LECTURE No. 8. Kidney failure. Clinic, diagnosis, treatment

The main functions of the kidneys are the removal of metabolic products, maintaining a constant water-electrolyte composition and acid-base state, carried out by renal blood flow, glomerular filtration and tubules (reabsorption, secretion, concentration ability).

Renal failure - this syndrome develops with severe disorders of the renal processes, leads to a disorder of hemostasis, is characterized by azotemia, a violation of the water-electrolyte composition and the acid-base state of the body.

1. Acute renal failure

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

1) violation of renal hemodynamics (shock, collapse, etc.);

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

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 changes in homeostatic constants (pH, osmolarity, etc.) as a result of significant impairment of renal function and is an outcome or complication of diseases conventionally divided into renal (glomerulonephritis, pyelonephritis), prerenal (hypovolemia, dehydration, disseminated intravascular coagulation) and postrenal (obstructive uropathy). ) Acute renal failure is characterized by a sudden disruption of homeostasis (hyperazotemia, electrolyte disturbances, acidosis) due to an acute disturbance of the basic functions of the kidneys (nitrogen excretion, regulation of metabolic balance, water-electrolyte balance). Acute renal failure can develop in diseases manifested by hypotension and hypovolemia (shock, burn, etc.) with a subsequent decrease in renal blood flow; DIC syndrome 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 surge arrest:

1) initial period;

2) oligoanuric period;

3) polyuric period;

4) recovery period.

Clinic. The initial period is characterized by symptoms of the underlying disease (poisoning, painful shock, anaphylactic or bacterial), hemolysis, acute poisoning, and infectious disease. On the first day, you can detect a decrease in diuresis (less than 500 ml/day), i.e., a period of oliguria, anuria begins, and homeostasis changes. In plasma, the level of creatinine, urea, residual nitrogen, sulfates, phosphates, magnesium, potassium is increased, the level of sodium, chlorine, and calcium is decreased. Adynamia, loss of appetite, nausea, vomiting appear; in the first days, oliguria and anuria can be observed. With increasing azotemia, the level of urea increases daily by 0,5 g/l; with increasing acidosis, overhydration and ectrolyte disorders, muscle twitching, lethargy, drowsiness are observed, shortness of breath appears due to acidosis, pulmonary edema, the early stage of which is determined by x-ray. Characteristic changes in the cardiovascular system: tachycardia, expansion of the borders of the heart, dull heart sounds appear on auscultation, systolic murmur at the apex, pericardial friction noise. Heart rhythm disturbances develop as a result of hyperkalemia, which can cause death. With hyperkalemia, the ECG shows a tall, pointed T wave, the QRS complex is widened, and the R wave is reduced. Heart block and ventricular fibrillation can lead to cardiac arrest. Anemia develops during all periods of acute renal failure. The period of oliguria and anuria is characterized by the appearance of leukocytosis. There may be complaints of abdominal pain, liver enlargement, and symptoms of acute uremia. Death in acute renal failure develops against the background of uremic coma, changes in hemodynamics, and sepsis. In acute renal failure, hypoisosthenuria appears.

The oligoanuric period is manifested by a rapid (within several hours) decrease in diuresis to 100-300 ml/day with a low specific gravity of urine of no more than 1012, lasting 8-10 days, a gradual increase in weakness, anorexia, nausea, vomiting, itching of the skin. With unlimited administration of fluid and salt, hypervolemia and hypertension occur; Peripheral edema and pulmonary edema may occur. Hyperazotemia quickly increases (up to 5-15 mmol/day 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, 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 occurs gradually: the level of azotemia decreases and homeostasis is restored. During an attack of polyuria, hypokalemia (less than 3,8 mmol/l) may develop, and the ECG shows characteristic changes (decrease in T wave voltage, U wave, extrasystole). With the normalization of residual nitrogen in the blood, homeostasis is restored, a period of glomerular filtration and concentration develops, kidney function is preserved, and in case of chronic failure, the course becomes chronic, with associated pyelonephritis playing a special role. The recovery period lasts about 1 year and is manifested by the gradual restoration of renal functions.

