglycosides are fixed on the apical membrane of the cells of the proximal tubules and the loop of Henle, bind to vesicles, are absorbed by pinocytosis, and are sequestered in the lysosomes of the tubular epithelium. At the same time, the concentration of the drug in the cortical substance becomes higher than in plasma. Damage to the kidneys by aminoglycosides is characterized by an increase in anionic phospholipids in the membranes, in particular, phosphatidylinositol, damage to mitochondrial membranes, accompanied by a loss of intracellular potassium and magnesium, impaired oxidative phosphorylation and energy deficiency. The combination of these changes leads to necrosis of the tubular epithelium.

Characteristically, the ions prevent the fixation of aminoglycosides on the brush border and thus reduce their nephrotoxicity. It was noted that the tubular epithelium, regenerating after damage by aminoglycosides, becomes resistant to the toxic effects of these drugs.

Therapy osmotic diuretins(solutions of glucose, urea, dextrans, mannitol, etc.) can be complicated by hydropic and vacuolar degeneration of nephrocytes. At the same time, the osmotic gradient of fluids on both sides of the tubular cell changes in the proximal tubules - blood washing the tubules and provisional urine. Therefore, it is possible for water to move into tubular epithelial cells from peritubular capillaries or from provisional urine. Hydropia of epithelial cells with the use of osmotic diuretins persists for a long time and, as a rule, is associated with partial reabsorption of osmotically active substances and their retention in the cytoplasm. Water retention in the cell dramatically reduces its energy potential and functionality. Thus, osmotic nephrosis is not the cause of acute renal failure, but an undesirable effect of its treatment or a consequence of replenishment of energy substrates in the body. parenteral administration hypertonic solutions.

The composition of urine in renal acute renal failure is similar in composition to the glomerular filtrate: low specific gravity, low osmolarity. The content in the urine is increased due to a violation of its reabsorption.

Postrenal acute renal failure occurs due to a violation of the outflow of urine through the urinary tract as a result of the following disorders:

occlusion of the urinary tract with stones or blood clots;

obstruction of the ureters or ureter by a tumor located outside the urinary tract;

Violation of the outflow of urine is accompanied by overstretching of the urinary tract (ureters, pelvis, calyces, collecting ducts, tubules) and the inclusion of the reflux system. Backflow of urine from the urinary tract into the interstitial space of the renal parenchyma occurs (pyelorenal reflux). But pronounced edema is not observed due to the outflow of fluid through the system of venous and lymphatic vessels. (pyelovenous reflux). Therefore, the intensity of hydrostatic pressure on the tubules and glomerulus is very moderate, and filtration is reduced slightly. There are no pronounced disorders of the peritubular blood flow and, despite anuria, renal function is preserved. After removing the obstruction to the outflow of urine, diuresis is restored. If the duration of occlusion does not exceed three days, the phenomena of acute renal failure after the restoration of the patency of the urinary tract quickly disappear.

With prolonged occlusion and high hydrostatic pressure, filtration and peritubular blood flow are disturbed. These changes, combined with persistent refluxes, contribute to the development of interstitial edema and tubular necrosis.

Clinical course of acute renal failure has a certain regularity and staging, regardless of the cause that caused it.

1st stage- short in duration and ends after the termination of the factor;

2nd stage - the period of oligoanuria (the volume of urine excreted does not exceed 500 ml / day), azotemia; in case of prolonged oliguria (up to 4 weeks) sharply increases the likelihood of cortical necrosis;

3rd stage- period of polyuria - restoration of diuresis with a phase of polyuria (the volume of urine excreted exceeds 1800 ml / day);

4th stage- restoration of kidney function. Clinically, the 2nd stage is the most difficult.

Extracellular and intracellular hyperhydration, non-gas excretory renal acidosis develops (depending on the localization of tubular damage, acidosis of the 1st, 2nd, 3rd types is possible). The first sign of overhydration is shortness of breath due to interstitial or cardiogenic pulmonary edema. A little later, the fluid begins to accumulate in the cavities, hydrothorax, ascites, and edema occur. lower extremities and in the lumbar region. This is accompanied by pronounced changes in blood biochemical parameters: azotemia (the content of creatinine, urea, uric acid is increased), hyperkalemia, hyponatremia, hypochloremia, hypermagnesemia, hyperphosphatemia.

The level of blood creatinine rises regardless of the nature of the patient's diet and the intensity of protein breakdown. Therefore, the degree of creatinemia gives an idea of the severity of the course and prognosis in acute renal failure. The degree of catabolism and necrosis of muscle tissue reflects hyperuricemia.

Hyperkalemia occurs as a result of a decrease in potassium excretion, an increased release of potassium from cells, and developing renal acidosis. Hyperkalemia 7.6 mmol/l is clinically manifested by disorders heart rate up to a complete cardiac arrest; hyporeflexia occurs, muscle excitability decreases with subsequent development of muscle paralysis.

Electrocardiographic indicators in hyperkalemia: T wave - high, narrow, ST line merges with T wave; disappearance of the P wave; widening of the QRS complex.

Hyperphosphatemia is caused by impaired phosphate excretion. The origin of hypocalcemia remains unclear. As a rule, shifts in phosphorus-calcium homeostasis are asymptomatic. But with the rapid correction of acidosis in patients with hypocalcemia, tetany and seizures may occur. Hyponatremia is associated with water retention or excess water intake. There is no absolute sodium deficiency in the body. Hypersulfatemia, hypermagnesemia, as a rule, are asymptomatic.

Within a few days, anemia develops, the genesis of which is explained by hyperhydration, hemolysis of erythrocytes, bleeding, inhibition of erythropoietin production by toxins circulating in the blood. Usually anemia is combined with thrombocytopenia.

The second stage is characterized by the appearance of signs of uremia, while symptoms from the gastrointestinal tract (lack of appetite, nausea, vomiting, flatulence, diarrhea) predominate.

With the appointment of antibiotics at the beginning, the symptoms of diarrhea increase. Subsequently, diarrhea is replaced by constipation due to severe intestinal hypokinesia. In 10% of cases, gastrointestinal bleeding (erosion, ulcers of the gastrointestinal tract, bleeding disorders) is observed.

Timely prescribed therapy prevents the development of coma, uremic pericarditis.

During the oliguric stage (9-11 days), the urine is dark in color, proteinuria and cylindruria are pronounced, natriuria does not exceed 50 mmol / l, urine osmolarity corresponds to plasma osmolarity. In 10% of patients with acute drug-induced interstitial nephritis, diuresis is preserved.

3rd stage characterized by the restoration of diuresis by the 12-15th day from the onset of the disease and polyuria (more than 2 l / day), which persists for 3-4 weeks. The genesis of polyuria is explained by the restoration of the filtration function of the kidneys and the insufficient concentration function of the tubules. In the polyuric stage, the body is unloaded from the fluid accumulated during the period of oliguria. Secondary dehydration, hypokalemia and hyponatremia are possible. The severity of proteinuria is reduced.

Differential diagnosis of prerenal and renal acute renal failure

Acute renal failure (ARF) is a sudden impairment of the functions of both kidneys, caused by a decrease in renal blood flow and a slowdown in the processes of glomerular filtration and tubular reabsorption. As a result, there is a delay or complete cessation of the excretion of toxic substances from the body and a disorder of the acid-base, electrolyte and water balance.

