Symptoms and treatment of acute renal failure. Renal failure - acute and chronic forms, symptoms and treatment, prognosis Renal causes of acute renal failure
Renal 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:
- The blood entering the vessels of the kidney from the aorta reaches the glomerulus from the capillaries, surrounded by a special capsule (Shumlyansky-Bowman's capsule). Under high pressure, the liquid part of the blood (plasma) with the substances dissolved in it seeps into the capsule. This is how primary urine is formed.
- Then the primary urine 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 with the primary, it loses in 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 cups, then into the pelvis and into the ureter.
- Excretion of harmful metabolic products from the body.
- Regulation of osmotic blood pressure.
- Hormone production. For example, renin, which is involved in the regulation 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 red blood cells (red blood cells).
The causes of kidney failure
Causes of Acute Renal Failure
Classification of acute renal failure, depending on the cause:- Prerenal... It is caused by impaired renal blood flow. The kidney is not getting enough blood. As a result, the process of urine formation is disrupted, pathological changes... It occurs in about half (55%) of patients.
- Renal... Associated with the pathology of the renal tissue. The kidney receives enough blood, but cannot make urine. It occurs in 40% of patients.
- Post-renal... Urine forms in the kidneys, but cannot flow due to an obstruction in the urethra. If an obstacle occurs in one ureter, then the function of the affected kidney will be taken over by a healthy one - 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 |
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| Renal |
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| Post-renal |
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Causes of Chronic Kidney Failure
Kidney failure symptoms
Symptoms of Acute Renal Failure
Symptoms of acute renal failure depend on the stage:- initial stage;
- the stage of reducing the daily volume of urine less than 400 ml (oliguric stage);
- stage of restoration of urine volume (polyuric stage);
- full recovery stage.
| Stage | Symptoms |
| Initial | At this stage, as such, there is still no renal failure. The person is worried about the symptoms of the underlying disease. But abnormalities in the kidney tissue are already taking place. |
| Oliguric | Kidney dysfunction increases, the amount of urine decreases. Due to this, harmful metabolic products are retained in the body, and violations of the water-salt balance occur. Symptoms:
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| Polyuric | The patient's condition is normalized, the amount of urine increases, as a rule, even more than normal. At this stage, dehydration of the body, infections can develop. |
| Full recovery | Final restoration of kidney function. It usually lasts 6 to 12 months. If during acute renal failure from work was turned off most of renal tissue, then full recovery impossible. |
Chronic kidney failure symptoms
- On initial stage chronic renal failure has no manifestations. The patient feels relatively normal. Usually, the first symptoms appear when 80% -90% of the kidney tissue ceases to perform its functions. But until that time, a diagnosis can be made if an examination is carried out.
- Usually the first to appear general symptoms: lethargy, weakness, increased fatigue, frequent malaise.
- Urinary excretion is impaired. In a day, it is formed more than it should be (2-4 liters). This can lead to dehydration. Frequent urination at night is noted. In the later stages of chronic renal failure, the amount of urine decreases sharply - this is bad sign.
- Nausea and vomiting.
- Twitching of muscles.
- Itchy skin.
- Dryness and bitterness in the mouth.
- Stomach ache.
- Diarrhea.
- Nose, stomach bleeding due to decreased blood clotting.
- Hemorrhage on the skin.
- Increased susceptibility to infections. Such patients often suffer from respiratory infections, pneumonia.
- In the late stage: the condition worsens. There are attacks of shortness of breath, bronchial asthma. The patient may lose consciousness, fall into a coma.
Diagnosis of renal failure
| Diagnostic method | Acute renal failure | Chronic renal failure |
| General urine analysis | In the general analysis of urine in acute and chronic renal failure, it is possible to identify:
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| Bacteriological examination of urine | If the impaired renal function was caused by an infection, then the pathogen will be detected during the study. Also, this analysis allows you to identify an infection that has arisen against the background of renal failure, to determine the sensitivity of the pathogen to antibacterial drugs.  |
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| General blood analysis | In acute and chronic renal failure, the general blood test reveals changes:
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| Blood chemistry | Helps to assess pathological changes in the body caused by impaired renal function. In a biochemical blood test in acute renal failure, changes can be detected:
| With chronic renal failure in biochemical analysis blood changes are usually detected:
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| These methods allow you to examine the kidneys, their internal structure, renal cups, pelvis, ureters, and bladder. In acute renal failure, CT, MRI and ultrasound are most often used to find the cause of the narrowing of the urinary tract.  |
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| Doppler ultrasound | Ultrasound examination, during which you can assess the blood flow in the vessels of the kidneys. | |
| X-ray chest | It is used to detect disorders of the respiratory system, some diseases that can cause kidney failure.
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| Chromocystoscopy |
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| Kidney biopsy | The doctor receives a fragment of the kidney tissue and sends it to the laboratory for examination under a microscope. Most often, this is done using a special thick needle that the doctor inserts into the kidney through the skin. Biopsy is used in doubtful cases, when it is not possible to establish a diagnosis.