When treated with peritoneal dialysis and hemodialysis in the complex therapy of acute renal failure, mortality decreased to 20-30%; an outcome in chronic renal failure, as well as the development of acute renal failure against the background of chronic renal failure, is rarely observed.

Prerenal acute renal failure Etiology. Dehydration, hypovolemia, and hemodynamic disturbances lead to impaired renal blood flow. Surveys.

1. When collecting anamnesis and physical examination, signs of dehydration, hypovolemia, shock, and decreased cardiac output can be identified.

2. Blood pressure and central venous pressure are measured, a urinary catheter is inserted in order to assess diuresis, which indicates severe oliguria, you can also obtain urine for a general urine test to determine osmolarity, sodium, potassium, and creatinine levels. After this, the catheter must be removed.

The diagnosis of prerenal acute renal failure is established on the basis of a sodium level in the urine of less than 15 mEq/L and an excreted sodium fraction (ESF) of less than 1%. EF# = (urine Na+ / plasma Na+) / (urine creatinine / plasma creatinine) x 100%. Renal insufficiency index (RII) < 1%, RFI = urine Na + / (urine creatinine / plasma creatinine) x 100%. Urine urea/plasma urea ratio > 10, urine creatinine/plasma creatinine > 40, urine osmolarity > 500 mOsmol/kg. The potassium level in the urine is at least 40 mEq/L. Rehydration therapy increases diuresis and blood volume. GFR increases with improved cardiac performance.

Treatment of prerenal AKI is aimed at restoring renal perfusion and function.

1. Vein catheterization is prescribed to administer medications. Sometimes monitoring of central venous pressure is necessary.

2. Restore BCC.

3. If, after restoration of bcc, oliguria and anuria persist, prescribe mannitol - 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 this does not occur, the administration of mannitol is stopped.

4. After restoration of blood volume, a test dose of furosemide is administered, 1 mg/kg intravenously.

5. If significant oliguria or anuria persists, it is necessary to exclude parenchymal or postrenal AKI.

Renal (parenchymal) acute renal failure

Etiology. A history of prolonged marked reduction in renal perfusion suggests acute tubular necrosis. Other causes of parenchymal acute renal failure include glomerulonephritis, malignant hypertension, hemolytic uremic syndrome, urate nephropathy and vasculitis.

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

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

2. Assess kidney function.

Parenchymal acute renal failure is characterized by the following symptoms:

1) urine creatinine/blood creatinine ratio < 20;

2) urine osmolarity below 350 mosmol/kg;

3) urinary sodium level above 40 mEq/l, EFN > 3%, PPI > 1%;

4) renal scintigraphy evaluates renal blood flow and renal function; this method can also exclude cortical necrosis of the kidneys; ultrasound can exclude urinary tract obstruction.

Treatment. If severe oliguria or anuria is caused by kidney damage, remove the urinary catheter immediately. Weigh the patient 2 times a day. The volume of injected and excreted fluid is measured. With water-electrolyte balance in the absence of edema and overhydration, the amount of administered fluid and electrolytes is calculated along with diuresis and hidden water losses. Calorie intake should be maximum; parenteral nutrition is used only when usual is not possible. With parenteral nutrition, 10-15% glucose can be injected into the patient’s peripheral vein, and up to 30% into the central vein. After diuresis is restored, losses of water and electrolytes in the urine must be replaced with infusion solutions. If potassium is lost, replace it until plasma levels normalize.

1. If the plasma potassium level is 5,5-7,0 mEq/L, it is necessary to administer sodium polystyrene sulfonate in sorbitol solution 1 g/kg orally, administered every 4-6 hours until the plasma potassium level decreases. When potassium is excreted, sodium is excreted and may develop hypernatremia.

