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Acute renal failure

Acute renal failure occurs suddenly due to acute, often reversible, kidney disease. Causes of acute renal failure:

1) impaired renal hemodynamics (shock, collapse, etc.);

2) exogenous intoxication: the bites of poisonous snakes, insects, drugs, poisons, which are used in the national economy, life, drugs;

3) infectious diseases (hemorrhagic fever with renal syndrome and leptospirosis);

4) acute kidney disease (acute glomerulonephritis and acute pyelonephritis);

5) urinary obstruction;

6) arena state (injury or removal of a single kidney).

Renal failure is characterized by a change in the homeostatic constants (pH, osmolarity, etc.) as a result of significant impairment of renal function and is the outcome or complication of diseases conventionally divided into renal (glomerulonephritis, pyelonephritis), prerenal (hypovolemia, dehydration, disseminated intravascular coagulation) and postrenal (obstructive) pathologies. ). Acute renal failure is characterized by a sudden disturbance of homeostasis (hyperazotemia, electrolyte disturbances, acidosis) due to acute impairment of the basic functions of the kidneys (nitrogen-excretion, regulation of ECB, water-electrolyte balance). Acute renal failure may develop in diseases manifested by hypotension and hypovolemia (shock, burn, etc.) with a subsequent decrease in renal blood flow; DIC in septic shock, HUS; with glomerulonephritis, pyelonephritis, with cortical necrosis of the kidneys in newborns, with difficulty in the outflow of urine from the kidneys.

There are 4 periods of the surge arrester:

1) the initial period;

2) oligoanuric period;

3) polyuric period;

4) recovery period.

Clinic. The initial period is characterized by symptoms of the underlying disease (poisoning, pain, anaphylactic or bacterial shock), hemolysis, acute poisoning, and an infectious disease. On the first day, you can detect a decrease in diuresis (less than 500 ml / day), that is, the period of oliguria, anuria begins, homeostasis changes. Plasma elevated levels of creatinine, urea, residual nitrogen, sulfates, phosphates, magnesium, potassium, reduced levels of sodium, chlorine, calcium. Adynamia, loss of appetite, nausea, vomiting, in the first days you can observe oliguria, anuria. With an increase in azotemia, the level of urea increases daily by 0.5 g / l, with an increase in acidosis, overhydration and ectrolytic disturbances, muscular twitching, lethargy, drowsiness, shortness of breath due to acidosis, pulmonary edema are observed, the early stage of which is determined radiographically. Characterized by changes in the cardiovascular system: tachycardia, expansion of the borders of the heart, with auscultation, there are muffled heart tones, systolic murmur at the apex, pericardial friction noise. A heart rhythm disorder develops as a result of hyperkalemia, which can be the cause of death. With hyperkalemia, a high, pointed T wave is recorded on the ECG, the QRS complex is expanded, the R wave is reduced. Heart block and ventricular fibrillation can lead to cardiac arrest. Anemia develops during all periods of acute renal failure. For the period of oliguria, anuria is characterized by the appearance of leukocytosis. There may be complaints of abdominal pain, enlargement of the liver, symptoms of acute uremia occur. Death in acute renal failure develops on the background of uremic coma, changes in hemodynamics, sepsis. In acute renal failure, hypoisostenuria appears.

The oligoanuric period is manifested by a rapid (within a few hours) decrease in diuresis to 100–300 ml / day with a low urine specific gravity of no more than 1012, lasts 8–10 days, a gradual increase in weakness, anorexia, nausea, vomiting, itching of the skin. With the unlimited introduction of fluid and salt, hypervolemia, hypertension occur; peripheral edema and pulmonary edema may occur. Hyperazotemia (up to 5-15 mmol / day of urea, creatinine more than 2 mmol / l), pronounced acidosis, hyperkalemia (up to 9 mmol / l), hyponatremia (below 115 mmol / l) cause uremic coma to quickly increase. Hemorrhages, gastrointestinal bleeding, decrease in hemoglobin, leukocytes to 2.0 x 109 / l. The color of urine is red due to gross hematuria, proteinuria is usually small - up to 9%. Clinical improvement comes gradually: the level of azotemia decreases and homeostasis is restored. During an attack of polyuria, hypokalemia may develop (less than 3.8 mmol / l), characteristic changes on the ECG (reduced T wave voltage, wave U, extrasystole). With the normalization of residual nitrogen in the blood, homeostasis is restored, the glomerular filtration period and concentration develops, the kidney function is maintained, and for chronic insufficiency, the course becomes chronic, the joined pyelonephritis plays a special role. The recovery period lasts about 1 year and is manifested by a gradual restoration of renal functions.