With proper and timely treatment, these pathological changes are reversible. According to medical statistics, cases of acute renal failure are recorded annually in approximately 200 people per 1 million.

Forms and causes of acute renal failure

Depending on what processes led to the onset of acute renal failure, prerenal, renal and postrenal forms are distinguished.

Prerenal form of acute renal failure

The prerenal form of acute renal failure is characterized by a significant reduction in renal blood flow and a decrease in glomerular filtration rate. Such disorders in the work of the kidneys are associated with a general decrease in the volume of circulating blood in the body. If the normal blood supply to the organ is not restored as soon as possible, ischemia or necrosis of the renal tissue is possible. The main reasons for the development of prerenal acute renal failure are:

decrease in cardiac output;
pulmonary embolism;
operations and injuries accompanied by significant blood loss;
extensive burns;
dehydration caused by diarrhea, vomiting;
taking diuretics;
sudden decrease in vascular tone.

Renal form of acute renal failure

In the renal form of acute renal failure, damage to the kidney parenchyma is observed. It can be caused by inflammatory processes, toxic effects, or pathologies of the kidney vessels, which lead to insufficient blood supply to the organ. Renal acute renal failure is a consequence of necrosis of the epithelial cells of the tubules of the kidneys. As a result, there is a violation of the integrity of the tubules and the release of their contents into the surrounding tissues of the kidney. The following factors can lead to the development of the renal form of acute renal failure:

intoxication with various poisons, drugs, radiopaque compounds, heavy metals, snake or insect bites, etc.;
kidney disease: interstitial nephritis, acute pyelonephritis and glomerulonephritis;
damage to the renal vessels (thrombosis, aneurysm, atherosclerosis, vasculitis, etc.);
kidney injury.

Important: Long-term use of drugs that have a nephro toxic effect, without prior consultation with a doctor, can cause acute renal failure.

Postrenal acute renal failure

Postrenal acute renal failure develops as a result of an acute violation of the passage of urine. With this form of acute renal failure, kidney function is preserved, but the process of urination is difficult. Ischemia of the renal tissue may occur, as the pelvis overflowing with urine begins to compress the surrounding tissues of the kidney. Causes of postrenal AKI include:

spasm of the sphincter of the bladder;
blockage of the ureters due to urolithiasis;
tumors of the bladder, prostate, urinary canals, pelvic organs;
injuries and hematomas;
inflammatory diseases of the ureters or bladder.

Stages and symptoms of acute renal failure

The characteristic symptoms of acute renal failure develop very quickly. There is a sharp deterioration in the general condition of the patient and impaired renal function. In the clinical picture of acute renal failure, stages are distinguished, each of which is characterized by certain signs:

initial stage;
stage of oligoanuria;
stage of polyuria;
recovery stage.

In the first stage of acute renal failure, the symptoms are determined by the cause of the disease. These may be signs of intoxication, shock, or manifestations of some kind of disease. So, with an infectious lesion of the kidneys, fever, headache, muscle weakness are noted. When intestinal infection there is vomiting and diarrhea. For toxic damage to the kidneys, manifestations of jaundice, anemia, and convulsions are possible. If the cause of acute renal failure is acute glomerulonephritis, then there is a discharge of urine mixed with blood and pain in the lumbar region. The first stage of acute renal failure is characterized by a decrease in blood pressure, pallor, rapid pulse, a slight decrease in diuresis (up to 10%).
The stage of oligoanuria in acute renal failure is the most severe and poses the greatest danger to the patient's life. It is characterized by the following symptoms:

a sharp decrease or cessation of urine output;
intoxication with products of nitrogen metabolism, manifested in the form of nausea, vomiting, itching of the skin, increased respiration, loss of appetite, tachycardia;
increased blood pressure;
confusion and loss of consciousness, coma;
swelling of the subcutaneous tissue, internal organs and cavities;
weight gain due to the presence of excess fluid in the body;
general severe condition.

The further course of acute renal failure is determined by the success of the therapy at the second stage. With a favorable outcome, the stage of polyuria and subsequent recovery occurs. First, there is a gradual increase in diuresis, and then polyuria develops. Excess fluid is removed from the body, swelling is reduced, the blood is cleared of toxic products. The polyuric stage can be dangerous due to the occurrence of dehydration and electrolyte imbalances (eg, hypokalemia). After about a month, diuresis returns to normal and a recovery period begins, which can last up to 1 year.

If the treatment was chosen incorrectly or carried out too late and turned out to be ineffective, then the terminal stage of acute renal failure develops with a high probability of death. She is characterized by:

shortness of breath, cough, caused by the accumulation of fluid in the lungs;
secretion of sputum with an admixture of blood;
subcutaneous hemorrhages and internal bleeding;
loss of consciousness, coma;
muscle spasms and cramps;
severe cardiac arrhythmias.

Tip: If you find even a slight decrease in diuresis, especially if kidney disease or other pathologies are present, you should immediately contact a nephrologist. Such violations may be the beginning of the development of acute renal failure.

OPN diagnostics

In acute renal failure, the diagnosis of the disease is carried out using both laboratory and instrumental methods. AT laboratory tests the following deviations from the norm are present:

a general blood test is characterized by a decrease in the level of hemoglobin, an increase in the concentration of leukocytes, an increase in ESR;
in general analysis urine reveals protein, cylinders, decreased density, increased content of erythrocytes and leukocytes, decreased platelet count;
daily urine analysis is characterized by a significant decrease in diuresis;
in biochemical analysis blood is detected elevated level creatinine and urea, as well as an increase in the concentration of potassium and a decrease in the concentration of sodium and calcium.

Of the instrumental diagnostic methods used:

ECG is used to monitor the work of the heart, which may be impaired due to hyperkalemia;
Ultrasound, allows you to assess the size of the kidneys, the level of blood supply and the presence of obstruction;
kidney biopsy;
radiography of the lungs and heart.

Treatment and emergency care for acute renal failure

For acute renal failure urgent care is to quickly deliver a person to a hospital hospital. In this case, the patient needs to provide a state of rest, warmth and horizontal position body. It's best to call ambulance, as in this case, qualified doctors will be able to take all necessary measures right on the spot.

In acute renal failure, treatment is carried out taking into account the stage of the disease and the cause of its cause. After elimination of the etiological factor, it is necessary to restore homeostasis and excretory function of the kidneys. Depending on the cause of acute renal failure, you may need:

taking antibiotics for infectious diseases;
replenishment of fluid volume (with a decrease in circulating blood volume);
use of diuretics and fluid restriction to reduce swelling and increase urine production;
taking heart medications in violation of the work of the heart;
taking drugs to lower blood pressure in case of its increase;
surgery to restore kidney tissue damaged as a result of trauma or to remove obstacles that interfere with the outflow of urine;
taking drugs to improve blood supply and blood flow in the nephrons;
detoxification of the body in case of poisoning (gastric lavage, administration of antidotes, etc.).

To remove toxic products from the blood, hemodialysis, plasmapheresis, peritoneal dialysis, and hemosorption are used. Acid-base and water-electrolyte balance is restored by introducing saline solutions of potassium, sodium, calcium, etc. These procedures are used temporarily until renal function is restored. With timely treatment of acute renal failure has a favorable prognosis.

But perhaps it is more correct to treat not the consequence, but the cause?

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Forms and causes of acute renal failure

Depending on what processes led to the onset of acute renal failure, prerenal, renal and postrenal forms are distinguished.