2. When the plasma potassium level is more than 7 mEq/L, characteristic changes appear on the ECG, the following measures are immediately taken while monitoring the ECG:

1) administer a 10% solution of calcium gluconate at a dose of 0,5-1 ml/kg IV for 5-10 minutes;

2) sodium bicarbonate is administered at a dose of 2 mEq/kg intravenously in a stream over 5-10 minutes.

3. If hyperkalemia persists, prescribe insulin 0,1 IU/kg, administered intravenously with 25% glucose, 0,5 g/kg (2 ml/kg), over 30 minutes.

It is necessary to monitor blood glucose levels using the express method and prepare everything for hemodialysis. Emergency hemodialysis is indicated if plasma potassium levels are greater than 7,5 mEq/L and previous interventions are ineffective. Acidosis usually improves with glucose administration. Bicarbonate, citrate, lactate can be prescribed for administration at 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 are not used for anuria.

Postrenal acute renal failure

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

Examination and diagnosis. Obstruction of the urinary tract is established on the basis of anamnesis (congenital anomalies of the urinary tract, genital organs, trauma to the lower abdomen); a mass formation in the lateral abdomen and a full bladder are palpated. Anuria may indicate bilateral ureteral obstruction. Ultrasound and kidney scintigraphy are performed. If these methods cannot be carried out, the serum creatinine level is determined; less than 5 mg% - excretory urography is indicated. It is necessary: ​​eliminate dehydration and administer a minimal amount of low-osmolar contrast agent, consult a urologist, and in case of 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 and the degree of intoxication. In case of hemodynamic disorders, anti-shock therapy is prescribed, replacement of blood loss with transfusion of blood components, blood substitutes (100-400 mg of prednisolone is administered intravenously). In case of hypotension (after replenishment of blood loss), an intravenous drip of 1 ml of 0,2% solution of norepinephrine in 200 ml of isotonic sodium chloride solution is prescribed. In case of poisoning, measures are used 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 antishock therapy and antibiotics are prescribed. In the initial period of oligurianuria, furosemide is prescribed intravenously to stimulate diuresis, 160 mg 4 times a day.

Further therapy should be aimed at resolving homeostasis. A diet is prescribed with limited intake of protein and potassium, but with sufficient calories from carbohydrates and fats. The amount of fluid administered should be greater than diuresis, the amount of water lost with vomiting and diarrhea, no more than 500 ml, this volume should include 400 ml of a 20% glucose solution with 20 units of insulin; for hyperkalemia, 10- 20 ml of a 10% solution of calcium gluconate, also 200 ml of a 5% solution of sodium bicarbonate intravenously (after establishing the degree of acidosis and under blood pH control). Indications for hemodialysis and peritoneal dialysis: if the level of urea in 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 uremia.

Contraindications are cerebral hemorrhage, gastric bleeding, intestinal bleeding, severe hemodynamic disturbances, and decreased blood pressure. A contraindication to peritoneal dialysis is a recent operation on the abdominal organs, or adhesions in the abdominal cavity. Treatment includes surgery or urinary diversion. Obstruction of the lower urinary tract is identified 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 administered.

2. Chronic renal failure (CRF)

Chronic renal failure develops gradually as a result of progressive irreversible loss of functioning parenchyma.

Diagnosed in children with diseases of the urinary system if they persist for 3-6 months and a decrease in glomerular filtration is less than 20 ml/min, an increase in the level of serum creatinine and urea. Over 50 diseases manifest as kidney damage and lead to chronic renal failure, which is characterized by progression and irreversibility.

