Acute Renal Failure

What is Acute Renal Failure?

Acute renal failure is a sudden and rapidly progressing violation of renal function, manifested by oligoanuria, azotemia, and disturbances in water-electrolyte balance.

Causes of Acute Renal Failure

The causes of acute renal failure are diverse. E. M. Tareev identifies the following groups of causes: 1) shock kidney, 2) toxic kidney, 3) acute infectious kidney, 4) vascular obstruction, 5) urinary tract obstruction.
The development of a shock kidney can result in traumatic shock, electrical injuries, burns, massive blood loss, muscle crush syndrome, surgical shock, transfusion of incompatible blood, pregnancy toxicosis, myocardial infarction, depleting vomiting. A toxic kidney occurs when poisoning with heavy metal salts, primarily mercury salts, organic poisons (carbon tetrachloride, dichloroethane, acetic acid, methyl alcohol, etc.), certain medications (barbiturates, quinine, pachycarpine), plant and animal poisons origin (snake, mushroom poison and insect venom).
Acute infectious kidney occurs with sepsis of various origins, primarily with anaerobic, and in patients with septic abortion. Acute renal failure can also occur with thrombosis and embolism of the renal arteries, with periarteritis nodosa, acute diffuse glomerulonephritis and acute pyelonephritis. Finally, this syndrome can be caused by mechanical obstruction to the outflow of urine in case of kidney stone disease, compression of the ureters.

Pathogenesis during Acute Renal Failure

Given the variety of reasons leading to the development of acute renal failure, it is hardly possible to reduce its development to any one mechanism. The most important is the ischemic factor.
With a significant decrease in heart function, a decrease in stroke volume of blood due to blood loss, loss of a significant amount of fluid or pathological redistribution of blood during shock and collapse, renal blood flow sharply decreases. Impaired renal circulation inevitably leads to a decrease in filtration and a violation of other functions of the kidneys. In some cases, a decrease in circulating blood volume occurs due to a decrease in plasma volume.
An important mechanism of impaired renal circulation in various types of shock is a spasm of the renal vessels due to neuro-humoral effects on the vessels of the kidneys, histamine and serotonin, released during shock or destruction of blood cells and tissues in pathological conditions.
The ultimate mechanism of renal ischemia is renal tissue anoxia, to which the latter is very sensitive. However, a decrease in renal blood flow is not a direct cause of oligoanuria. In chronic kidney diseases, a sharp decrease in renal blood flow and filtration does not reduce diuresis. Therefore, a drop in renal blood flow and a sharp decrease in filtration is difficult to explain oligoanuria. Apparently, the filtrate is almost completely reabsorbed in the damaged tubules. Due to damage to the basal membrane of the tubules, the glomerular filtrate can directly contact the renal interstitium and is easily absorbed back into the blood and lymph.
Another important factor is nephro-toxins. Various nephrotropic poisons disrupt the enzymatic processes in the renal tissue, and damaging the lysosomal cell membranes can lead to necrosis. According to modern ideas, tubular obstruction should not be considered as a cause of impaired renal function, but rather as a consequence of oligoanuria, although this obstruction may be an additional factor that worsens the course of acute renal failure.

Pathological Anatomy

Macroscopically, in acute renal failure, the kidneys are enlarged, flabby, the cortical layer swollen, the pattern of the cortex loses its clarity. The basis of patho-morphological changes in acute renal failure is the defeat of the tubules, primarily tubulonecrosis and tubulorexis, as well as edema of the interstitial tissue of the kidneys. For a toxic kidney, tubulonecrosis is more characteristic, for a shock one – damage to the basement membrane of the tubules with fragmentation of the main membrane, referred to as tubulo-rexis. In the tubule epithelium, swelling of the cytoplasm, granular, vacuole, and less often fatty degeneration are noted. With electron microscopy, swelling, edema and decay of mitochondria are noted. Morphological changes in acute renal failure undergo rapid dynamics. Necrotic epithelium is desquamated and rejected, interstitial tissue edema decreases and epithelial regeneration begins along the preserved main membrane. However, where the rupture of the basement membrane occurred, complete recovery of the nephron does not occur. The consequence of the transferred process is focal nephron fibrosis.

Symptoms of Acute Renal Failure

During acute renal failure, four periods or stages are distinguished: 1) shock, 2) oligoanuria, 3) restoration of diuresis with a phase of initial diuresis and a phase of polyuria and, finally, 4) recovery period. In the first period, the symptoms of the underlying disease, leading to acute renal failure and shock, are most pronounced. Tachycardia, a decrease in blood pressure, which, however, can be transient, is noted. In the period of oligoanuria, urination decreases or completely stops. This is accompanied by a gradual increase in all components of the residual nitrogen of the blood, phenol and other excreted metabolic products.

Sometimes at the beginning of this period, patients feel better for a while, despite the absence of urine. Gradually, they begin to complain of weakness, loss of appetite, headache. Nausea, vomiting appear. With the progression of the disease during breathing, the smell of ammonia is determined.