Prerenal form of acute renal failure

decrease in cardiac output;
pulmonary embolism;
operations and injuries accompanied by significant blood loss;
extensive burns;
dehydration caused by diarrhea, vomiting;
taking diuretics;
sudden decrease in vascular tone.

Renal form of acute renal failure

intoxication with various poisons, drugs, radiopaque compounds, heavy metals, snake or insect bites, etc.;
kidney disease: interstitial nephritis, acute pyelonephritis and glomerulonephritis;
damage to the renal vessels (thrombosis, aneurysm, atherosclerosis, vasculitis, etc.);
kidney injury.

Antibiotics, sulfonamides, aminoglycosides, antitumor agents, have a toxic effect on the kidneys

Important: Long-term use of drugs that have a nephrotoxic effect, without prior consultation with a doctor, can cause acute renal failure.

Postrenal acute renal failure

spasm of the sphincter of the bladder;
blockage of the ureters due to urolithiasis;
tumors of the bladder, prostate, urinary canals, pelvic organs;
injuries and hematomas;
inflammatory diseases of the ureters or bladder.

Stages and symptoms of acute renal failure

initial stage;
stage of oligoanuria;
stage of polyuria;
recovery stage.

In the first stage of acute renal failure, the symptoms are determined by the cause of the disease. These may be signs of intoxication, shock, or manifestations of some kind of disease. So, with an infectious lesion of the kidneys, fever, headache, muscle weakness are noted. In the case of an intestinal infection, vomiting and diarrhea are present. For toxic damage to the kidneys, manifestations of jaundice, anemia, and convulsions are possible. If the cause of acute renal failure is acute glomerulonephritis, then there is a discharge of urine mixed with blood and pain in the lumbar region. The first stage of acute renal failure is characterized by a decrease in blood pressure, pallor, rapid pulse, a slight decrease in diuresis (up to 10%).
The stage of oligoanuria in acute renal failure is the most severe and poses the greatest danger to the patient's life. It is characterized by the following symptoms:

a sharp decrease or cessation of urine output;
intoxication with products of nitrogen metabolism, manifested in the form of nausea, vomiting, itching of the skin, increased respiration, loss of appetite, tachycardia;
increased blood pressure;
confusion and loss of consciousness, coma;
swelling of the subcutaneous tissue, internal organs and cavities;
weight gain due to the presence of excess fluid in the body;
general severe condition.

shortness of breath, cough, caused by the accumulation of fluid in the lungs;
secretion of sputum with an admixture of blood;
subcutaneous hemorrhages and internal bleeding;
loss of consciousness, coma;
muscle spasms and cramps;
severe cardiac arrhythmias.

Tip: If you find even a slight decrease in diuresis, especially if kidney disease or other pathologies are present, you should immediately contact a nephrologist. Such violations may be the beginning of the development of acute renal failure.

OPN diagnostics

In acute renal failure, the diagnosis of the disease is carried out using both laboratory and instrumental methods. In laboratory tests, the following deviations from the norm are present:

a general blood test is characterized by a decrease in the level of hemoglobin, an increase in the concentration of leukocytes, an increase in ESR;
in the general analysis of urine, protein, cylinders, a decrease in density, an increased content of erythrocytes and leukocytes, a decrease in the level of platelets are found;
daily urine analysis is characterized by a significant decrease in diuresis;
in a biochemical blood test, an increased level of creatinine and urea is detected, as well as an increase in the concentration of potassium and a decrease in the concentration of sodium and calcium.

Urinalysis can detect kidney dysfunction

Of the instrumental diagnostic methods used:

ECG is used to monitor the work of the heart, which may be impaired due to hyperkalemia;
Ultrasound, allows you to assess the size of the kidneys, the level of blood supply and the presence of obstruction;
kidney biopsy;
radiography of the lungs and heart.

Treatment and emergency care for acute renal failure

In acute renal failure, emergency care consists in the rapid delivery of a person to a hospital hospital. In this case, the patient needs to provide a state of rest, warmth and a horizontal position of the body. It is best to call an ambulance, as in this case, qualified doctors will be able to take all necessary measures right on the spot.

In severe condition in case of acute renal failure, the patient must be taken to the hospital

taking antibiotics for infectious diseases;
replenishment of fluid volume (with a decrease in circulating blood volume);
use of diuretics and fluid restriction to reduce swelling and increase urine production;
taking heart medications in violation of the work of the heart;
taking drugs to lower blood pressure in case of its increase;
surgery to restore kidney tissue damaged as a result of trauma or to remove obstacles that interfere with the outflow of urine;
taking drugs to improve blood supply and blood flow in the nephrons;
detoxification of the body in case of poisoning (gastric lavage, administration of antidotes, etc.).

Modern methods of treatment of acute renal failure
Modern methods of treatment of acute renal failure

Acute renal failure (ARF)

Acute renal failure(ARF) is a clinical and biochemical syndrome characterized by a rapid decrease in the predominantly excretory function of the kidneys (within hours or days), which is clinically manifested by a decrease in glomerular filtration rate, an increase in the content of nitrogenous metabolites in the blood, changes in the volume of extracellular fluid, acid-base and electrolyte disorders. homeostasis.

Classification. Depending on the causes and mechanisms of development, prerenal, renal and postrenal acute renal failure is considered.
In addition, acute renal failure is often divided into oliguric and neoliguric, and four periods are distinguished during oliguric acute renal failure: the period of initial manifestations ( clinical picture There is no acute renal failure as such, the clinic is determined by the condition that leads to acute renal failure), the period of anurioliguria, the period of polyuria, the period of recovery.
However, such a clear periodization can usually be observed only in acute tubular necrosis (ATN).

Etiology. OTN dominates - 45%; prerenal cases account for 21%; ARF developing against the background of existing CRF (“ARC on CRF”) - 13%; obstruction of the urinary tract - 10%; parenchymal diseases of the kidneys - 4.5%; OTIN - 1.6%. share vascular pathology is only 1%.

Causes of prerenal acute renal failure:
- conditions associated with a decrease in extracellular fluid volume (ECV);
- hypovolemia (renal fluid loss - diuretics, osmotic diuresis in diabetes, adrenal insufficiency; losses through the gastrointestinal tract and skin, as well as blood loss of any etiology; redistribution of fluid into the abdominal cavity with hepatopathy, NS, hypoalbuminemia of other etiologies, intestinal obstruction, pancreatitis, peritonitis) ;
- decrease in cardiac output (severe heart failure, cardiogenic shock, heart valve damage, myocardial pathology, arrhythmias, pulmonary embolism, pericardial tamponade, etc.);
- violation of the ratio between systemic and renal vascular resistance in arterial hypotension, sepsis, hypoxemia, anaphylaxis, treatment of IL 2 and IFN, ovarian hyperstimulation syndrome; renal vasoconstriction, blockade of prostaglandin synthesis, hypercalcemia;
- hypoperfusion of the kidneys due to impaired renal vascular autoregulation due to excessive dilatation of the efferent arteriole when using ACE inhibitors, blockers of AT1 angiotensin II receptors (A II); - syndrome of increased blood viscosity (myeloma, macroglobulinemia, polycythemia).

