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Acute renal failure

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

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

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

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

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

5) urinary tract obstruction;

6) arenal condition (trauma or removal of a single kidney).

Renal failure is characterized by a change in homeostatic constants (pH, osmolarity, etc.) as a result of significant impairment of renal function and is the outcome or complication of diseases conditionally divided into renal (glomerulonephritis, pyelonephritis), prerenal (hypovolemia, dehydration, DIC) and postrenal (obstructive uropathy ) Acute renal failure is characterized by a sudden violation of homeostasis (hyperazotemia, electrolyte disturbances, acidosis) due to acute impairment of the main functions of the kidneys (nitrogen excretion, regulation of CBS, water-electrolyte balance). Acute renal failure can develop in diseases manifested by hypotension and hypovolemia (shock, burn, etc.), followed by a decrease in renal blood flow; DIC-syndrome with 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 acute renal failure:

1) the initial period;

2) oligoanuric period;

3) the polyuric period;

4) the recovery period.

Clinic. The initial period is characterized by symptoms of the underlying disease (poisoning, shock pain, anaphylactic or bacterial), hemolysis, acute poisoning, infectious disease. On the first day, a decrease in diuresis (less than 500 ml / day) can be detected, that is, the period of oliguria, anuria begins, homeostasis changes. In plasma, the level of creatinine, urea, residual nitrogen, sulfates, phosphates, magnesium, potassium is increased, the level of sodium, chlorine, calcium is reduced. Adynamia, loss of appetite, nausea, vomiting appears, in the first days you can observe oliguria, anuria. With an increase in azotemia, the urea level rises daily by 0.5 g / l, with an increase in acidosis, hyperhydration and ectrolitic disturbances, muscle twitching, lethargy, drowsiness, dyspnea due to acidosis, pulmonary edema, the early stage of which is determined radiologically. Changes in the cardiovascular system are characteristic: tachycardia, expansion of the borders of the heart, with auscultation, deaf heart sounds, systolic murmur at the apex, pericardial friction noise appear. Heart rhythm disturbance develops as a result of hyperkalemia, which can be the cause of death. In case of hyperkalemia, an 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, the appearance of leukocytosis is characteristic. Complaints of abdominal pain, enlargement of the liver, and symptoms of acute uremia may occur. Death in acute renal failure develops against a background of uremic coma, hemodynamic changes, and sepsis. In acute renal failure, hypoisostenuria appears.

The oligoanuric period is manifested by a rapid (within several hours) decrease in urine output to 100-300 ml / day with a low specific gravity of urine of not more than 1012, lasts 8-10 days, a gradual increase in weakness, anorexia, nausea, vomiting, and itching of the skin. With the unlimited introduction of fluid and salt, hypervolemia, hypertension occur; peripheral edema and pulmonary edema may appear. Hyperazotemia rises rapidly (up to 5-15 mmol / day of urea, creatinine more than 2 mmol / l), severe acidosis, hyperkalemia (up to 9 mmol / l), hyponatremia (below 115 mmol / l) cause uremic coma. Hemorrhages, gastrointestinal bleeding, decreased hemoglobin, white blood cells to 2.0 x 109 / L. The color of urine is red due to macrohematuria, proteinuria is usually small - reaches 9%. Clinical improvement occurs 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 (decrease in the voltage of the T wave, wave U, extrasystole). With the normalization of residual nitrogen in the blood, homeostasis is restored, a period of glomerular filtration and concentration develops, kidney function persists, and in chronic insufficiency, the course takes on a chronic nature, 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 treatment of acute renal failure, mortality decreased to 20-30%, rarely there is an outcome in chronic renal failure, as well as the development of acute renal failure in patients with chronic renal failure.

Prerenal acute renal failure

Etiology. The renal blood flow is disturbed by dehydration, hypovolemia, and hemodynamic disturbances.


1. When collecting an anamnesis and physical examination, you can identify signs of dehydration, hypovolemia, shock, decreased cardiac output.

2. Blood pressure and CVP are measured, a urinary catheter is inserted in order to evaluate diuresis, which indicates pronounced oliguria; urine can also be obtained for examination for general urinalysis with determination of osmolarity, level of sodium, potassium, creatinine. After this, the catheter must be removed.

The diagnosis of prerenal acute renal failure is based on the level of sodium in the urine of less than 15 meq / l, the excreted sodium fraction (EFN) less than 1%. EF№ = (Na + urine / Na + plasma) / (urine creatinine / plasma creatinine) x 100%. Renal failure index (IDI) <1%, IDI = Na + urine / (urine creatinine / plasma creatinine) x 100%. The ratio of urine urea / plasma urea> 10, urine 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 improved cardiac activity.

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

1. Vein catheterization is prescribed for the administration of drugs. Sometimes monitoring of CVP is necessary.

2. Restore bcc.

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

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

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

Renal (parenchymal) acute renal failure

Etiology. A long-term marked decrease in renal perfusion in the anamnesis indicates acute canalicia necrosis. Other causes of parenchymal acute renal failure may be glomerulonephritis, malignant arterial hypertension, hemolytic uremic syndrome, urate nephropathy and vasculitis.

