Treatment of acute renal failure in adults. Acute renal failure - symptoms and treatment
The kidneys are a pair of small (about the size of a fist) bean-shaped organs that lie on either side of the spine and are located just below the line of the ribs. The kidneys remove waste products and toxins from the blood and maintain optimal electrolyte balance. They also eliminate excess water in the body, and by absorbing, beneficial chemicals and waste allow free passage into the bladder as urine.
The kidneys allow a person to consume a variety of foods, medications, vitamins and nutritional supplements, and excess fluids without fear of toxic foods reaching dangerous levels.
In the first stage of filtration, the blood passes through complex structures consisting of blood vessels woven together. Substances present in the blood are selectively filtered through the outer linings of the vessels and excreted in the urine or absorbed for further filtration. The cycle continues until all nutrients are absorbed into the blood and all waste products are eliminated from the body.
After urine leaves the kidney, it passes through long, thin, tubular ureters into the bladder and out of the urethra during urination.
The kidneys help regulate blood pressure and secrete hormones that promote the production of red blood cells.
Kidney failure occurs when the kidneys lose part or all of their ability to filter blood.
The accumulation of toxic substances excreted from the body by the kidneys can cause dangerous health problems.
Acute kidney failure develops asymptomatically over many years, slowly destroying the kidneys. The disease progresses so gradually that symptoms manifest themselves only when the organ is able to perform its functions only to 1/10th of a share.
Causes of acute renal failure
The causes of kidney failure fall into several categories:
- Prerenal - disruption of blood flow to the organ;
- Postrenal - disturbance of urine outflow;
- Renal - functional disorders in the kidney itself;
Prerenal renal failure the most common type of acute renal failure (60% - 70% of all cases). Perenal insufficiency develops against the background of:
- Dehydration: vomiting, diarrhea, diuretics, or blood loss;
- Drop in blood pressure associated with injury or burn;
- Blockage or narrowing of the blood vessel that carries blood to the kidneys;
- Heart failure or heart attacks.
At the first stages of the development of perenal insufficiency, actual damage to the kidney does not occur. With appropriate treatment, complete remission is possible. At the same time, the lack of qualified assistance for a long time can cause pathological damage to organ tissue.
Postrenal failure sometimes called obstructive because it is often caused by something blocking the elimination or production of urine by the kidneys. It is a rare cause of acute kidney failure (5 to 10% of all cases). This problem can be completely resolved if the obstruction does not last too long to cause damage to the kidney tissue.
Ureteral obstruction can be caused by the following reasons:
- Kidney stones;
- Urinary tract cancer;
- Medicines;
- Obstruction at the level of the bladder may be caused by;
- Stones in the bladder;
- Enlarged prostate (most common cause in men);
- Blood clot;
- Bladder cancer;
- Neurological bladder disorder.
The essence of treatment is to eliminate the root cause of the obstruction. Once the obstruction is removed, the kidneys will recover within 1-2 weeks, unless there is infection or other problems.
Primary kidney damage is the most complex cause of renal failure (occurs in 25% to 40% of cases). Kidney causes of acute kidney failure include those that affect the filtration function of the kidneys, those that affect the blood supply within the kidney, and those that affect the kidney tissue that processes water and salt processing.
What can cause kidney failure:
- Diseases of the blood vessels;
- Thrombus in a vessel;
- Kidney tissue injury;
- Glomerulonephritis;
- Acute interstitial nephritis;
- Acute tubular necrosis;
- Polycystic kidney disease.
Glomerulonephritis: glomeruli - the original filtration systems of the kidney, can be damaged by various diseases, including infectious diseases. As a result of the inflammatory process, kidney function deteriorates.
A typical example is a complication after a sore throat. Streptococcal bacterial infections can also damage the glomeruli.
Symptoms of globular damage include pain in the lumbar region and a change in the color of the urine, becoming like strong tea or cola.
Other symptoms include producing less urine than usual, blood in the urine, high blood pressure, and swelling.
Treatment is usually prescribed medication. But if kidney function cannot be restored, dialysis is prescribed to artificially remove toxic substances dangerous to health and life from the body.
Acute interstitial nephritis: This is a sudden decline in kidney function caused by inflammation of the interstitial kidney tissue, which primarily processes salt and regulates water balance.
Medicines such as antibiotics, anti-inflammatory drugs (eg, aspirin, ibuprofen), and diuretics are the most common causes of acute interstitial nephritis.
Other causes include diseases such as lupus, leukemia, lymphoma and sarcoidosis.
All pathological changes as a result of acute interstitial nephritis are reversible if the patient receives timely medical care. The essence of treatment is the removal of toxic medications, treatment of infections and dialysis if necessary.
Acute tubular necrosis- This is damage to the renal tubules and disruption of their full functioning. Tubular necrosis is usually the end result of other causes of acute renal failure. The tubes are very delicate structures that perform the main function during blood filtration. Damaged cells forming the tubules become dysfunctional and die.
Polycystic kidney disease is a genetic disease characterized by the formation of numerous cysts in the kidneys. During polycystic kidney disease, the kidneys enlarge, most of their normal structure is replaced by connective tissue, which leads to dysfunction and leads to renal failure.
Symptoms of acute renal failure
Acute renal failure is characterized by:
- Reduced urine production;
- Edema;
- Problems with concentration;
- Confusion;
- Fatigue;
- Lethargy;
- Nausea, vomiting;
- Diarrhea;
- Abdominal pain;
- Metallic taste in the mouth.
Convulsions and coma occur only in very severe and advanced cases of renal failure.
When to seek medical help?
Contact your doctor if you experience the following symptoms:
- Loss of strength, inability to fully perform usual actions;
- Increased blood pressure;
- swelling of the legs, around the eyes, or in other parts of the body;
- shortness of breath or change in normal breathing rhythm;
- Nausea or vomiting;
- Prolonged absence of urination;
- Dizziness;
Emergency assistance is required in the following cases:
- Changes in level of consciousness, drowsiness;
- Fainting;
- Chest pain;
- Difficulty breathing;
- Extremely high blood pressure;
- Severe nausea and vomiting
- Severe bleeding (from any source);
- Severe weakness;
- Inability to urinate.
Diagnosis of kidney failure
Many people with acute kidney failure do not notice any symptoms. Even if symptoms are observed, they are nonspecific and may be misinterpreted. Therefore, only on the basis of a complete medical examination can one draw conclusions about the presence or absence of kidney problems. Most often, kidney failure is noticed during a blood or urine test.
Kidney disease is indicated by:
- High levels of urea and creatinine;
- Abnormally low or high electrolyte levels in the blood;
- Decreased red blood cell levels (anemia).
If the doctor is unsure of the diagnosis, after laboratory tests. Additionally, an ultrasound examination of the kidneys and bladder is prescribed to identify specific causes of renal failure. Sometimes a biopsy is performed for this purpose.