Causes of renal acute renal failure:
- acute tubular necrosis in violation of hemodynamics (cardiovascular surgery, sepsis), toxic effects of antibiotics, iodine-containing radiopaque drugs, anesthetics, immunosuppressants and cytostatics, mercury-containing drugs, snake venom;
- myoglobin rhabdomyolysis: muscle injury, infections, polymyositis, metabolic disorders, hyperosmolar coma, diabetic ketoadiosis, severe hyperkalemia, hypernatremia, hyponatremia, hypophosphatemia, hyperthyroidism, high hyperthermia, exposure to ethylene glycol, CO, mercury chloride, medication (fibrates, statins, opioids, amphetamine), congenital diseases (muscular dystrophy, carnitine deficiency, McArdle's disease)
- hemolysis and hemoglobinuria: malaria, mechanical destruction of erythrocytes in extracorporeal circulations or metal prostheses, post-transfusion reactions, hemolysis of other etiologies, heat stroke, burns, glucose-6-phosphate dehydrogenase deficiency and other erythrocyte fermentopathies, Marchiafava-Micheli syndrome, influence organic matter(aniline, phenol, quinine, glycerol, benzene, phenol, hydralazine), insect poisons;
- acute tubulointerstitial nephritis: allergic (when taking p-lactams, trimethoprim, sulfonamides, cyclooxygenase inhibitors, diuretics, captopril, rifampicin); infectious (bacterial - acute pyelonephritis, leptospirosis, etc.; viral, fungal); with leukemia, lymphomas, sarcoidosis; idiopathic;
- violations of vascular patency (bilateral stenosis of the renal artery due to thrombosis / embolism, thrombosis of the renal veins; atheroembolism, thrombotic microangiopathy, hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, postpartum thrombosis, APS, DIC, scleroderma, PAH, post-radiation lesions, vasculitis);
- glomerulopathies: AGN, RPGN (ANCA-associated vasculitis, low immune GN), IgA nephropathy, MzPGN, lupus nephritis, Shenlein-Henoch disease, mixed cryoglobu lineemia, Goodpasture's disease;
- cortical necrosis, abruptio placentae, septic abortion, DIC.

Causes of postrenal acute renal failure:
- obstruction of the ureters: urolithiasis disease, thrombi, papillary necrosis, tumors, compression from the outside (tumors, retroperitoneal fibrosis), ureterocele, iatrogenic ligation of the ureter;
- bladder obstruction: neurogenic bladder, benign prostatic hyperplasia, urolithiasis, blood clots, tumors, bladder diverticulosis;
- urethral obstruction: phimosis, urethral stricture, congenital urethral valves.

clinical picture. Clinically, acute renal failure can manifest itself in several ways:
1. Latent (neoliguric acute renal failure) - characterized only by laboratory changes (azotemia and decreased GFR), but the volume of urine in patients does not decrease.
The content of creatinine (Cgr) and urea nitrogen (Ur) in blood serum are traditionally the most accessible indicators in clinical practice, which are markers of a decrease in GFR and, thus, allow assessing the functional state of the kidneys.
Cgr correlates more reliably with the level of GFR. However, it should be remembered that an increase in Cgr is not always associated with the development of PI.
This applies to cases of massive intake of creatinine from damaged striated muscles with various options rhabdo myolysis and blockade of its tubular secretion by trimethoprim and cimetidine. In most cases, the concentrations of creatinine and urea in the blood increase as the GFR falls, proportionally, approximately in a ratio of 1:60 (in mmol / l).

A disproportionate increase in serum urea can be observed with a decrease in urine flow in the distal nephron in cases of prerenal acute renal failure or postrenal urinary tract obstruction. In addition, fever, the use of corticosteroids and tetracycline, as well as excess consumption squirrel.

Neoliguric are from 20-30% to half of cases of acute renal failure.
The neoliguric variant is more common with the use of aminoglycosides and radiopaque drugs, although it can develop with an acute decrease in renal function of any etiology.
Neoliguric acute renal failure has a more favorable course and prognosis, since it is associated with less pronounced morphological and functional changes in the renal tissue.
In these patients, GFR is 2-3 times higher, the severity of azotemia is less than in oliguric patients.
Naturally, the need for RRT in non-oliguric patients is much lower.

2. Oligo- and anuria.
Oliguria - a decrease in the volume of daily urine less than 400 ml.
The development of oliguria indicates either the shutdown of most of the glomeruli, or an extremely pronounced decrease in GFR in each of them.
Anuria is determined by a decrease in diuresis less than 50 ml / day.
The development of this symptom is most often associated with complete obstruction of the urinary tract, as well as rapidly progressive glomerulonephritis, cortical necrosis and renal infarction. Alternating oliguria and polyuria suggests partial urinary obstruction.

3. The predominance of clinical symptoms of the underlying disease that caused acute renal failure. The polyetiology of acute renal failure suggests the presence of symptoms of the disease that caused this condition in addition to clinical signs of reduced kidney function.

4. Expanded PI (uremia, anemia, dyselectrolytemia, metabolic acidosis). The severity of the clinical symptoms of the uremic syndrome and related conditions, reflecting a violation of the partial functions of the kidneys, depends on the time of detection of acute renal failure, the speed of its development, the cause and residual function. Usually pronounced azotemia and uremia reflect the fact of delayed diagnosis of acute renal failure and are associated with an unfavorable prognosis.

Uremic symptoms include: appearance skin itching, nausea, vomiting, disorders of the central nervous system, up to a coma, the development of pleurisy and pericarditis. Uremia is usually accompanied by the development of anemia, metabolic acidosis, electrolyte disorders (hyperkalemia, hyperphosphatemia, more often moderate hypocalcemia and hyponatremia, less often hypercalcemia and hypernatremia), overhydration (especially with a decrease in diuresis).
However, these complications in one combination or another may also occur in other clinical variants of acute renal failure. Each of these conditions requires observation and timely correction.

Diagnostics.
In the diagnosis of acute renal failure, it is important to observe several principles - timeliness, urgency and consistency, which is of great practical importance.
Early diagnosis of any variant of acute renal failure allows you to start timely conservative treatment, prevent the development of severe uremia and its complications, the need for RRT, prevent or reduce damage to the renal tissue and improve the immediate and long-term prognosis. Therefore, when monitoring patients belonging to risk groups, screening studies should be carried out regularly in relation to indicators of the functional state of the kidneys - control of diuresis, urinalysis, determination of Cgr and urea in the blood serum, parameters of the CBS of blood, ultrasound of the kidneys.

In practical work, each case of acute renal failure requires the fastest possible determination of the type of acute renal failure, its etiology.
It must be borne in mind that untimely diagnosis of prerenal acute renal failure is fraught with the formation of renal.
Early diagnosis of postrenal acute renal failure allows timely minimization of urinary tract obstruction by surgical methods.

The main stages in the diagnosis of acute renal failure in detecting a decrease in GFR and / or azotemia:
1. Confirmation of azotemia, decrease in GFR, i.e. PN.
2. Differential diagnosis of acute renal failure and chronic renal failure.
3. Conducting differential diagnosis of pre- and postrenal acute renal failure.
When determining prerenal acute renal failure, correct hypovolemia and systemic hemodynamics as quickly as possible. If postrenal acute renal failure is detected, eliminate urinary tract obstruction.
4. If pre- and postrenal acute renal failure is excluded, clarify the etiology of renal acute renal failure (renal vascular pathology, tubular necrosis, cortical necrosis, ATIN, glomerulopathy).
At each stage of diagnosis, it is necessary to resolve the issue of indications for replacement renal therapy(RT).