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

1. Prior to invasive diagnostic procedures, the patient's condition must be stabilized.

2. Assess kidney function.

The following symptoms are characteristic of parenchymal acute renal failure:

1) urine creatinine / blood creatinine ratio <20;

2) urine osmolarity below 350 mosmol / kg;

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

4) renal scintigraphy evaluates renal blood flow, renal function, cortical necrosis of the kidneys can also be eliminated with this method, ultrasound can exclude obstruction of the urinary tract.

Treatment. If severe oliguria or anuria is caused by kidney damage, the urinary catheter is removed immediately. The patient is weighed 2 times a day. The volume of injected and released fluid is measured. With a water-electrolyte balance in the absence of edema and hyperhydration, the amount of injected liquid and electrolytes is calculated together with diuresis and latent water loss. Calorie intake should be maximum; parenteral nutrition is used only when normal is not possible. With parenteral nutrition, 10-15% glucose can be introduced into the peripheral vein, up to 30% into the central vein. After the restoration of diuresis, the loss of water and electrolytes with urine must be compensated for by infusion solutions. With a loss of potassium, it is compensated until the plasma level normalizes.

1. If the level of potassium in the plasma is 5.5-7.0 meq / l, it is necessary to administer sodium polystyrenesulfonate in a solution of sorbitol 1 g / kg inside, injected every 4-6 hours until the level of potassium in the plasma decreases. When potassium is excreted, sodium is excreted and hypernatremia may develop.

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

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

2) sodium bicarbonate in a dose of 2 meq / kg is injected intravenously for 5-10 minutes.

3. If hyperkalemia persists, insulin 0.1 IU / kg is prescribed, iv is administered 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 express method, prepare everything for hemodialysis. Emergency hemodialysis is indicated if the potassium level in the plasma is more than 7.5 meq / l and the previous measures are not effective. Acidosis usually decreases with the introduction of glucose. You can prescribe for the introduction of bicarbonate, citrate, lactate in a dose of 1-3 meq / l. But you need to 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 for anuria are not used.

Postrenal acute renal failure

Etiology. Urinary obstruction develops with congenital valve abnormalities, with structural disorders of the urethra, with hematuria, a tumor, or retroperitoneal fibrosis.

Examination and diagnostics. Obstruction of the urinary tract is established on the basis of anamnesis (congenital malformations of the urinary tract, genitals, lower abdominal trauma); palpable volume formation in the lateral abdomen, overflowing bladder. Anuria may indicate bilateral obstruction of the ureters. Ultrasound and kidney scintigraphy are performed. If these methods cannot be carried out, serum creatinine level is determined, less than 5 mg% - excretory urography is indicated. Necessary: ​​eliminate dehydration and introduce a minimum amount of low-osmolar contrast medium, consult a urologist, with anuria, urinary tract obstruction, perform cystoscopy and retrograde pyelography.

Treatment. Pathogenetic therapy is prescribed based on the cause of acute renal failure. Plasmapheresis should be performed, the volume of which can be determined by the severity of the patient's condition, the degree of intoxication. In case of hemodynamic disorders, antishock therapy is prescribed, replenishment of blood loss by transfusion of blood components, blood substitutes (100-400 mg of prednisolone is administered intravenously). With hypotension (after replenishing blood loss), an intravenous drip of 1 ml of a 0.2% solution of norepinephrine in 200 ml of an isotonic sodium chloride solution is prescribed. In case of poisoning, measures are taken to remove poison from the body. With large intravascular hemodialysis, if the hematocrit is below 20%, a replacement 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, furosemide IV 160 mg 4 times a day is prescribed to stimulate diuresis.

Further therapy should be aimed at resolving homeostasis. Prescribe a diet with a limited intake of protein and potassium, but with sufficient calorie intake due to carbohydrates and fats. The amount of injected fluid should be more than urine output, the amount of water lost with vomiting and diarrhea, not more than 500 ml, this volume should include 400 ml of a 20% glucose solution with 20 IU of insulin, with hyperkalemia, 10- 20 ml of a 10% solution of calcium gluconate, also in / drip 200 ml of a 5% solution of sodium bicarbonate (after establishing the degree of acidosis and under the 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 - more than 6.5 mmol / l; if there is decompensated metabolic acidosis; if there are clinical manifestations of acute uremia.

Contraindications are cerebral hemorrhage, stomach bleeding, intestinal bleeding, severe hemodynamic disturbances, decreased blood pressure. Contraindication to peritoneal dialysis is the just performed operation on the abdominal organs, adhesions in the abdominal cavity. Treatment includes surgery or urinary diversion. Obstruction of the lower urinary tract is detected and eliminated by catheterization of the bladder, obstruction of the ureters is detected by ultrasound. After restoration of patency of the urinary tract, polyuria develops, which leads to dehydration; in these cases, 0.45% NaCl is introduced.

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Acute renal failure

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