Prognosis for acute renal failure
Recovery from acute kidney failure depends on what caused the illness. If the cause of the disease is secondary factors and the organ tissue is not damaged, there is a high probability of the patient’s complete recovery. Particularly severe cases of kidney failure can cause death. In the long term (from 1 to 10 years). Approximately 12.5% of surviving patients require dialysis. Between 9 and 31% suffer chronically from chronic kidney disease.
Video podcast: About the diagnosis and treatment of kidneys
(AKI) is a syndrome of sudden, rapid decline or cessation of the function of both kidneys (or a single kidney), leading to a sharp increase in nitrogen metabolism products in the body, a disruption of general metabolism. Impaired function of the nephron (the structural unit of the kidney) occurs due to a decrease in blood flow in the kidneys and a sharp decrease in oxygen delivery to them.
Acute renal failure develops within a few hours and up to 1-7 days, lasting more than 24 hours. With timely treatment and correct treatment, it results in complete restoration of kidney function. Acute renal failure is always a complication of other pathological processes in the body.
Causes of acute renal failure
1. Shock kidney. Acute renal failure develops during traumatic shock with massive tissue damage, due to a decrease in the volume of circulating blood (blood loss, burns), and reflex shock. This is observed in accidents and injuries, severe operations, damage and decay of liver and pancreas tissue, myocardial infarction, burns, frostbite, transfusion of incompatible blood, abortion.
2. Toxic kidney. ARF occurs when poisoned by nephrotropic poisons, such as mercury, arsenic, Berthollet's salt, snake venom, insect venom, and mushrooms. Intoxication with drugs (sulfonamides, antibiotics, analgesics), X-ray contrast agents. Alcoholism, drug addiction, substance abuse, professional contact with salts of heavy metals, ionizing radiation.
3. Acute infectious kidney. Develops in infectious diseases: leptospirosis, hemorrhagic fever. Occurs in severe infectious diseases accompanied by dehydration (dysentery, cholera), and bacterial shock.
4. Obstruction (obstruction) of the urinary tract. Occurs with tumors, stones, compression, trauma to the ureter, with thrombosis and embolism of the renal arteries.
5. Develops in acute pyelonephritis (inflammation of the renal pelvis) and acute glomerulonephritis (inflammation of the renal glomeruli).
Prevalence of acute renal failure
- 60% of all cases of acute renal failure are associated with surgery or trauma.
- In 40% of cases, the patient develops acute renal failure during treatment in medical institutions.
- 1-2% - in women during pregnancy.
Symptoms of acute renal failure
In the initial period, the symptoms of the disease that led to the development of acute renal failure come to the fore. These are symptoms of poisoning, shock, the disease itself. At the same time, the amount of urine excreted begins to decrease (diuresis), first to 400 ml per day (oliguria), and then to 50 ml per day (anuria). Nausea, vomiting, and decreased appetite appear. Drowsiness, inhibition of consciousness occurs, convulsions and hallucinations may appear. The skin becomes dry, pale with hemorrhages, and swelling appears. Breathing is deep and frequent. Tachycardia, cardiac arrhythmia are heard, and blood pressure rises. Characterized by bloating and loose stools.
With timely treatment, a period of diuresis recovery begins. The amount of urine excreted increases to 3-5 liters per day. All symptoms of acute renal failure gradually disappear. For complete recovery it takes from 6 months to 2 years.
Treatment of acute renal failure
All patients with acute renal failure require urgent hospitalization in the nephrology and dialysis department or in the intensive care unit.
Of decisive importance is the early treatment of the underlying disease and the elimination of the factors that caused kidney damage. Since shock is the cause in most cases, it is necessary to begin anti-shock measures as quickly as possible. In case of massive blood loss, blood loss is compensated by administering blood substitutes. In case of poisoning, toxic substances are removed from the body by washing the stomach, intestines, and using antidotes. In case of severe renal failure, sessions of hemodialysis or peritoneal dialysis are performed.
Stages of treatment for patients with acute renal failure:
- Eliminate all causes of decreased renal function that are amenable to specific therapy, including correction of prerenal and postrenal factors;
- Try to achieve a stable volume of urine excreted;
- Conservative therapy:
- reduce the amounts of nitrogen, water and electrolytes entering the body to such an extent that they correspond to their excreted amounts;
- provide adequate nutrition to the patient;
- change the nature of drug therapy;
- ensure monitoring of the patient’s clinical condition (the frequency of measurements of vital signs is determined by the patient’s condition; measurement of the amounts of substances entering and released from the body; body weight; inspection of wounds and intravenous infusion sites; physical examination should be performed daily);
- ensure control of biochemical parameters (the frequency of determining the concentrations of BUN, creatinine, electrolytes and calculating the blood formula will be dictated by the patient’s condition; in patients suffering from oliguria and catabolism, these indicators should be determined daily, the concentrations of phosphorus, magnesium and uric acid - less often)
4. Perform dialysis therapy
A number of manifestations of acute renal failure can be controlled using conservative therapy. After any disturbances in intravascular fluid volume have been corrected, the amount of fluid entering the body should exactly correspond to the sum of its measured output and insensible losses. The amounts of sodium and potassium introduced into the body should not exceed their measured excreted amounts. Daily monitoring of fluid balance and body weight makes it possible to determine whether the patient’s normal volume of intravascular fluid is impaired. In patients with acute renal failure receiving adequate treatment, body weight decreases by 0.2-0.3 kg/day. A more significant decrease in body weight suggests hypercatabolism or a decrease in the volume of intravascular fluid, and a less significant one suggests that excess amounts of sodium and water are entering the body. Since most drugs are eliminated from the body, at least in part, by the kidneys, careful attention must be paid to the use of drugs and their dosage. Serum sodium concentration serves as a guide to determine the required amount of water administered. A decrease in sodium concentration indicates that there is excess water in the body, while an unusually high concentration indicates that there is not enough water in the body.
In order to reduce catabolism, it is necessary to ensure a daily intake of at least 100 g of carbohydrates into the body. Some recent studies suggest that administration of a mixture of amino acids and a hypertonic glucose solution into the central veins improves the condition of patients and reduces mortality in a group of patients suffering from acute renal failure following surgery or trauma. Because parenteral administration of excessively large quantities of nutrients can be associated with significant difficulties, this type of nutrition should be reserved for catabolic patients who do not achieve satisfactory results with conventional oral administration of nutrients. Previously, anabolic androgens were used to reduce the level of protein catabolism and reduce the rate of increase in BUN. Currently, this treatment is not used. Additional measures to reduce the level of catabolism include timely removal of necrotic tissue, control of hyperthermia, and early initiation of specific antimicrobial therapy.