Diagnosis of prerenal acute renal failure
Prerenal azotemia should first be suspected in the presence of conditions that can lead to hypovolemia and associated clinical symptoms.
Of great importance at this stage is the correct interpretation of urine tests. Normal analyzes or minor changes in the first place suggest the presence of prerenal acute renal failure, while proteinuria, changes in the cellular composition of urine, cylindruria make one think of a true renal pathology.
At this stage of diagnosis, it is advisable to determine the renal indices, which can be of great help in distinguishing between variants of acute renal failure, and primarily prerenal acute renal failure and ARF.
In most patients with prerenal acute renal failure, the ratio of Ur/Cr in the blood serum is increased to more than 60:1. Fractional excretion of sodium (EF Na) and urinary sodium concentration (U Na) are reduced, respectively.< 1 % и < 20 ммоль/л.
The EF Na indicator has sufficient sensitivity and specificity for the diagnosis of prerenal acute renal failure.
However, it should be remembered that decreased EF Na can also occur in cases of ATN in immune glomerulopathies, in the initial stages (first hours) of urinary tract obstruction, in ATN, which complicates the use of radiopaque agents.
In one fifth of patients with ATN and non-oliguric form of AKI, the excreted sodium fraction also remains low (< 1%).
The value of EF Na will be increased with the development of prerenal acute renal failure against the background of pre-existing CKD or with the use of loop diuretics.

In these cases, the final diagnosis of acute renal failure is established ex juvantibus (significant improvement in the nitrogen excretion function of the kidneys after correction of hypovolemia).
In patients with chronic renal failure, the adaptive capacity of the kidneys to developed hypovolemia is reduced due to pronounced tubulointerstitial changes.
Finally, EF Na in patients with prerenal AKI may increase in situations of osmotic diuresis, for example, when diabetic ketoacidosis or intravenous glucose.
In these cases, determining the concentration of chlorine in the urine (U Q) can provide more significant diagnostic information.

Thus, in a significant proportion of patients at the stage of diagnosing prerenal acute renal failure, symptoms of absolute or relative hypovolemia can be detected and, accordingly, a preliminary diagnosis can be established.
In this case, it is necessary to immediately begin conservative treatment aimed at correcting the BCC, stabilizing blood pressure, and increasing cardiac output (CO).
Timely initiation of therapy, on the one hand, has a diagnostic value, since fast recovery diuresis and a decrease in azotemia against the background of this treatment, undoubtedly, testifies in favor of prerenal acute renal failure.
On the other hand, restoration or improvement of renal perfusion reduces the risk of ischemic changes in the renal tissue and may prevent the development of ATN.

Diagnosis of variants of renal acute renal failure
The main variants of true renal acute renal failure.
Acute tubular necrosis.
Prerenal AKI and ischemic OTN have common mechanisms of development and are considered different stages of the same process.
Ischemic ATN should be considered in the presence of signs of systemic hemodynamic disturbance and hypovolemia. In contrast to prerenal acute renal failure, in the case of deeper ischemia of the kidney tissue or its longer exposure, leading to the development of tubular necrosis, after the correction of systemic hemodynamics, there is no improvement in the indicators of the functional state of the kidneys.
The development of ATN may be associated with damage to the tubules by exogenous and endogenous nephrotoxic effects. Most common causes the last ones are medicines.

In the diagnosis of this variant of acute renal failure, it is important to determine the relationship between the development of acute renal failure, the time of taking the drug, the duration, the total dose, and the achievement of a critical concentration in the blood. Acute tubulointerstitial nephritis.

This variant of renal acute renal failure in the vast majority of cases occurs against the background of the use of a number of drugs.
The course of the disease is often accompanied by systemic symptoms of allergy - hyperthermia, arthralgia, erythema.
Laboratory findings indicate eosinophilia in the blood.

An important sign of ATIN of drug etiology is an increase in the content of eosinophils in the urine.
It should be noted that the development of ATN is also associated with drug-induced kidney injury, the treatment of which differs from the treatment of drug-induced ATIN.
Therefore, if it is not possible to conduct a differential diagnosis between these conditions, it is advisable to conduct a morphological study of the renal tissue.
Thus, a kidney biopsy is indicated in any case of renal ARF with an unexplained etiology.
Diagnosis of ATIN should also be associated with the search for other etiological factors - infections, blood diseases, SLE, kidney transplant rejection in patients with a transplanted kidney. Glomerulopathy as a cause of acute renal failure.

A number of diseases of the renal glomeruli can lead to the development of acute renal failure.
Suspicion of this form of acute renal failure should arise when changes characteristic of glomerular pathology are detected. Examination of such patients should include a number of parameters to clarify the specific disease that is the direct culprit of glomerular lesions. In vasculitis with glomerulopathies, it is necessary to investigate antinuclear factor, ANCA, AT to GBM, LE cells, blood cultures, complement, cryoglobulins, rheumatoid factor, form 50, HbsAg, anti-HCV.
With plasma cell dyscrasias - light chains of immunoglobulins, Ben-Jones protein, proteinogram.

When establishing the diagnosis of acute renal failure against the background of glomerular diseases or vasculitis, for the final diagnosis, an urgent kidney biopsy is necessary, indications for which in acute renal failure are: gradual onset, absence of an obvious external cause, proteinuria more than 1 g / day, hematuria, systemic clinical manifestations, a long period of oliguria / anuria (10-14 days).
In this case, a morphological study of the renal tissue is necessary first of all, to exclude variants of RPGN.
Timely diagnosis and immunosuppressive therapy of this renal pathology can significantly delay the development of CRF.
Empiric immunosuppressive therapy may be prescribed in case of reasonable suspicion of RPGN and in the absence of the possibility of performing a morphological study or contraindications to a kidney biopsy.

Occlusion of the vessels of the kidneys.
Diagnosis of bilateral occlusion of large renal vessels (arteries and veins) requires the inclusion of dopplerography of renal vessels as a screening method in the examination program for a patient with acute renal failure.
The final diagnosis is established after angiography.

Diseases of small vessels that can lead to acute renal failure (see etiology) require appropriate diagnostics, which is described in the relevant sections of the site and numerous manuals.

Cortical necrosis is due to severe damage to the glomeruli and tubules.
It develops rarely and is mainly associated with obstetric pathology - placental abruption.
This condition can also complicate the course of sepsis and DIC.
Cortical necrosis can be suspected with the development of persistent anuria. Confirmation in the acute period can only be obtained by morphological examination.
Clinically, the diagnosis can be established retrospectively, in the absence of resolution of the alleged
OTN for 1-1.5 months.

Diagnosis of postrenal acute renal failure.
Urinary tract obstruction should be suspected in the presence of nocturia, calculi, signs of UTI, bladder tumors, prostate tumors, abdominal masses, symptoms renal colic, pain in the suprapubic region.

For screening detection of possible urinary tract obstruction with the development of acute renal failure, in most cases, ultrasound of the kidneys and bladder is sufficient.
In the absence of typical signs of expansion of the pelvicalyceal system in cases suspected of postrenal AKI, it is necessary to perform a second ultrasound of the kidneys after 24 hours.