In the treatment of peritoneal dialysis and hemodialysis in the complex therapy of acute renal failure, mortality decreased to 20–30%, the outcome is rarely observed in chronic renal failure, as well as the development of ARF in the presence of chronic renal failure.

Prerenal acute renal failure

Etiology. Dehydration, hypovolemia, and hemodynamic disturbances lead to impaired renal blood flow.


1. When collecting anamnesis and physical examination, signs of dehydration, hypovolemia, shock, decrease in cardiac output can be detected.

2. Measure blood pressure and CVP, inject a urinary catheter in order to evaluate diuresis, which indicates pronounced oliguria, you can also get urine for a urinalysis test with the definition of osmolarity, sodium, potassium, creatinine levels. After that, the catheter must be removed.

The diagnosis of prerenal ARF is established on the basis of urine sodium level less than 15 meq / l, the sodium fraction excreted (EFN) is less than 1%. EFN = (Na + urine / Na + plasma) / (creatinine urine / plasma creatinine) x 100%. Renal failure index (PPI) <1%, PPI = Na + urine / (urine creatinine / plasma creatinine) x 100%. The ratio of urea urine / plasma urea> 10, urinary creatinine / plasma creatinine> 40, urine osmolarity> 500 mosmol / kg. The level of potassium in the urine is not less than 40 mEq / l. Rehydration therapy increases diuresis and bcc. GFR increases with cardiac performance.

Treatment for prerenal ARF is aimed at restoring perfusion and kidney function.

1. Catheterization of a vein is prescribed for drug administration. Sometimes monitoring of CVP is necessary.

2. Restore the BCC.

3. If, after restoring the BCC, oliguria, anuria are preserved, mannitol is prescribed - a 20% solution at a dose of 0.5 g / kg, intravenously over a period of 10-20 minutes, and subsequently diuresis should increase by 6 ml / kg, if does not occur, the administration of mannitol is stopped.

After restoring the BCC, a test dose of furosemide, 1 mg / kg intravenously, is administered.

5. If significant oliguria or anuria persists, parenchymal or postrenal acute renal failure must be excluded.

Renal (parenchymal) arrester

Etiology. A long pronounced decrease in renal perfusion in history shows acute canalicular necrosis. Other causes of parenchymal acute renal failure can be glomerulonephritis, malignant hypertension, hemolytic uremic syndrome, urate nephropathy and vasculitis.

Examination and diagnosis. First, exclude prerenal and postrenal causes of acute renal failure.

1. Before invasive diagnostic interventions, the patient’s condition must be stabilized.

2. Assess kidney function.

The following signs are characteristic of parenchymal ARF:

1) urinary creatinine / blood creatinine ratio <20;

2) urine osmolarity below 350 mosmol / kg;

3) urine sodium level is above 40 meq / l, EFNO> 3%, IIT> 1%;

4) kidney scintigraphy assesses renal blood flow, kidney function, also using this method, you can eliminate the cortical necrosis of the kidneys, ultrasound allows to exclude obstruction of the urinary tract.

Treatment. If severe oliguria or anuria is caused by kidney damage, the urinary catheter is immediately removed. Weigh the patient 2 times a day. Measure the amount of injected and excreted fluid. When water-electrolyte balance in the absence of edema and overhydration, the amount of injected fluid and electrolytes is calculated along with diuresis and latent water loss. Caloric intake should be maximized; parenteral nutrition is used only when it is impossible to normal. With parenteral nutrition, 10-15% of glucose can be injected into the patient in the peripheral vein, and up to 30% into the central vein. After the restoration of diuresis, the loss of water and electrolytes in the urine must be replaced by infusion solutions. When potassium is lost, it is reimbursed until plasma levels are normalized.

1. If the level of potassium in plasma is 5.5–7.0 meq / l, sodium polystyrenesulfonate must be injected in a solution of sorbitol 1 g / kg orally, injected every 4-6 hours until the level of potassium in plasma decreases. When potassium is excreted, sodium is excreted and hypernitraemia may develop.