Patients with a mild degree of metabolic acidosis associated with acute renal failure are not prescribed treatment, with the exception of those whose serum bicarbonate concentration does not decrease below 10 mEq/L. An attempt to restore the acid-base state by urgently introducing alkalis can reduce the concentration of ionized calcium and provoke the development of tetany. Hypocalcemia is usually asymptomatic and rarely requires specific correction. Hyperphosphatemia should be controlled by oral administration of 30-60 ml of aluminum hydroxide 4-6 times a day, since soft tissue calcification develops when the calcium x phosphorus product is more than 70. Timely initiation of dialysis therapy will help control elevated serum phosphorus concentrations in patients with severe hyperphosphatemia. If the patient does not have acute nephropathy caused by uric acid, then secondary hyperuricemia in acute renal failure most often does not require the use of allopurinol. The decrease in the magnitude of the glomerular filtration rate makes the proportion of uric acid filtered out and, therefore, the deposition of uric acid inside the tubules negligible. In addition, for unknown reasons, acute renal failure, despite hyperuricemia, is rarely complicated by clinically manifested gout. For timely detection of gastrointestinal bleeding, it is important to carefully monitor changes in the hematocrit number and the presence of occult blood in the stool. If the hematocrit number decreases rapidly and the rate of this decrease is inadequate to the severity of renal failure, then alternative causes of anemia should be sought.
Congestive heart failure and hypertension are indicators of excess fluid in the body and require appropriate action. It must be remembered that many drugs, such as digoxin, are excreted primarily by the kidneys. As noted earlier, persistent hypertension is not always caused by increased fluid volume in the body; Factors such as hyperreninemia may contribute to its development. In a number of cases, in order to prevent gastrointestinal bleeding in some seriously ill patients, selective blockade of histamine-2 receptors (cimetidine, ranitidine) was successfully carried out, but the feasibility of such treatment in acute renal failure has not yet been studied. To avoid infection and damage to the integrity of anatomical barriers, prolonged catheterization of the bladder should be avoided, the oral cavity and skin should be sanitized, the insertion sites of intravenous catheters and the skin incision site for tracheostomy should be treated in compliance with the rules of asepsis, and careful clinical observation should be carried out. If the patient's body temperature rises, it is necessary to carefully examine him, paying special attention to the condition of the lungs, urinary tract, wounds and places of insertion of the catheter for intravenous infusion.
In acute renal failure, hyperkalemia often develops. If the increase in potassium concentration in the blood serum is small (less than 6.0 mmol/l), then to correct it it is enough to simply exclude all sources of potassium from the diet and conduct constant careful laboratory monitoring of biochemical parameters. If the serum potassium concentration increases to levels exceeding 6.5 mmol, and especially if any changes appear on the ECG, then active treatment of the patient should be started. Treatment can be divided into emergency and routine forms. Emergency treatment includes intravenous calcium (5-10 ml of 10% calcium chloride solution is administered intravenously over 2 minutes under ECG monitoring), bicarbonate (44 mEq is administered intravenously over 5 minutes) and glucose with insulin (200-300 ml 20 % glucose solution containing 20-30 units of regular insulin is administered intravenously over 30 minutes). Routine treatment involves administration of potassium-binding ion exchange resins such as sodium polystyrene sulfonate. They can be administered orally every 2-3 hours per dose. 25-50 g with 100 ml of 20% sorbitol to prevent constipation. On the other hand, for a patient who cannot take medications by mouth, 50 g of sodium polystyrene sulfonate and 50 g of sorbitol in 200 ml of water can be administered at intervals of 1-2 hours through a retention enema. If refractory hyperkalemia develops, hemodialysis may be necessary.
Some patients with acute renal failure, especially those without oliguria and catabolism, can be successfully treated without or with minimal use of dialysis therapy. There is an increasing trend to use dialysis therapy in the early stages of acute kidney failure to prevent possible complications. Early (prophylactic) dialysis often simplifies the management of the patient, creating the possibility of a more liberal approach to ensuring that the body receives appropriate amounts of potassium and fluid and allowing for an improvement in the general well-being of the patient. The absolute indications for dialysis are symptomatic uremia (usually manifested by central nervous system and/or gastrointestinal symptoms); development of resistant hyperkalemia, severe acidemia or accumulation of excess fluid in the body that is not amenable to medication, and pericarditis. In addition, many centers try to maintain predialysis serum BUN and creatinine levels below 1000 and 80 mg/L, respectively. To ensure adequate prevention of uremic symptoms, patients without oliguria and catabolism may require dialysis only in rare cases, and patients whose condition is aggravated by catabolism and trauma may require daily dialysis. Peritoneal dialysis is often an acceptable alternative to hemodialysis. Peritoneal dialysis may be particularly useful in patients with non-catabolic renal failure who are candidates for infrequent dialysis. To control the volume of extracellular fluid in patients with acute renal failure, slow continuous filtration of blood using high-permeability filters can be used. Currently commercially available filters connected to the circulatory system through an arteriovenous shunt allow the removal of 5 to 12 liters of blood plasma ultrafiltrate per day without the use of a pump. Therefore, such devices appear to be particularly useful in the treatment of patients who suffer from oliguria and have increased extravascular fluid volume and unstable hemodynamics.
Nutrition for such patients is very important.
Nutrition for acute renal failure
Hunger and thirst sharply worsen the condition of patients. A low-protein diet is prescribed (no more than 20 g of protein per day). The diet consists mainly of carbohydrates and fats (porridge with water, butter, kefir, bread, honey). If it is impossible to eat, nutritional mixtures and glucose are administered intravenously.
Complications of acute renal failure
In the initiating and maintenance phases of acute renal failure, the excretion of nitrogen metabolism products, water, electrolytes and acids from the body in the urine is disrupted. The severity of the changes that occur in the chemical composition of the blood depends on the presence of oliguria and the state of catabolism in the patient. In patients who do not suffer from oliguria, higher levels of glomerular filtration are noted than in patients with oliguria, and as a result, the former excrete more products of nitrogen metabolism, water and electrolytes in the urine. Therefore, disturbances in the chemical composition of the blood in acute renal failure in patients who do not suffer from oliguria are usually less pronounced than in those suffering from oliguria.
Patients suffering from acute renal failure accompanied by oliguria are at increased risk of developing salt and water overload, leading to hyponatremia, edema and blood stagnation in the lungs. Hyponatremia is a consequence of the intake of excessive amounts of water, and edema is a consequence of excessive amounts of both water and sodium.
Acute renal failure is characterized by hyperkalemia, caused by reduced elimination of potassium by the kidneys with its continued release from tissues. The usual daily increase in serum potassium concentration in non-oliguric and catabolic patients is 0.3-0.5 mmol/day. A greater daily increase in serum potassium concentration indicates a possible endogenous (tissue destruction, hemolysis) or exogenous (drugs, diet, blood transfusion) potassium load or release of potassium from cells due to acidemia. Typically, hyperkalemia is asymptomatic until the serum potassium concentration increases to values exceeding 6.0-6.5 mmol/L. If this level is exceeded, changes are observed in the electrocardiogram (bradycardia, deviation of the electrical axis of the heart to the left, pointed T waves , expansion of the ventricular complexes, an increase in the P-R interval and a decrease in the amplitude of the P waves) and ultimately cardiac arrest may occur. Hyperkalemia can also lead to muscle weakness and flaccid tetraparesis.
In acute renal failure, hyperphosphatemia, hypocalcemia and mild hypermagnesemia are also observed.
Soon after the development of significant azotemia, normocytic, normochromic anemia develops, and the hematocrit number stabilizes at 20-30 percent by volume. Anemia is caused by a weakening of erythropoiesis, as well as a slight decrease in the lifespan of red blood cells.