Etiology. Causes of chronic renal failure: chronic pyelonephritis, chronic glomerulonephritis. hereditary nephritis, nephritis in systemic diseases, nephroangiosclerosis, polycystic kidney disease, diabetic glomerulonephrosis, renal amyloidosis, urological diseases The pathogenetic mechanism of chronic renal failure is a progressive decrease in the number of active nephrons, which leads to a decrease in the efficiency of renal processes and to impaired renal function. Chronic kidney disease can last for 2 years or more before chronic kidney failure develops. They go through several stages, when glomerular filtration and tubular reabsorption are at normal levels, the underlying disease is in a stage not accompanied by disturbances in renal processes. Over time, glomerular filtration becomes lower than normal, the ability of the kidneys to concentrate urine decreases, and the disease progresses to the stage of impaired renal processes. At this stage, homeostasis is preserved and there is no renal failure yet. If the number of active nephrons and the glomerular filtration rate is below 50 ml/min, the level of creatinine in the blood plasma is increased by more than 0,02 g/l and urea by more than 0,5/g/l, at this stage conservative treatment of chronic renal failure is required. When filtration is below 10 ml/min, azotemia and other disturbances of homeostasis increase and the end stage of chronic renal failure occurs, which requires the use of dialysis. The cause of development is acquired and hereditary diseases of the urinary system, factors leading to the development of acute renal failure and chronic renal failure. With progressive kidney diseases, they gradually decrease in size and become sclerotic. Morphological changes appear in the form of sclerotic glomeruli and tubules with hypertrophied glomeruli and dilated tubules, with areas of fibrosis of interstitial tissue. In infants, chronic renal failure progresses against the background of structural and functional immaturity of the kidneys, with urolithiasis, with kidney destruction, hydronephrosis, and pyelonephritis.

1. When 75-80% of nephrons are sclerotic, others lose the ability for further hypertrophy, which causes minimal reserve capabilities, clinically manifested by a decrease in tolerance to potassium and sodium intake, and decompensation of chronic renal failure.

2. Clinical signs of chronic renal failure: decrease in excretory and other renal functions, activation of secondary factors aimed at compensating for primary disorders (removal of calcium from bones to compensate for acidosis), as well as damage to other organs (pericarditis, etc.), in conditions of change homeostatic constants (acidosis, hyperazotemia, etc.).

Clinic. Complaints of fatigue, decreased performance, headache, decreased appetite. CRF is characterized by the gradual development of weakness, pale skin, and anorexia. Sometimes an unpleasant taste in the mouth is noted, nausea and vomiting appear. The skin is pale, the skin is dry, flabby.

Muscle tone is reduced, small muscle twitching, tremors of the fingers and hands are observed. Pain appears in the bones and joints. Anemia develops, leukocytosis and bleeding appear. Arterial hypertension develops with underlying kidney disease. The borders of the heart are expanded, during auscultation the heart sounds are muffled, characteristic changes on the ECG (sometimes they are associated with dyskalemia). Conservative therapy regulates homeostasis, the patient’s general condition is satisfactory, but physical activity, mental stress, errors in diet, infection, and surgery can lead to a deterioration in kidney function and the appearance of uremic symptoms. Blood pressure is normal in the initial and polyuric stages. Arterial hypertension appears in the oligoanuric and uremic stages. In the polyuric stage of chronic renal failure (diuresis reaches 2-3 l/day), which can last for years, hyperazotemia is moderate, glomerular filtration is 20-30 ml/min. the relative density of urine is lower than the relative density of blood plasma (1010-1012). With congenital nephropathies (proteinuria up to 1 g/day), proteinuria, hematuria, and leukocyte-turia appear. In the oligoanuric stage, the patient’s condition sharply worsens, which is due to the addition of hemorrhagic syndrome and cardiovascular failure. When glomerular filtration is below 10 ml/min, conservative therapy is carried out, homeostasis is impossible. The terminal stage of chronic renal failure is characterized by emotional lability (apathy is replaced by excitement), disturbance of night sleep, lethargy and inappropriate behavior. Puffy face, gray-yellow color, itchy skin, scratches on the skin, dull, brittle hair, dystrophy, hypothermia is characteristic. Decreased appetite Voice is hoarse. An ammonia smell appears from the mouth, and aphthous stomatitis develops. The tongue is coated, vomiting, regurgitation, sometimes diarrhea, foul-smelling, dark-colored stools. Anemia, hemorrhagic syndrome, muscle twitching appear. With prolonged uremia, pain in the arms and legs and brittle bones appear, which can be explained by uremic nephropathy and renal osteodystrophy. Uremic intoxication can be complicated by pericarditis, pleurisy, ascites, encephalopathy and uremic coma. Children with chronic renal failure experience symptoms of rickets (bone and muscle pain, bone deformities, growth retardation), which is associated with insufficient production of the biologically active metabolite of vitamin D.