In each specific case, especially if obstructive acute renal failure is suspected against the background of oncological pathology, computed tomography or magnetic resonance imaging can provide useful information about the state of the urinary tract. resonance imaging. The use of radiological methods to detect obstruction (dynamic scintigraphy) is justified if the renal blood flow is relatively preserved, as can be seen with the help of renal Doppler sonography.

Diagnostic methods with parenteral administration of X-ray contrast agents should not be used, as they may have an additional nephrotoxic effect.
It should be emphasized that with continued uncertainty regarding urinary tract obstruction and the need for additional research, the diagnosis and exclusion of other variants of AKI should not be suspended.

Treatment. Therapy for prerenal acute renal failure depends on the cause of acute renal failure - hypovolemia, low CO, a decrease in peripheral vascular resistance.
BCC reduction correction. Isotonic NaCl is the treatment of choice for most patients with significant hypovolemia resulting in prerenal AKI.
However, large volumes of intravenous NaCl can lead to the development of hyperchloremic metabolic acidosis, especially in patients with preserved diuresis and defecation (due to loss of bicarbonate).
Therefore, with a tendency to hyperchloremic metabolic acidosis, infusion therapy should be started with lactate Ringer's solution, since lactate itself is metabolized in the liver to bicarbonate and allows you to control the development / progression of acidosis.

Another alternative to saline may be a hypotonic NaCl solution with added bicarbonate (eg 0.25-0.45% NaCl + 50-100 mEq sodium bicarbonate).

In conditions of a slight deficiency of BCC and with the development of hypernatremia, a hypotonic NaCl solution should be used.
Hypertonic solutions of NaCl are used for acute renal failure on the background of traumatic injury or burns, since small volumes of this drug can cause a significant increase in BCC due to the active movement of water from the extracellular to the intravascular space. It should be emphasized that, unlike crystalloids, colloidal solutions, including hydroxyethyl starch (HES), dextrans, and gelatins, are not recommended for use in prerenal AKI.
Despite their effectiveness in the treatment of hypovolemia, the concomitant significant increase in colloid osmotic (oncotic) blood pressure can lead to a further drop in GFR.

In the case of the development of pre-ARF against the background of acute hemorrhagic shock, the treatment of hypovolemia, of course, should begin with the introduction of blood products. If the latter are not available, the first step therapy is the administration of crystalloids (isotonic NaCl solution), and in the absence of an effect on systemic hemodynamics, non-protein colloidal solutions and albumin.
With prerenal acute renal failure against the background of hypoalbuminemia and redistribution of volumes into third spaces (cavities, subcutaneous tissue), measures are shown that lead to an increase in the effective arterial blood volume - immersion of the body in water and intravenous administration of albumin.

Severe peripheral and cavitary edema with hypoalbuminemia is often resistant to diuretic treatment. In addition, the isolated use of diuretics in these patients can cause an increase in hypovolemia and azotemia.

A temporary effect can be obtained with the combined use of furosemide and albumin at a dose of 50 g / day.
Doses of furosemide can vary from 40 to 1000 mg/day. The use of albumin significantly improves the diuretic effect of diuretics, leads to an increase in diuresis, a decrease in body weight and, most importantly, to a decrease or resolution of prerenal azotemia.
About 90% of the administered furosemide binds to albumin, therefore, with hypoalbuminemia, the distribution of the diuretic in the vascular and extravascular space changes.

The addition of albumin to the treatment, in addition to a temporary increase in the oncotic pressure of the blood plasma and the attraction of fluid from the interstitial spaces, leads to an increase in the delivery of furosemide to its receptors in the thick ascending loop of Henle. So, in patients with hypoalbuminemia in monotherapy, the content of furosemide in the urine was 7-12% of the administered dose.
Combination therapy with furosemide and albumin increases the urinary excretion of the former up to 24-30%.

Correction of low cardiac output.
Treatment should be aimed at increasing CO and reducing afterload. The tactic for increasing CO is to reduce the increased extracellular volume with diuretics or ultrafiltration (UF); improvement of cardiac function with the use of inotropic drugs and/or peripheral vasodilators.
The use of diuretics (in particular, furosemide) leads to a decrease in the end-diastolic volume of the left ventricle and an improvement in subendocardial perfusion.
In addition, against the background of furosemide therapy, the contractile function of the heart improves in the process of reducing the wedge pressure of the pulmonary capillaries.

Theoretically, treatment with loop diuretics can lead to a critical decrease in LV filling and a fall in CO.
Therefore, the introduction of diuretics should occur under careful control of the water balance, CVP.

Some patients with severe heart failure and acute renal failure have a very low CB, a high level of endogenous vasopressors and are practically resistant to therapy with diuretics, inotropic agents and vasodilators.
In this case, hardware ultrafiltration (UF) can have a significant effect, the use of which leads to an increase in diuresis and an improvement in the response to drug therapy and a decrease in the level of pressor factors in the circulation.

Other diseases with eu or hypervolemia against the background of low CO, which can lead to the development of pre-ARF, are myocardial infarction, pericardial tamponade, massive pulmonary embolism.
In these cases, the resolution of prerenal azotemia depends primarily on the treatment of the underlying process.
Correction of conditions with reduced peripheral vascular resistance.
An isotonic NaCl solution is used.
The effectiveness of the use of non-protein colloidal solutions and albumin has not been proven.

Prerenal azotemia often occurs in patients with cirrhosis and other liver diseases complicated by liver failure and ascites.
These patients are shown to limit the intake of NaCl.
Diuretics are effective in resolving ascites in 73% of patients. However, stimulation of diuresis (furosemide + spironolactone) can lead to a deterioration in the functional state of the kidneys.
In this case, the treatment of choice is albumin infusion at a dose of 40 g IV along with paracentesis (4-6 liters per session).
Paracentesis with the introduction of albumin can significantly reduce the time of hospitalization.
Therefore, the combination of paracentesis and albumin should be used as initial therapy in cases of liver failure, severe ascites (both with and without prerenal azotemia); maintenance therapy should be carried out with diuretics.

To prevent deterioration of renal function during paracentesis in patients with severe ascites, the administration of dextran (dextran 70) is indicated.
The feasibility of using dopamine for vasodilation of the renal arterial bed in prerenal acute renal failure has not yet been proven.

Treatment of renal acute renal failure.
AKI of ischemic and nephrotoxic etiology.
Correction of BCC and water-electrolyte disturbances should be carried out with saline solutions, since there are experimental data on a decrease in the severity of ATN against the background of sodium chloride preload.
The principles of the use of crystalloids are similar to those in the treatment of prerenal acute renal failure (see below).

Of undoubted importance in the prevention of ATN is caution in choosing diagnostic procedures and drugs that have potential nephrotoxicity, monitoring the patient's condition, especially those belonging to risk groups, and timely correction of systemic and regional hemodynamic disorders.
Traditional methods of drug prevention have been related to the use of osmotic and loop diuretics, as well as dopamine.
It was previously thought that diuretics, by increasing urine output, could prevent tubular obstruction, which is partly associated with a decrease in GFR in ATN. Later, however, it was demonstrated that both loop diuretics and mannitol do not have preventive properties in relation to the development of ATN and do not affect the prognosis of full-blown ATN in any way.