Infectious diseases complicate the course of acute renal failure in 30-70% of patients and are considered the leading cause of mortality. The portals of infection are often the respiratory tract, surgical sites, and urinary tract. In this case, septicemia often develops, caused by both gram-positive and gram-negative microorganisms.
Cardiovascular complications of acute renal failure include circulatory failure, hypertension, arrhythmias, and pericarditis.
Acute renal failure is often accompanied by neurological disorders. Patients not on dialysis experience lethargy, drowsiness, confusion, disorientation, fluttering, restlessness, myoclonic muscle twitching, and seizures. To a greater extent, they are typical for elderly patients and can be easily corrected with dialysis therapy.
Acute renal failure is often accompanied by gastrointestinal complications, which include anorexia, nausea, vomiting, intestinal obstruction and vague complaints of abdominal discomfort.
Acute renal failure during pregnancy.
Most often, acute renal failure develops in the early or late stages of pregnancy. In the first trimester of pregnancy, acute renal failure usually develops in women after a criminal abortion under unsterile conditions. In these cases, decreased intravascular fluid volume, sepsis, and nephrotoxins contribute to the development of acute renal failure. The prevalence of this form of acute renal failure has noticeably decreased nowadays due to the widespread availability of abortion in a medical facility.
Acute kidney failure may also develop as a result of major postpartum hemorrhage or preeclampsia in late pregnancy. Most patients with this type of acute renal failure usually experience complete recovery of kidney function. However, in a small number of pregnant women suffering from acute renal failure, renal function is not restored, and in these cases, histological examination reveals diffuse necrosis of the renal cortex. The presence of massive bleeding during placental abruption usually complicates this condition. Along with this, clinical and laboratory signs of intravascular coagulation are detected.
A rare form of acute renal failure has been described that developed 1-2 weeks after uncomplicated childbirth, called postpartum glomerulosclerosis. This form of the disease is characterized by irreversible, rapidly progressing renal failure, although less severe cases have been described. Typically, patients suffer from concomitant microangiopathic hemolytic anemia. Histopathological changes in the kidneys in this form of renal failure are indistinguishable from similar changes that occur with malignant hypertension or scleroderma. The pathophysiology of this disease has not been established. There are also no methods of treating patients that would ensure permanent success, although the use of heparin is considered appropriate.
Prevention of kidney failure.
Preventive treatment deserves special attention due to the high morbidity and mortality rates among patients with acute renal failure. During the Vietnam War, military personnel experienced a fivefold reduction in mortality rates due to acute renal failure compared with similar rates during the Korean War. This reduction in mortality occurred in parallel with the provision of earlier evacuation of the wounded from the battlefield and an earlier increase in the volume of intravascular fluid. Therefore, it is very important to promptly identify patients with a high incidence of acute renal failure, namely: patients with multiple injuries, burns, rhabdomyolysis and intravascular hemolysis; patients receiving potential nephrotoxins; patients who have undergone surgical operations during which it became necessary to temporarily interrupt renal blood flow. Particular attention should be paid to maintaining optimal values of intravascular fluid volume, cardiac output and normal urine flow in such patients. Caution when using potentially nephrotoxic drugs and early treatment in cases of cardiogenic shock, sepsis and eclampsia can also reduce the incidence of acute renal failure.
General practitioner Vostrenkova I.N.
Kidney failure- a pathological condition that occurs in various diseases and is characterized by a violation of all kidney functions.
The kidney is an organ of the urinary system. Its main function is the formation of urine. 
It goes like this:
- Blood entering the kidney vessels from the aorta reaches the glomerulus from the capillaries, surrounded by a special capsule (Shumlyansky-Bowman capsule). Under high pressure, the liquid part of the blood (plasma) with substances dissolved in it seeps into the capsule. This is how primary urine is formed.
- Primary urine then moves through the convoluted tubule system. Here, water and substances necessary for the body are absorbed back into the blood. Secondary urine is formed. Compared to the primary one, it loses volume and becomes more concentrated; only harmful metabolic products remain in it: creatine, urea, uric acid.
- From the tubular system, secondary urine enters the renal calyces, then into the pelvis and into the ureter.
- Excretion of harmful metabolic products from the body.
- Regulation of blood osmotic pressure.
- Hormone production. For example, renin, which is involved in the regulation of blood pressure.
- Regulation of the content of various ions in the blood.
- Participation in hematopoiesis. The kidneys secrete the biologically active substance erythropoietin, which activates the formation of erythrocytes (red blood cells).
Causes of kidney failure
Causes of acute renal failure
Classification of acute renal failure, depending on the causes:- Prerenal. Caused by impaired renal blood flow. The kidney does not receive enough blood. As a result, the process of urine formation is disrupted, and pathological changes occur in the kidney tissue. Occurs in approximately half (55%) of patients.
- Renal. Associated with pathology of renal tissue. The kidney receives enough blood, but cannot produce urine. Occurs in 40% of patients.
- Postrenal. Urine is produced in the kidneys, but cannot flow out due to an obstruction in the urethra. If an obstruction occurs in one ureter, the healthy kidney will take over the function of the affected kidney - renal failure will not occur. This condition occurs in 5% of patients.
In the picture: A - prerenal renal failure; B - postrenal renal failure; C - renal renal failure.Causes of acute renal failure:
| Prerenal |
|
| Renal |
|
| Postrenal |
|
Causes of chronic renal failure
Symptoms of kidney failure
Symptoms of acute renal failure
Symptoms of acute renal failure depend on the stage:- initial stage;
- stage of decrease in daily urine volume to less than 400 ml (oliguric stage);
- stage of restoration of urine volume (polyuric stage);
- full recovery stage.
| Stage | Symptoms |
| Initial | At this stage, there is no renal failure as such yet. The person is concerned about the symptoms of the underlying disease. But disturbances in the kidney tissue are already occurring. |
| Oliguric | Renal dysfunction increases and the amount of urine decreases. Due to this, harmful metabolic products are retained in the body, and disturbances in the water-salt balance occur. Symptoms:
|
| Polyuric | The patient's condition returns to normal, the amount of urine increases, usually even more than normal. At this stage, dehydration and infections may develop. |
| Full recovery | Final restoration of kidney function. Usually lasts from 6 to 12 months. If during acute renal failure a large part of the kidney tissue was turned off, then complete recovery is impossible. |
Symptoms of chronic renal failure
- At the initial stage, chronic renal failure has no manifestations. The patient feels relatively normal. Typically, the first symptoms appear when 80%-90% of the kidney tissue ceases to perform its functions. But before this time, a diagnosis can be made if an examination is carried out.
- Usually the first to appear are general symptoms: lethargy, weakness, increased fatigue, frequent malaise.
- Urine excretion is impaired. More of it is produced per day than it should be (2-4 liters). Because of this, dehydration may develop. There is frequent urination at night. In the later stages of chronic renal failure, the amount of urine decreases sharply - this is a bad sign.