Disorders of the central nervous system are manifold. Most often there is apathy, but sometimes the patient can be excited, poor orientation, confusion. Often hyper reflection and convulsive seizures are noted.

In cases where acute renal failure was the result of sepsis, herpetic eruptions around the mouth and nose can be noted. The nature of skin changes in acute renal failure resulting from allergic reactions can be diverse: fixed erythema, urticaria rash, toxicoderma. The pulse exceeds 100 beats per minute. The boundaries of the heart are expanding. Particularly demonstrative expansion of the heart is determined on radiographs. Above the apex of the heart, systolic murmur is heard, an accent of the II tone, a gallop rhythm is detected. Systolic blood pressure in some patients is elevated. Sometimes there is a decrease in diastolic pressure, in some patients – to zero. Rhythm and conduction disturbances are noted: atrioventricular extrasystole and intraventricular block, mainly associated with violations of 13–143 electrolyte metabolism and acidosis. Fibrinous pericarditis with a noise of pericardial friction, pain in the region of the heart, changes in the electrocardiogram may be noted. Interestingly, the symptoms of pericarditis intensify after hemodialysis.

Nausea and vomiting, loss of appetite are observed in almost all patients. Less common are diarrhea and melena. Especially often, phenomena from the digestive organs are noted in hemorrhagic fever with renal syndrome. The occurrence of gastrointestinal lesions is primarily associated with the development of excretory gastritis and enterocolitis, which are erosive in nature. However, some of the symptoms are due to profound electrolyte imbalance. In the lungs, interstitial edema develops, which is based on the increased permeability of the alveolar capillaries. Pulmonary edema is clinically poorly recognized and diagnosed mainly with a chest radiograph. In this case, bilateral, symmetrical, with fuzzy contours, dimming in the basal zone is detected.

The predominant clinical sign at this stage is oligoanuria. The amount of daily urine ranges from 20 to 300 ml at a density of 1003-1008. The urine is cloudy, dark brown or bloody. The sediment is large, it contains many red blood cells, white blood cells, blocks of hemin-impregnated cylinders. There is a lot of protein in the urine. Urea and creatinine excretion in urine is reduced. High leukocytosis, a marked shift in the leukocyte formula, anemia, and an increase in ESR are noted in the blood.

Anemia in acute renal failure is constantly developing. Anemia is most pronounced in cases where acute renal failure is preceded by intravascular hemolysis. Anemia, growing during the period of oliguria, reaches a maximum in the initial phase of recovery of diuresis and stubbornly continues during the recovery period.

Pronounced disorders of homeostasis develop. The content of residual nitrogen increases from 14–26 to 140–260 mmol / l (from 20–40 to 200–400 mg%). Urea nitrogen rises to a greater extent than residual nitrogen in general. Creatinine levels increase more rapidly than urea, especially in patients with massive muscle damage. The ammonia content in the blood also increases sharply, especially with combined renal and hepatic insufficiency. Concentrations of uric acid and indoxin increase not so significantly. Metabolic acidosis develops, usually uncompensated. Acute renal failure is characterized by hyperkalemia and hypermagnesemia, manifested by an electrocardiographically high T wave, a decrease or disappearance of the U wave, and a violation of atrioventricular and intraventricular conduction. High potassium levels are explained by the appearance of pathological neuromuscular symptoms such as increased muscle irritability, hyperreflexia, and even paralysis.

However, in some cases of acute renal failure, with repeated vomiting, profuse diarrhea, on the contrary, excessive excretion of potassium and the development of hypokalemia with weakness, decreased reflexes, and bloating due to intestinal paresis are observed. At the same time, an ST segment decline, a decrease in the voltage of the T wave, and a high Q wave are noted on the electrocardiogram. The S — T interval is significantly extended.

During oligoanuria, as a rule, hyperhydration is observed with a decrease in the hematocrit. *
Damage to the liver in acute renal failure is observed almost constantly. Clinical lesions of the liver are manifested by icteric sclera and yellowness of the skin.

Anuria or oliguria usually lasts 5-10 days, but in some cases 30 or more days. It is clear that in the latter case, methods of active = therapy of renal failure are required to maintain the patient’s life.
An increase in diuresis can begin a few days after oliguria and occurs gradually. First, the amount of urine exceeds 500 ml, and then, gradually increasing, is more than 2000 ml / day. From this time begins the third period of acute renal failure.

In this period, clinical improvement does not develop immediately, and sometimes the condition of patients may worsen. At the beginning of the diuretic period, the level of azotemia may increase, hyperkalemia may increase. The concentration ability of the kidneys remains low. The patient during polyuria is losing weight. The period of polyuria usually lasts 4-6 days. Patients’ appetite improves, pathological changes from the nervous system and circulatory system disappear.