However, the use of diuretics can transform oliguric OTN variants into non-oliguric ones and thus reduce the need for RRT.
For this purpose, low doses of mannitol (15-25 g), bolus or drip administration of furosemide are used, which are effective only on early stages REL.
In the absence of an increase in diuresis after therapy with these diuretics, further administration of these diuretics should not be continued and doses should not be increased.
This may lead to undesirable consequences- hyperosmolar coma, pancreatitis, deafness.
In addition, with the introduction of mannitol in high doses in individuals with reduced urine output, there is a high risk of developing pulmonary edema.
The results of recent developments, including meta-analyses, confirmed that the use of furosemide in patients with AKI or high risk its development does not significantly affect in-hospital mortality, the need for subsequent RRT, the number of subsequent hemodialysis sessions, and the number of patients with persistent oliguria.

At the same time, high doses of this loop diuretic, which are usually used in patients with acute renal failure, were associated with a distinct increase in the risk of ototoxicity of this drug.
Systemic hemodynamic disorders are the dominant cause of ATN, so the main goals of treatment include stabilization of circulatory disorders, blood pressure and maintenance of regional renal circulation.
The first task is solved with the help of BCC correction and the use of systemic vasopressors. The scope of vasopressor agents, as a rule, is shock, more often septic, less often - another etiology. Data published to date on the use of vasopressors in patients with septic shock and prerenal acute renal failure do not yet allow definitive recommendations on the use of this group of drugs, either in relation to the control of systemic hemodynamics or in relation to renal effects.

In practice, for the treatment and prevention of acute renal failure in severe patients, dopamine is most widely used at doses of 0.5-2 mcg / kg / min (some recommendations provide for higher doses - 1-5 mcg / kg / min, suggesting that as the "gold standard" 3 µg/kg/min) for 6 hours.

In certain situations, the time of dopamine infusion can be increased, but usually no more than 24 hours. The possible positive effects of dopamine on the course of acute renal failure are associated with an increase in renal blood flow and a decrease in tubular Na transport through the activation of DA1 receptors. However, clinical trials have not found a significant value of dopamine infusion in the prevention and treatment of ATN, probably due to the activation of not only DAl-type receptors, but also other receptors (DA2 and adrenergic), leveling the positive effects of the first on renal hemodynamics and tubular sodium reabsorption.

It is possible that fenoldapam, a selective DA1 receptor agonist, may be more useful in the treatment of ATN.

This drug is little known to Russian nephrologists.
Significant evidence of the effectiveness of this substance in the treatment of acute renal failure has not yet been presented, since the results of a number of studies have been contradictory.
The schemes for its application have not been developed either.
For example, for the prevention of X-ray contrast nephropathy, it is suggested to prescribe it 15 minutes-12 hours (!) to 0-12 (!) hours after the procedure at a rate of 1 μg / kg / min.
On the other hand, as shown in a number of studies (including double-blind, randomized and placebo-controlled), norepinephrine infusion is more effective in stabilizing systemic hemodynamics compared to dopamine.
The theoretical probability of violation of regional blood circulation of the abdominal organs and kidneys due to adrenergic stimulation with the use of norepinephrine has not been clinically confirmed.
The use of epinephrine is indicated in cases where the use of other pressor agents does not give the desired increase in blood pressure.
Dobutamine may be effective in reducing the risk of in-hospital mortality when given early in patients with septic shock, but it has not been found to have a positive effect on either urine output or creatinine clearance. The role of an effective vasopressor in prerenal acute renal failure can be claimed by the recently entered clinical practice vasopressin (ADH), which in pilot studies in septic shock was effective in raising systemic BP, allowing dosage reduction or discontinuation of other pressor drugs.

In any case, prospective studies are needed to clarify the situation with the choice of vasopressors in this very difficult category of patients. Since specific therapy for acute renal failure associated with exposure to nephrotoxic agents is practically not developed, the prevention of renal dysfunction is the cornerstone in the management of these patients.

The main principle is prevention through a sparing regimen of drug use taking into account risk factors, timely correction of reversible risk factors and immediate withdrawal of drugs in case of acute renal dysfunction.
In some cases, early treatment preventive actions can prevent the development and improve the long-term prognosis of acute renal failure.

Kidney dysfunction that develops rapidly and is accompanied by painful sensations called acute renal failure. This is a serious pathology, as a result of which there is a violation of the production and excretion of urine. Such negative changes provoke a number of complications that adversely affect the general condition, well-being and lead to other, more serious diseases. It is extremely important to provide timely assistance at the first manifestation of the disease and prevent the degeneration of the acute form into a chronic one, which will accompany a person until the end of his life, reminding himself of exacerbations, pain and other symptoms. Start treatment medicines recommended after a thorough examination and diagnosis. Often, in order to get rid of the disease, patients resort to traditional medicine, which also have a beneficial effect on the body when acute form kidney failure.

What is acute renal failure?

Acute renal failure is a pathological disorder of the kidneys that develops quickly over several hours or days and is accompanied by a number of unpleasant symptoms, intoxication of the body and provokes the appearance of various complications. The main cause of the disease is damage to the kidney tissue or disruption of the functioning of other internal organs.

In its development, the disease goes through several stages:

The first stage is characterized by minimal pathological changes in the functioning of the kidneys, a decrease in the amount of urine excreted.
The second stage is characterized by a significant deterioration in kidney function, a decrease in urine volume and a strong increase in toxic substances in the blood (creatinine). Due to poor urine output, fluid accumulates in the body, which provokes swelling, the development of heart disease, and a hypertensive crisis.
The third stage is characterized by the death of nephrons, the filling of the urinary ducts with blood plasma. Often the patient is tormented by tachycardia, peeling of the skin and its dryness appear. In particularly difficult cases, the patient may fall into a coma.
The final stage is characterized by the restoration of kidney function, which is extremely slow and can take from 6 to 12 months to complete recovery.

Causes of the disease

kidney failure in an acute form develops under the influence of the most various reasons: from disruption of the functioning of internal organs, to damage by poisons or mechanical damage to kidney tissues. The most common and frequently occurring factors provoking the disease include:

Depending on the prerequisites that provoke the development of the disease, acute renal failure can be divided into three types:

Prerenal acute renal failure - the main factor in the development is a violation of the blood circulation of the kidneys or a decrease in the filtration rate, resulting in a significant increase in the level of cretinin, there is a violation of the functioning of the kidneys. With timely assistance, the disease responds well to treatment, but in the case of its advanced form, necrosis or coronary disease is possible.
Obstructive acute renal failure - the development of this type of disease is facilitated by a violation of the patency of urine in urinary tract. That is, the kidneys perform their functions to the full, but due to damage to the ureters, urine is not excreted, which is most often caused by the presence of tumor diseases, hematomas or stones.
Parenchymal acute renal failure is kidney damage provoked by mechanical, toxic, chemical, ischemic effects.

Symptoms of acute renal failure

Acute renal failure syndrome is characterized by the following symptoms:

Diagnosis of the disease

Before proceeding with the choice of treatment, it is necessary to correctly establish the diagnosis and degree of kidney damage. First of all, you need a consultation and a therapist. At the first visit to the doctor's office, he conducts a thorough examination, collects an anamnesis, and establishes possible causes that could provoke the disease. To obtain a complete picture of the patient's health status, the doctor prescribes the following diagnostic procedures:

Treatment of acute renal failure

Treatment of symptoms and causes of acute renal failure depends on the stage of the disease, the presence of complications, and the general health of the patient. So, at the first stage, doctors set the main goal - to eliminate the cause that provoked the disease, and the main therapy is aimed at solving this problem. If the patient has a second or third stage, then the treatment consists in restoring kidney function and eliminating all complications.
The treatment of ARF is aimed at:

Elimination of factors that led to disruption of the functioning of the kidneys.
Restoration of the normal functioning of the body.
Normalization of the volume of urine excreted per day.