During this period, anemia, hyperkalemia, and impaired renal function due to osmotic dilution increase, which leads to the development of hypovolemia with inadequate fluid administration.

Treatment. Treatment of chronic renal failure in conjunction with treatment of the underlying kidney disease, which leads to renal failure. In the initial stage, when there is no impairment of renal processes, etiotropic and pathogenetic therapy is prescribed, which will cure the patient and prevent the development of renal failure or lead to remission and a slow course of the disease. In the stage of impaired renal processes, pathogenetic therapy is carried out with symptomatic treatment methods (hypotensive drugs, antibacterial treatment, protein restriction in the daily diet, spa treatment, etc.).

Conservative treatment of chronic renal failure is aimed at restoring homeostasis, reducing azotemia, and reducing symptoms of uremia. The glomerular filtration rate is below 50 ml/min, the level of creatinine in the blood is above 0,02 g/l - it is necessary to reduce the amount of protein consumed to 30-40 g/day. The diet should be high in calories and contain essential amino acids (potato-egg diet without meat and fish). Food is prepared with a limited (up to 2-3 g) amount of table salt. To reduce the level of phosphates in the blood, use almagel 1-2 tsp. 4 times a day. During treatment, it is necessary to control the level of calcium and phosphorus in the blood. For acidosis, depending on the degree, 100-200 ml of 5% sodium bicarbonate solution is administered intravenously. When diuresis decreases, Lasix is ​​prescribed in doses (up to 1 g/day) that provide polyuria. Antihypertensive drugs are prescribed to lower blood pressure. For anemia, iron supplements are prescribed. When the hematocrit is 25% and below, fractional red blood cell transfusions are indicated. Antibiotics and their chemotherapeutic drugs for chronic renal failure are used carefully: doses are reduced by 2-3 times. Nitrofuran derivatives are contraindicated in chronic renal failure. In heart failure and chronic renal failure, cardiac glycosides are used cautiously in reduced doses, especially in case of hypokalemia. Hemodialysis may be indicated for exacerbation of renal failure, after the exacerbation has subsided. If the patient's condition improves, conservative therapy is carried out. Plasmapheresis courses provide a good effect in chronic renal failure. In the terminal stage, the patient is transferred to hemodialysis. Regular hemodialysis is used when creatinine clearance is below 10 ml/min and its plasma level is above 0,1 g/l. CRF must be differentiated from acute renal failure, which is distinguished by a sudden onset with an oligoanuric stage and reverse development, from neurohypophyseal diabetes insipidus, the difference being that there is no hyperazotemia and other signs of chronic renal failure, from anemic syndrome and other diseases (hypoplastic anemia, etc.), in which there are no symptoms of chronic renal failure.

Treatment is aimed at reducing hyperazotemia and correcting water and electrolyte metabolic disorders. Basic principles as in the treatment of acute renal failure. The "dialysis-kidney transplant" program remains the most promising in the treatment of children with chronic renal failure, which helps patients return to normal life. Indications for the implementation of the program are the lack of effect from conservative therapy, an increase in serum creatinine levels to 0,6 mmol/l (6 mg%) and potassium in the blood above 7 mmol/l.

Forecast. Hemodialysis and kidney transplantation change the fate of patients with chronic renal failure, allowing them to prolong life and achieve rehabilitation. The selection of patients for these types of treatment is carried out by specialists from hemodialysis and organ transplantation centers.

Author: Pavlova N.V.

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