- Nausea and vomiting.
- Muscle twitching.
- Skin itching.
- Dryness and bitter feeling in the mouth.
- Stomach ache.
- Diarrhea.
- Nose and stomach bleeding due to decreased blood clotting.
- Hemorrhages on the skin.
- Increased susceptibility to infections. Such patients often suffer from respiratory infections, pneumonia.
- At a late stage: the condition worsens. Attacks of shortness of breath and bronchial asthma occur. The patient may lose consciousness or fall into a coma.
Diagnosis of kidney failure
| Diagnostic method | Acute renal failure | Chronic renal failure |
| General urine test | A general urine test for acute and chronic renal failure can reveal:
 |
|
| Bacteriological examination of urine | If the renal dysfunction was caused by an infection, the pathogen will be detected during the study. This analysis also makes it possible to identify an infection that has occurred against the background of renal failure and determine the sensitivity of the pathogen to antibacterial drugs.  |
|
| General blood test | In acute and chronic renal failure, a general blood test reveals changes:
 |
|
| Biochemical blood test | Helps evaluate pathological changes in the body caused by impaired renal function. In a biochemical blood test in acute renal failure, changes can be detected:
| In chronic renal failure, biochemical blood tests usually reveal changes:
|
| These methods allow you to examine the kidneys, their internal structure, renal calyces, pelvis, ureters, and bladder. In acute renal failure, CT, MRI and ultrasound are most often used to find the cause of narrowing of the urinary tract.  |
|
| Doppler ultrasound | Ultrasound examination, during which you can evaluate the blood flow in the vessels of the kidneys. | |
| Chest X-ray | It is used to identify disorders of the respiratory system and some diseases that may cause renal failure.
|
|
| Chromocystoscopy |
| |
| Kidney biopsy | The doctor obtains a piece of kidney tissue and sends it to the laboratory for examination under a microscope. Most often this is done using a special thick needle, which the doctor inserts into the kidney through the skin. Biopsy is resorted to in doubtful cases when it is not possible to establish a diagnosis.
|
|
| Electrocardiography (ECG) | This study is mandatory for all patients with acute renal failure. It helps to identify heart problems and arrhythmias.  |
|
| Zimnitsky test | The patient collects all urine during the day into 8 containers (each for 3 hours). Determine its density and volume. The doctor can assess the state of kidney function, the ratio of daytime and nighttime urine volumes. | |
Treatment of kidney failure
Acute renal failure requires immediate hospitalization of the patient in a nephrology hospital. If the patient is in serious condition, he is placed in the intensive care unit. Therapy depends on the causes of renal dysfunction. For chronic renal failure, therapy depends on the stage. At the initial stage, treatment of the underlying disease is carried out - this will help prevent severe renal dysfunction and make it easier to cope with them later. When the amount of urine decreases and signs of renal failure appear, it is necessary to combat pathological changes in the body. And during the recovery period, you need to eliminate the consequences.
Directions for treatment for renal failure:
| Direction of treatment | Events |
| Eliminating the causes of prerenal acute renal failure. |
|
| Eliminating the causes of renal acute renal failure |
|
| Eliminating the causes of postrenal acute renal failure | It is necessary to remove the obstacle that interferes with the outflow of urine (tumor, stone, etc.). Most often, this requires surgical intervention. |
| Eliminating the causes of chronic renal failure | Depends on the underlying disease. |
| Measures to combat disorders that occur in the body during acute renal failure |
|
| Elimination of water-salt imbalances |
|
| Fighting blood acidification | The doctor prescribes treatment when the acidity (pH) of the blood drops below the critical value of 7.2. A sodium bicarbonate solution is injected intravenously until its concentration in the blood rises to certain values and the pH rises to 7.35. |
| Fighting Anemia | If the level of red blood cells and hemoglobin in the blood decreases, the doctor prescribes blood transfusions and epoetin (a drug that is an analogue of the kidney hormone erythropoietin and activates hematopoiesis). |
| Hemodialysis, peritoneal dialysis | Hemodialysis and peritoneal dialysis are methods of purifying the blood from various toxins and unwanted substances. Indications for acute renal failure:
In peritoneal dialysis, a blood purification solution is injected into the abdominal cavity. As a result of the difference in osmotic pressure, it absorbs harmful substances. It is then removed from the abdomen or replaced with a new one.
|
| Kidney transplant | Kidney transplantation is carried out in case of chronic renal failure, when severe disorders occur in the patient’s body, and it becomes clear that it will not be possible to help the patient in other ways. The kidney is taken from a living donor or a cadaver. After the transplant, a course of therapy is administered with drugs that suppress the immune system to prevent rejection of the donor tissue.
|
Diet for acute renal failure
Prognosis for renal failure
Prognosis for acute renal failure
Depending on the severity of acute renal failure and the presence of complications, from 25% to 50% of patients die.The most common causes of death:
- Damage to the nervous system - uremic coma.
- Severe circulatory disorders.
- Sepsis is a generalized infection, “blood poisoning”, in which all organs and systems are affected.
Prognosis for chronic renal failure
Depends on the disease against which the kidney function was impaired, the age, and the condition of the patient’s body. Since hemodialysis and kidney transplantation began to be used, patient deaths have become less frequent.Factors that worsen the course of chronic renal failure:
- arterial hypertension;
- improper diet when food contains a lot of phosphorus and protein;
- high protein content in the blood;
- increased function of the parathyroid glands.
- kidney injury;
- urinary tract infection;
- dehydration.
Prevention of chronic renal failure
If proper treatment of a disease that can lead to chronic renal failure is started in a timely manner, then kidney function may not be affected or, at least, its impairment will not be as severe.Some drugs are toxic to kidney tissue and can lead to chronic renal failure. You should not take any medications without a doctor's prescription.
Most often, kidney failure develops in people suffering from diabetes, glomerulonephritis, and arterial hypertension. Such patients need to be constantly monitored by a doctor and undergo timely examinations.
Acute kidney failure (ARF) is a rapid, acute decline or complete cessation of all kidney functions due to severe damage to most of the kidney tissue, resulting in the accumulation of protein waste products in the body.
Due to a violation of the excretory (excretory) function of the kidneys, nitrogenous wastes enter the human blood, which, during normal activity of the body, are removed along with urine. Their number increases, the patient’s general condition worsens, and metabolism is significantly impaired. The disease is also characterized by a sharp decrease in the amount of urine excreted (oliguria) to its complete absence (anuria).
In most cases, acute renal failure is a reversible process, but in the absence of timely medical care and the formation of deep damage to the renal tissue, the process becomes irreversible and becomes chronic.
Diagnosis of the disease is carried out on the basis of data from clinical and biochemical tests of blood and urine, as well as instrumental studies of the urinary system.
Treatment depends on the current stage of acute renal failure.
Etiology of acute renal failure (ARF)
The occurrence and condition of acute renal failure depends on the causes, which can be divided into three groups:
- Prerenal. Collapse, shock, severe arrhythmias, sepsis, heart failure, circulatory disorders, a significant decrease in circulating blood volume (as a result of excessive blood loss), anaphylactic or bacteriotoxic shock, a decrease in the amount of extracellular fluid and many other reasons can cause conditions in which prerenal acute renal failure develops .