To achieve their goals, doctors use the following methods of treatment:

Prevention of kidney failure

In order to prevent the development of acute renal failure, it is necessary to eliminate all factors that can provoke the disease in time: take medications under the strict supervision of a doctor (especially if there is a predisposition to this kind of disease); timely receive the help of specialists in case of poisoning with poisons or chemicals; timely treat dysfunctions of internal organs that can provoke acute renal failure; undergo preventive examinations.

Treatment of acute renal failure must begin with the treatment of the underlying disease that caused it.

To assess the degree of fluid retention in the patient's body, daily weighing is desirable. For a more accurate determination of the degree of hydration, volume infusion therapy and indications for it, it is necessary to install a catheter into the central vein. It should also take into account the daily diuresis, as well as the patient's blood pressure.

In prerenal acute renal failure, it is necessary to restore the BCC as soon as possible and normalize blood pressure.

For the treatment of renal acute renal failure caused by various substances of medicinal and non-drug nature, as well as some diseases, it is necessary to start detoxification therapy as early as possible. It is desirable to take into account the molecular weight of the toxins that caused acute renal failure, and the clearance capabilities of the efferent therapy method used (plasmapheresis, hemosorption, hemodiafiltration or hemodialysis), the possibility of the earliest administration of the antidote.

In postrenal acute renal failure, immediate drainage of the urinary tract is necessary to restore adequate urine flow. When choosing the tactics of surgical intervention on the kidney in conditions of acute renal failure, even before the operation, information about the sufficient function of the contralateral kidney is necessary. Patients with a single kidney are not so rare. During the stage of polyuria, which usually develops after drainage, it is necessary to control the fluid balance in the patient's body and the electrolyte composition of the blood. The polyuric stage of acute renal failure may present with hypokalemia.

Medical treatment of acute renal failure

With an intact passage through the gastrointestinal tract, adequate enteral nutrition is necessary. If it is impossible, the need for proteins, fats, carbohydrates, vitamins and minerals is satisfied with the help of intravenous nutrition. Given the severity of glomerular filtration disorders, protein intake is limited to 20-25 g per day. The required caloric intake should be at least 1500 kcal / day. The amount of fluid required by the patient before the development of the polyuric stage is determined based on the volume of diuresis for the previous day and an additional 500 ml.

The combination of acute renal failure and urosepsis causes the greatest difficulty in treatment. The combination of two types of uremic and purulent intoxication at once significantly complicates the treatment, and also significantly worsens the prognosis for life and recovery. In the treatment of these patients, it is necessary to use efferent methods of detoxification (hemodiafiltration, plasmapheresis, indirect electrochemical blood oxidation), selection antibacterial drugs according to the results of a bacteriological analysis of blood and urine, as well as their dosing, taking into account the actual glomerular filtration.

Treatment of a patient with hemodialysis (or modified hemodialysis) cannot serve as a contraindication to surgical treatment diseases or complications leading to acute renal failure. Modern possibilities of monitoring the blood coagulation system and its drug correction allow avoiding the risk of bleeding during operations and in postoperative period. For efferent therapy, it is desirable to use short-acting anticoagulants, for example, sodium heparin, the excess of which can be neutralized by the end of treatment with an antidote - protamine sulfate; sodium citrate can also be used as a coagulant. To control the blood coagulation system, the study of activated partial thromboplastin time and the determination of the amount of fibrinogen in the blood are usually used. The method for determining blood clotting time is not always accurate.

Treatment of acute renal failure even before the development of the polyuric stage requires the appointment of loop diuretics, such as furosemide up to 200-300 mg per day fractionally.

Anabolic steroids are prescribed to compensate for catabolism processes.

With hyperkalemia, intravenous administration of 400 ml of a 5% glucose solution with 8 IU of insulin, as well as 10-30 ml of a 10% solution of calcium gluconate, is indicated. If hyperkalemia cannot be corrected conservative methods, then the patient is indicated for emergency hemodialysis.

Surgical treatment of acute renal failure

To replace kidney function during the period of oliguria, you can use any method of blood purification:

hemodialysis;
peritoneal dialysis;
hemofiltration;
hemodiafiltration;
low flow hemodiafiltration.

With multiple organ failure, it is better to start with low-flow hemodiafiltration.

Treatment of acute renal failure: hemodialysis

Indications for hemodialysis or its modification in chronic and acute renal failure are different. In the treatment of acute renal failure, the frequency, duration of the procedure, dialysis load, the amount of filtration and the composition of the dialysate are selected individually at the time of the examination, before each treatment session. Treatment with hemodialysis is continued, preventing an increase in the urea content in the blood above 30 mmol / l. With the resolution of acute renal failure, the blood creatinine concentration begins to decrease earlier than the blood urea concentration, which is regarded as a positive prognostic sign.

Emergency indications for hemodialysis (and its modifications):

"uncontrolled" hyperkalemia;
severe hyperhydration;
hyperhydration of lung tissue;
severe uremic toxicity.

Planned indications for hemodialysis:

the content of urea in the blood is more than 30 mmol / l and / or the concentration of creatinine in excess of 0.5 mmol / l;
pronounced clinical signs of uremic intoxication (such as uremic encephalopathy, uremic gastritis, enterocolitis, gastroenterocolitis);
hyperhydration;
severe acidosis;
hyponatremia;
a rapid (within a few days) increase in the content of uremic toxins in the blood (daily increase in urea exceeding 7 mmol / l, and creatinine - 0.2-0.3 mmol / l) and / or a decrease in diuresis

With the onset of the stage of polyuria, the need for hemodialysis treatment disappears.

Possible contraindications to efferent therapy:

afibrinogenemic bleeding;
unreliable surgical hemostasis;
parenchymal bleeding.

As a vascular access for dialysis treatment, a two-way catheter is used, installed in one of the central veins (subclavian, jugular or femoral).

Etiology of prerenal acute renal failure

Etiology of renal acute renal failure

Etiology of postrenal acute renal failure

Symptoms of acute renal failure

Complications of acute renal failure

OPN diagnostics

Treatment of acute renal failure

Treatment in the initial phase

Treatment in the phase of oliguria

Indications for hemodialysis

Forms and causes of acute renal failure

Prerenal form of acute renal failure

Renal form of acute renal failure

Postrenal acute renal failure

Stages and symptoms of acute renal failure

OPN diagnostics

Treatment and emergency care for acute renal failure

But perhaps it is more correct to treat not the consequence, but the cause?

Forms and causes of acute renal failure

Prerenal form of acute renal failure

Renal form of acute renal failure

Postrenal acute renal failure

Stages and symptoms of acute renal failure

OPN diagnostics

Treatment and emergency care for acute renal failure

What is acute renal failure?

Causes of the disease

Symptoms of acute renal failure

Diagnosis of the disease

Treatment of acute renal failure

Prevention of kidney failure

Medical treatment of acute renal failure

Surgical treatment of acute renal failure

Treatment of acute renal failure: hemodialysis

Emergency indications for hemodialysis (and its modifications):

Planned indications for hemodialysis:

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