2. When the level of potassium in the plasma is more than 7 meq / l, characteristic changes on the ECG appear, immediately take the following measures, following the ECG:

1) inject a 10% solution of calcium gluconate at a dose of 0.5-1 ml / kg IV per 5-10 minutes;

2) Sodium bicarbonate is administered in a dose of 2 meq / kg intravenously in a jet for 5-10 minutes.

3. If hyperkalemia persists, insulin 0.1 IU / kg is administered, injected intravenously with 25% glucose, 0.5 g / kg (2 ml / kg) for 30 minutes.

It is necessary to monitor the level of glucose in the blood using the rapid method, to prepare everything for hemodialysis. Emergency hemodialysis is indicated if the level of potassium in the plasma is more than 7.5 mEq / L and the pre-event measures are not effective. Acidosis usually decreases with the introduction of glucose. You can assign for the introduction of bicarbonate, citrate, lactate at a dose of 1-3 mEq / l. But we must remember that 1 meq / l contains 1 meq / l of sodium and potassium. Treatment of severe acidosis is difficult due to overhydration, hemodialysis is indicated. Diuretics in anuria is not used.

Postrenal acute renal failure

Etiology. Obstruction of the urinary tract develops with congenital anomalies of the valve, with structural disorders of the urethra, with hematuria, tumors or retroperitoneal fibrosis.

Examination and diagnosis. Urinary tract obstruction is established on the basis of anamnesis (congenital anomalies of urinary tract development, genital organs, lower abdominal trauma); palpable mass education in the lateral abdomen, crowded bladder. Anuria may indicate bilateral obstruction of the ureters. Ultrasonography and kidney scintigraphy are performed. If these methods cannot be performed, determine serum creatinine level, less than 5 mg% - excretory urography is indicated. It is necessary to: eliminate dehydration and enter the minimum amount of low-osmolar contrast material, undergo a consultation with a urologist, with anuria, urinary tract obstruction, cystoscopy and retrograde pyelography.

Treatment. Pathogenetic therapy is prescribed based on the cause of the acute renal failure. Plasmapheresis should be carried out, the volume of which can be determined by the severity of the patient's condition, the degree of intoxication. In hemodynamic disorders, anti-shock therapy is prescribed, replacement of blood loss with a transfusion of blood components, blood substitutes (intravenous drip inject 100–400 mg of prednisolone). For hypotension (after completing blood loss), intravenous drip administration of 1 ml of a 0.2% norepinephrine solution in 200 ml of isotonic sodium chloride solution is prescribed. When poisoning using measures to remove poison from the body. With large intravascular hemodialysis, if the hematocrit is below 20%, an alternative transfusion of blood or plasma is performed. If the cause is bacterial shock, then anti-shock therapy and antibiotics are prescribed. In the initial period of oliguria-anuria, to stimulate diuresis, furosemide is prescribed i.v. at 160 mg 4 times a day.

Further therapy should be aimed at resolving homeostasis. Assign a diet to limit the intake of protein and potassium, but with sufficient calorie due to carbohydrates and fats. The amount of fluid injected should be more than diuresis, the amount of water lost with vomiting and diarrhea, not more than 500 ml, this volume should include 400 ml of 20% glucose solution with 20 U insulin, in case of hyperkalemia in / in 10— 20 ml of 10% calcium gluconate solution, also in / in drip 200 ml of 5% sodium hydrogen carbonate solution (after establishing the degree of acidosis and under control of blood pH). Indications for hemodialysis and peritoneal dialysis: if the level of urea in the plasma is more than 2 g / l, potassium is more than 6.5 mmol / l; if there is decompensated metabolic acidosis; if there are clinical manifestations of acute uraemia.

Contraindications are hemorrhage in the brain, gastric bleeding, intestinal bleeding, severe hemodynamic disturbances, lowering blood pressure. A contraindication to peritoneal dialysis is an abdominal organ surgery that has just been performed, adhesions in the abdominal cavity. Treatment includes surgery or urinary diversion. Obstruction of the lower urinary tract is detected and eliminated with the help of catheterization of the bladder, obstruction of the ureters is detected by ultrasound. After restoration of the patency of the urinary tract, polyuria develops, which leads to dehydration; in these cases, 0.45% NaCl is administered.

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Acute renal failure

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