- Renal. Toxic effects on the renal parenchyma of poisonous mushrooms, fertilizers, uranium, mercury, cadmium and copper salts. Develops with uncontrolled use of antibiotics, sulfonamides, antitumor drugs, etc. When a large amount of hemoglobin and myoglobin circulates in the blood (due to prolonged compression of tissues due to injury, transfusion of incompatible blood, alcoholic and drug coma, etc.). Less commonly observed is the development of renal acute renal failure due to inflammatory kidney disease.
- Postrenal. Mechanical obstruction of urine outflow caused by bilateral obstruction of the urinary tract by stones. Less commonly occurs with severe injuries, extensive surgical interventions, tumors of the bladder, prostate gland, urethritis, etc.
Unexpected kidney dysfunction in acute renal failure leads to pronounced metabolic disorders; if timely medical care is not provided, consequences incompatible with life arise.
The development of acute renal failure occurs from several hours to seven days and can last twenty-four hours. If you seek help from a doctor in a timely manner, the treatment will end with complete restoration of the functions of both kidneys.
Symptoms of kidney failure (KF)
There are four phases of acute renal failure. In the initial stage, the patient’s condition is determined by the underlying disease causing acute renal failure. There are no characteristic symptoms. Nonspecific symptoms of acute renal failure - deterioration of health, loss of appetite, nausea, vomiting, diarrhea, swelling of the lower and upper extremities, increased liver volume, lethargy or agitation of the patient - are masked by manifestations of the underlying disease, poisoning or injury.
During the first stage of the disease, which lasts from several hours to several days, pronounced pallor of the skin and characteristic abdominal pain caused by acute intoxication also appear.
During the second phase (oligoanuric), there is a sharp decrease in the amount of urine excreted. During this period, metabolic end products accumulate in the blood, the main of which are nitrogenous wastes. Due to the cessation of kidney functions, the acid-base balance and water-electrolyte balance are disturbed.
As a result of these processes, the following symptoms of acute renal failure occur: nausea, vomiting, loss of appetite, peripheral edema, cardiac arrhythmia and neuropsychiatric disorder.
Due to acute fluid retention in the body, cerebral, pulmonary edema, ascites or hydrothorax may develop.
The oligoanuria stage lasts on average two weeks, its duration depends on the extent of kidney damage, the adequacy of the treatment and the rate of restoration of the renal tubular epithelium.
The third stage (restorative) is characterized by a gradual restoration of diuresis and takes place in two stages. During the first, the daily amount of urine does not exceed 400 ml (initial diuresis), then there is a gradual increase in urine volume - up to two liters or more. This indicates regeneration of the glomerular function of the kidney.
The diuresis stage lasts 10-12 days. During this period, the activity of the cardiovascular and respiratory systems and digestive organs is normalized.
The fourth stage is the recovery stage. Completely regenerate kidney function. Recovery of the body after long-term treatment can last from several months to one year or more. During this period, the volume of urine excreted, water-electrolyte and acid-base balance are normalized. In some cases, acute renal failure can become chronic.
Diagnosis of acute renal failure (ARF)
As mentioned above, the main indicator of acute renal failure is an increase in nitrogen compounds and potassium in the blood with a significant decrease in the amount of urine excreted by the body, up to a state of anuria. The concentrating ability of the kidneys and the amount of daily urine are assessed based on the results of the Zimnitsky test. Monitoring levels of urea, creatinine and electrolytes is of great importance. They allow us to judge the severity of acute renal failure and the effectiveness of the treatment.
The main task in diagnosing the disease is to determine its form. To do this, an ultrasound of the kidneys and bladder is performed to identify or exclude blockage of the urinary tract. In some cases, bilateral catheterization of the pelvis is performed. If both catheters pass freely into the pelvis, but no urine discharge is observed through them, we can confidently exclude the postrenal form of acute renal failure.
In order to determine renal blood flow, an ultrasound scan of the renal vessels is performed. If acute glomerulonephritis, tubular necrosis, or systemic disease is suspected, a kidney biopsy procedure is performed.
Complications of acute renal failure
The danger to the health and condition of the patient with acute renal failure lies in its complications.
Violation of water-salt metabolism. With oliguria, the risk of developing water and salt overload increases. Insufficient excretion of potassium while maintaining the level of its release from body tissues is called hyperkalemia. In patients who do not suffer from this disease, the potassium level is 0.3-0.5 mmol/day. The first symptoms of hyperkalemia occur at levels of 6.0-6.5 mmol/day. Muscle pain appears, ECG changes are noted, bradycardia develops, and an increased level of potassium in the body can cause cardiac arrest.
In the first two stages of acute renal failure, hyperphosphatemia, hypocalcemia, and mild hypermagnesemia are observed.
Change in blood. Inhibition of erythropoiesis is a consequence of severe azotemia. In this case, the life of red blood cells decreases, and normocytic normochromic anemia develops.
Immune disorders. Infectious diseases occur in 30-70% of patients with acute renal failure due to weakened immunity. The associated infection complicates the course of the disease and often causes the death of the patient. The area of postoperative wounds becomes inflamed, the respiratory system, oral cavity, and urinary tract suffer. A common complication of acute renal failure is sepsis, which can be caused by both gram-positive and gram-negative flora.
Neurological disorders. In patients with acute renal failure, drowsiness and lethargy are recorded, alternating with periods of excitement; confusion and disorientation in space are observed. Peripheral neuropathy occurs more often in elderly patients.
Complications from the cardiovascular system. With acute renal failure, arrhythmia, arterial hypertension, pericarditis, and congestive heart failure may develop.
Disorders of the gastrointestinal tract. Patients with acute renal failure experience abdominal discomfort, loss of appetite, nausea and vomiting. In severe cases, uremic gastroenterocolitis develops, complicated by bleeding.
Treatment of acute renal failure (ARF)
The most important thing in the treatment of acute renal failure is the timely identification of all symptoms and elimination of the causes that provoked kidney damage.
Treatment in the initial phase. Therapy is aimed at eliminating the cause of renal dysfunction. In case of shock, it is necessary to normalize blood pressure and replenish the volume of circulating blood. In case of nephrotoxin poisoning, the patient's stomach and intestines are washed. In urology, extracorporeal hemocorrection is used, which allows you to quickly cleanse the body of toxins that cause the development of acute renal failure. For this purpose, hemosorption and plasmapheresis are performed. If obstruction is present, normal urine passage is restored. For this purpose, stones from the kidneys and ureters are removed, ureteral strictures are eliminated, and tumors are removed surgically.
Treatment in the oliguria phase. The patient is prescribed furosemide and osmotic diuretics to stimulate diuresis. Dopamine is administered to reduce vasoconstriction of the renal vessels. It is important to take into account sweating and respiration losses (400 ml) when determining the volume of fluid administered, in addition to losses due to vomiting, bowel movements and urination. The patient's intake of potassium from food is limited and he is put on a strict protein-free diet. The wounds are drained and areas of necrosis are removed. When choosing the dose of antibiotics, the severity of kidney damage is taken into account.