It is conventionally assumed that the recovery period begins on the day of the disease, when the level of residual nitrogen or urea becomes normal. It lasts 3-6-22 months, during which not only homeostasis is completely restored, but also the filtration, concentration ability of the kidneys, and tubular secretion gradually increase.
However, within 1-2 years, signs of functional insufficiency of individual organs and systems (heart, liver, etc.) may persist.

Acute renal failure, if not fatal, results in a gradual recovery without a tendency to develop chronic kidney disease.
After 6 months, more than half of the patients fully recover from working capacity, although in some patients by this time working capacity remains limited, and they are recognized as invalids of group III. In many ways, the ability to work of patients depends on the underlying disease that caused acute renal failure.

Treatment of Acute Renal Failure

Measures aimed at reducing the effect of nephrotoxins and preventing circulatory disturbances reduce tubular damage. Early removal of poison from the body, the appointment of specific antidotes and the use of drugs that prevent and eliminate circulatory disorders are also measures for the prevention of acute renal failure.
In cases where there is a risk of developing acute renal failure, in order to prevent it, intravenous mannitol can be administered in a 10% solution at the rate of 1 g per 1 kg of patient weight. It improves renal blood flow, increases glomerular filtration, and acts as an osmotic diuretic. In the oliguria stage, the use of mannitol is ineffective and impractical.
It should be noted that the etiological treatment of acute renal failure in most cases is effective only in the early stages of the disease. Patients with acute renal failure must be hospitalized. Careful care of the oral cavity, skin and mucous membranes is necessary. In normal cases, the amount of injected fluid should not exceed 600-700 ml / day. With polyuria, it is necessary to completely compensate for the loss of fluid and electrolytes.
The appointment of large amounts of fluid to the patient during the period of oliguria and anuria in the hope of stimulating diuresis and reducing the concentration of nitrogenous toxins does not give results. It enhances hyperhydration, reduces the effective osmotic pressure of plasma, and enhances water “intoxication.”
In the initial period of the disease, the most effective treatment is exchange blood transfusion. With its help, part of the non-dialyzed plasma hemoglobin is extracted, the bloodstream is replenished with red blood cells, and anemia is eliminated. If it is not possible to perform an exchange blood transfusion, a blood transfusion should be performed, the purpose of which is to eliminate anemia and restore the volume of circulating blood.
Measures are being taken to combat shock and blood loss. In cases where there is a picture of shock and compensation for blood loss does not eliminate hypotension, the use of corticosteroids (intravenously 30-60 mg of prednisolone or 100 mg of hydrocortisone) is indicated. However, the usefulness of such therapy is limited to the very initial period of the disease.
If there is an infection, antibiotic treatment is necessary, to which the allocated flora is sensitive, but antibiotics are often used for preventive purposes. However, we must not forget that most antibiotics are excreted by the kidneys, which makes it necessary to reduce the dosage and frequency of antibiotic administration. Antibiotics such as streptomycin, monomycin, neomycin, it is better not to use in acute renal failure due to their nephro-toxicity.
In connection with the danger of urinary tract infection, it is necessary to pay attention to the fact that the introduction of a permanent catheter, especially in men, in order to accurately control diuresis is dangerous due to the development of urethritis, prostatitis and cystitis, followed by pyelonephritis.
During the first three periods of the disease, protein is completely excluded from the patient’s diet. You can give patients cream, sour cream, syrups. With pornic dyspeptic disorders, the patient eats parenterally.
To combat acidosis, a 5% sodium bicarbonate solution is used from the initial calculation of 0.5-1 ml per 1 kg of mass under the control of determining acid-base balance indicators.
To correct protein catabolism, anabolic steroid hormones are introduced: methyl anrostrostenediol, nerobol, retabolil.
Effectively intravenous infusion of hypertonic solutions of 40% glucose (up to 100 ml / day). At the same time, insulin is used at the rate of 1 unit per 3-4 g of glucose.
Long-term gastric lavage is indicated in order to wash out nitrogenous slags; this relieves patients of indomitable nausea and vomiting. Parenteral administration of calcium salts is necessary, especially with the development of seizures.
Acute renal failure, which is not amenable to conservative treatment, is an indication for hemodialysis using an artificial kidney or peritoneal dialysis. In the early days of the development of oligoanuria, the use of hemodialysis is impractical, since in a significant part of the cases conservative treatment allows the restoration of renal function. Hemodialysis is indicated for blood creatinine levels above 114 mmol / L (15 mg% ‘), urea above 49 mmol / L (300 mg%), residual nitrogen above 113-140 mmol / L (160-200 mg%), potassium 6, 5 mmol / l. Indications for hemodialysis should be evaluated only in conjunction with the clinical picture. Contraindications to hemodialysis are the septic process, acute thromboembolism, myocardial infarction, gastrointestinal bleeding, severe heart and liver failure.
The issue of sanatorium-resort treatment is decided in each case individually and not earlier than 6 months after discharge from the hospital.
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