Indications for hemodialysis. Hemodialysis is performed for a patient with acute renal failure when the level of urea increases to 24 mmol/l, potassium to 7 mmol/l. Symptoms of uremia, acidosis and overhydration are indications for hemodialysis. Currently, to prevent complications arising from metabolic disorders, nephrologists are increasingly performing early and preventive hemodialysis.
Prognosis for acute renal failure
The outcome of acute renal failure is influenced by the patient’s age, the degree of renal dysfunction, and the presence of concomitant complications. The lethal outcome depends on the severity of the pathological condition that caused the development of acute renal failure.
If, when acute renal failure is detected, a diagnosis is made in a timely manner and treatment is carried out correctly in a hospital setting, then the recovery of patients is guaranteed by 40%. Partial restoration of kidney function is observed in 10-15% of cases; 1-3% of patients require constant hemodialysis.
Prevention of acute renal failure
Carrying out preventive measures to avoid acute renal failure includes the need to completely eliminate various etiological factors. If the patient has chronic kidney disease, then after undergoing an examination and consulting a doctor, it is necessary to gradually reduce the dose of previously prescribed medications.
Also, to prevent the manifestation of acute renal failure, it is necessary to undergo an annual X-ray contrast examination, one day before the procedure, injecting a hypotonic sodium solution so that a large amount of polyuria develops.
With effective prevention, timely and adequate treatment of a disease such as acute renal failure, it is possible to prevent all its severe consequences and maintain normal kidney function.
Acute renal failure (AKI) develops as a complication of many diseases and pathological processes. Acute renal failure is a syndrome that develops as a result of disturbances in renal processes (renal blood flow, glomerular filtration, tubular secretion, tubular reabsorption, renal concentrating ability) and is characterized by azotemia, disturbances in water-electrolyte balance and acid-base status.
Acute renal failure can be caused by prerenal, renal and postrenal disorders. Prerenal acute renal failure develops due to a violation of 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 OPN is acute tubulonecrosis, manifested by a decrease in the height of the brush border, a decrease in 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 renal function is preserved.
Causes of prerenal acute kidney injury:
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 circulating blood volume (blood loss, plasma loss, uncontrollable vomiting, diarrhea);
an increase in intravascular capacity, accompanied by a decrease in peripheral resistance (septicemia, endotoxemia, anaphylaxis);
decreased cardiac output (myocardial infarction, heart failure, pulmonary embolism).
The key element 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 surge arrester prerenal azotemia. With a long-term decrease in renal blood flow (more than 3 days) prerenal acute renal failure transforms into renal acute renal failure.
The degree of renal ischemia correlates with structural changes in the epithelium of the proximal tubules (reduction in the height of the brush border and the area of basolateral membranes). Initial ischemia increases the permeability of the membranes of tubular epithelial cells for [Ca 2+ ] ions, which enter the cytoplasm and are actively transported by a special carrier to the inner surface of mitochondrial membranes or to the sarcoplasmic reticulum. The energy deficit developing in cells due to ischemia and energy consumption during the movement of [Ca 2+ ] ions leads to cell necrosis, and the resulting cellular detritus obstructs the tubules, thereby aggravating anuria. The volume of tubular fluid under conditions of ischemia is reduced.
Damage to nephrocytes is accompanied by impaired sodium reabsorption in the proximal tubules and excess sodium intake into the distal tubules. Sodium stimulates macula densa production of renin; 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 components of the renin-apgiotensin-aldosterone system and catecholamines, afferent vasoconstriction and renal ischemia are maintained. In the glomerular capillaries, 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 tubular pressure is accompanied by a decrease in glomerular filtration. Hypoxia of the distal tubules that are most sensitive to it is manifested by necrosis of the tubular epithelium and basement membrane up to tubular necrosis. Obstruction of the tubules occurs with fragments of necrotic epithelial cells, cylinders, etc.
Under conditions of hypoxia in the medulla, changes in the activity of enzymes of the arachidonic cascade are accompanied by a decrease in the formation of prostaglandins, which have a vasodilator effect, and the release of biologically active substances (histamine, serotonin, bradykinin), which directly affect the renal vessels and disrupt renal hemodynamics. This, in turn, contributes to secondary damage to the renal tubules.
After restoration of renal blood flow, the formation of reactive oxygen species, free radicals and activation of phospholipase occurs, which maintains membrane permeability disorders for [Ca 2+ ] 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 scavenge free radicals, such as glutathione. Ions, adenine nucleotides protect mitochondria from damage.
The degree of kidney ischemia correlates with structural changes in the tubular epithelium; the development of vacuolar degeneration or necrosis of individual nephrocytes is possible. Vacuolar dystrophy is eliminated within 15 days after the cessation of the damaging factor.
Renal acute renal failure develops as a result of renal ischemia, that is, it occurs secondary to primary impaired renal perfusion or under the influence of the following reasons:
inflammatory process in the kidneys (glomerulonephritis, interstitial nephritis, vasculitis);
endo- and exotoxins (medicines, radiopaque substances, heavy metal salts - compounds of mercury, lead, arsenic, cadmium, etc., organic solvents, ethylene glycol, carbon tetrachloride, poisons of animal and plant origin;
renovascular diseases (thrombosis and embolism of the renal artery, dissecting aortic aneurysm, bilateral renal vein thrombosis);
pigmentemia - hemoglobinemia (intravascular hemolysis) and myoglobinemia (traumatic and non-traumatic rhabdomyolysis);
toxicosis of pregnancy;
hepatorenal syndrome.
This type of acute renal failure is characterized by acute tubular necrosis caused by ischemia or nephrotoxins that bind to renal tubular cells. 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 damage is usually minor.
To date, more than 100 nephrotoxins have been described that have a direct damaging effect on renal tubular cells (acute tubular necrosis, nephrosis of the lower nephron, vasomotor vasopathy). Acute renal failure caused by nephrotoxins accounts for about 10% of all patient admissions to acute hemodialysis centers.
Nephrotoxins cause damage to tubuloepithelial structures of varying severity - from dystrophies (hydropic, vacuolar, balloon, fatty, hyaline droplet) 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 of nephrotoxins on the cell membrane and in the cytoplasm, filtered through the glomerular filter. The occurrence of a particular dystrophy is determined by the operating 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 plasmacoagulating effect, which causes massive coagulative necrosis of the tubules. Sublimate causes selective kidney damage - “ mercuric nephrosis." Other substances in this group are not selective in action and damage kidney tissue, liver and red blood cells. For example, a feature of poisoning with copper sulfate, dichromates, and arsenous hydrogen is the combination of coagulation necrosis of the epithelium of the proximal tubules with acute hemoglobinuric nephrosis. In case of poisoning with dichromates and arsenic hydrogen, centrilobular necrosis of the liver with cholemia and chelation is observed.
Poisoning ethylene glycol and its derivatives is characterized by irreversible destruction of intracellular structures, called balloon dystrophy. Ethylene glycol and its breakdown products are reabsorbed by the epithelial cells of the renal tubules, a large vacuole is formed in them, which displaces the cellular organelles along with the nucleus to the basal sections. Such dystrophy, as a rule, ends with liquefaction necrosis and complete loss of function of the affected tubules. Sequestration of the damaged part of the cell along with the vacuole is also possible, and the preserved basal sections with the displaced nucleus can be a source of regeneration.
Poisoning dichloroethane, less often chloroform, accompanied by fatty degeneration nephrocytes (acute lipid nephrosis) proximal, distal tubules and 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 hyaline-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 and are 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, unreabsorbed pigment masses in the lumen of the tubules become denser and move into the loop of Henle and distal tubules. In the apical sections of epithelial cells overloaded with pigment granules, partial necrosis occurs. Individual 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 of free amino groups in the side chains in their molecules. Aminoglycosides are not metabolized in the body, and 99% of them are excreted unchanged in the urine. The 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. In this case, the concentration of the drug in the cortex becomes higher than in the plasma. Kidney damage caused by aminoglycosides is characterized by an increase in membrane anionic phospholipids, in particular phosphatidylinositol, damage to mitochondrial membranes, accompanied by loss of intracellular potassium and magnesium, impaired oxidative phosphorylation and energy deficiency. The combination of these changes leads to necrosis of the tubular epithelium.
It is characteristic that [Ca 2+ ] ions prevent the fixation of aminoglycosides on the brush border and thus reduce their nephrotoxicity. It has been 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.) may be complicated by hydropic and vacuolar degeneration of nephrocytes. At the same time, in the proximal tubules, the osmotic gradient of liquids on both sides of the tubular cell changes - blood washing the tubules and provisional urine. Therefore, it is possible for water to move into the tubular epithelial cells from peritubular capillaries or from provisional urine. Hydropy of epithelial cells when using 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 a cell sharply 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 by parenteral administration of 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 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 by stones or blood clots;
obstruction of the ureters or ureter by a tumor located outside the urinary tract;
kidney tumors;
necrosis of the papilla;
prostate hypertrophy.
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 slightly reduced. There are no significant disturbances in 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 restoration of patency of the urinary tract quickly disappear.
With prolonged occlusion and high hydrostatic pressure, filtration and peritubular blood flow are disrupted. These changes, combined with persistent reflux, contribute to the development of interstitial edema and tubular necrosis.
Clinical course of acute renal failure has a certain pattern and stages, regardless of the reason that caused it.
1st stage– short in duration and ends after the factor ceases to act;
2nd stage – period of oligoanuria (the volume of urine excreted does not exceed 500 ml/day), azotemia; in case of prolonged oliguria (up to 4 weeks) the likelihood of developing cortical necrosis sharply increases;
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, stage 2 is the most severe.
Extracellular and intracellular hyperhydration and non-gas excretory renal acidosis develop (depending on the location of tubular damage, acidosis of types 1, 2, 3 is possible). The first sign of overhydration is shortness of breath due to interstitial or cardiogenic pulmonary edema. Somewhat later, fluid begins to accumulate in the cavities, hydrothorax, ascites, and swelling of the lower extremities and lumbar region occur. This is accompanied by pronounced changes in biochemical blood parameters: azotemia (the content of creatinine, urea, uric acid is increased), hyperkalemia, hyponatremia, hypochloremia, hypermagnesemia, hyperphosphatemia.
The blood creatinine level increases regardless of the patient’s diet and the intensity of protein breakdown. Therefore, the degree of creatinemia gives an idea of the severity and prognosis of acute renal failure. The degree of catabolism and necrosis of muscle tissue reflects hyperuricemia.
Hyperkalemia occurs as a result of decreased potassium excretion, increased release of potassium from cells, and developing renal acidosis. Hyperkalemia 7.6 mmol/l is clinically manifested by cardiac arrhythmias up to complete cardiac arrest; hyporeflexia occurs, muscle excitability decreases with the subsequent development of muscle paralysis.
Electrocardiographic indicators for hyperkalemia: T wave – high, narrow, the ST line merges with the T wave; disappearance of the P wave; widening of the QRS complex.
Hyperphosphatemia is caused by impaired phosphate excretion. The genesis of hypocalcemia remains unclear. As a rule, shifts in phosphorus-calcium homeostasis are asymptomatic. But with 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 and hypermagnesemia are usually asymptomatic.
Anemia develops within a few days, the genesis of which is explained by overhydration, hemolysis of red blood cells, bleeding, and inhibition of erythropoietin production by toxins circulating in the blood. Anemia is usually combined with thrombocytopenia.
The second stage is characterized by the appearance of signs of uremia, with predominant symptoms from the gastrointestinal tract (lack of appetite, nausea, vomiting, flatulence, diarrhea).
When antibiotics are prescribed at the beginning, the symptoms of diarrhea increase. Subsequently, diarrhea gives way to constipation due to severe intestinal hypokinesia. In 10% of cases, gastrointestinal bleeding (erosions, ulcers of the gastrointestinal tract, bleeding disorders) is observed.
Timely prescribed therapy prevents the development of coma and uremic pericarditis.
During the oliguric stage (9-11 days), 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 restoration of diuresis by 12-15 days from the onset of the disease and polyuria (more than 2 l/day) that persists for 3-4 weeks. The genesis of polyuria is explained by the restoration of the filtration function of the kidneys and insufficient concentration function of the tubules. During 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 decreases.
Table 6
Differential diagnosis of prerenal and renal acute renal failure
For the differential diagnosis of prerenal and renal acute renal failure, the index of excreted sodium fraction and the index of renal failure are calculated (including the data in Table 6).
Excreted sodium fraction (Na + ex)
Na+ urine: Na+ blood
Na + ex = ------,
Urine Cr: Blood Cr
where Na + urine and Na + blood are, respectively, the content of Na + in urine and blood, and Cr urine and Cr blood are the content of creatinine in urine and blood
For prerenal acute renal failure, the index of the excreted sodium fraction is less than 1; for acute tubular necrosis, the index is greater than 1.
Renal Failure Index (RFI):
IPN = ------ .
Urine Cr: Blood Cr
The disadvantage of these indicators is that in acute glomerulonephritis they are the same as in prerenal acute renal failure.
Pathogenetic ways of correction in acute renal failure: replenishment of bcc - plasma, protein solution, polyglycans, rheopolyglucin (under the control of central venous pressure);
diuretics - mannitol, furosemide - wash out tubular detritus;
prevention of hyperkalemia - 16 units of insulin, 40% in 50 ml of glucose solution;
prevention of hypercalcemia - 10% in 20.0-30.0 ml of calcium gluconate solution (increasing the level of ionized Ca 2+ reduces cell excitability);
elimination of acidosis - administration of sodium bicarbonate.
Thus, treatment is aimed at eliminating shock, replenishing circulating blood volume, treating disseminated intravascular coagulation syndrome, preventing overhydration, correcting acid-base and water-electrolyte balance, and eliminating uremia.