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| Electrocardiography (ECG) | This study is mandatory for all patients with acute renal failure. It helps to identify violations of the heart, arrhythmias.  |
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| Zimnitsky test | The patient collects all urine during the day in 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. | |
Renal failure treatment
Acute renal failure requires immediate hospitalization of the patient in a nephrological hospital. If the patient is in grave condition- he is placed in the intensive care unit. Therapy depends on the cause of the kidney dysfunction. In chronic renal failure, therapy depends on the stage. At the initial stage, the underlying disease is treated - this will help prevent severe renal dysfunction and easier cope with them later. With a decrease in the amount of urine and the appearance of signs of renal failure, it is necessary to fight pathological changes in the body. And during the recovery period, you need to eliminate the consequences.
Directions of treatment for renal failure:
| Direction of treatment | activity |
| Eliminating the causes of prerenal acute renal failure. |
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| Eliminating the causes of renal acute renal failure |
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| Elimination of 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 in acute renal failure |
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| Elimination of violations of water-salt balance |
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| Fighting blood acidification | The doctor prescribes treatment when the acidity (pH) of the blood falls below the critical value of 7.2. A solution of sodium bicarbonate is injected intravenously until its concentration in the blood rises to certain values, and the pH rises to 7.35. |
| Combating anemia | With a decrease in the level of erythrocytes and hemoglobin in the blood, the doctor prescribes blood transfusions, epoetin (a drug that is an analogue of the renal 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 picks up harmful substances. Then it is removed from the abdomen or replaced with a new one.
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| 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 corpse. After the transplant, a course of therapy with drugs that suppress the immune system is carried out so that the donor tissue does not reject.
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Diet for acute renal failure
Prognosis for renal failure
Prognosis for Acute Renal Failure
Depending on the severity of the course of acute renal failure and the presence of complications, from 25% to 50% of patients die.Most common reasons 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 the background of which there was a violation of kidney function, age, condition of the patient's body. Since the introduction of hemodialysis and kidney transplantation, the death rate of patients has 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 blood protein;
- increased function of the parathyroid glands.
- kidney injury;
- an infection of the urinary system;
- dehydration.
Prevention of chronic renal failure
If you start on time correct treatment diseases that can lead to chronic renal failure, then kidney function may not be affected or, at least, its impairment will not be so severe.Some medications are toxic to renal tissue and can lead to chronic renal failure. You should not take any medications without a doctor's prescription.
Most often, renal failure develops in people suffering from diabetes mellitus, glomerulonephritis, arterial hypertension. Such patients need to be constantly monitored by a doctor, to undergo examinations in a timely manner.
How to make an accurate diagnosis?
In order to accurately determine the diagnosis of pathology, it is necessary to conduct a number of laboratory and instrumental studies. In acute renal failure, the diagnosis determines an increased level of potassium and nitrogenous substances in the blood. Such an increase is observed due to complications of the outflow of urine. This is the main marker for defining arresters.
No less important laboratory tests are:
- blood test (shows a decrease in hemoglobin, an increase in the erythrocyte sedimentation rate and leukocyte level), during biochemistry, an excess of creatine, urea and potassium is detected, reduced level calcium and sodium;
- urine analysis (as a result, there will be a decrease in the level of platelets, an increase in leukocytes and erythrocytes, a drop in density, the presence of protein and cylinders), with a daily urine analysis, a decrease in urine output is manifested.
Instrumental studies include:
- an electrocardiogram (used to monitor the work of the heart);
- ultrasound (evaluates kidney size, obstruction and blood supply);
- kidney biopsy;
- radiography of the lungs and myocardium.
Using the above diagnostic methods, an accurate diagnosis of acute renal failure in adults is established. Having established the etiological factor, the form and stage of the disease, the doctor prescribes the appropriate therapy.
ARF treatment and emergency care
Treatment of acute renal failure begins with providing the patient with an ambulance first aid... To do this, it is necessary to deliver the patient to the hospital department as soon as possible. During transportation or waiting for a qualified physician, the patient must be provided with complete rest, wrap the patient in a warm blanket, and lay in a horizontal position.
In acute renal failure, treatment is determined by the stage pathological condition and its etiological factor.
The first therapeutic approach is to eliminate the cause of acute renal failure: removing the patient from shock, restoring blood supply and urine passage in case of ureteral obstruction, detoxification in case of poisoning, etc.
To eliminate etiological factors, the following drugs are used:
- antibiotics for infectious diseases;
- diuretics to increase blood flow and prevent or eliminate peripheral edema;
- cardiac drugs for violations of the myocardium;
- salt solutions to restore electrolyte balance;
- antihypertensive drugs to lower blood pressure.
And also to eliminate the root cause, a number of therapeutic methods are carried out, including gastric lavage in case of intoxication of the body and surgery to repair injured kidney tissue or to remove factors blocking the outflow of urine. With hemodynamic disorders, blood substitutes are transfused, and with the development of anemia, erythrocyte mass is transfused.
After eliminating the root cause, a conservative drug therapy... And also provides full control over the clinical parameters of the patient. The patient needs to take anamnesis and physical examination every day, measure body weight, measure incoming and outgoing substances, inspect wounds and places of intravenous infusion.
The patient's diet is adjusted. The diet menu should be low in protein (20–25 g / day) and salt (up to 2–4 g / day). Foods with a high content of potassium, magnesium and phosphorus are completely excluded from the diet. Caloric intake is provided by fats and carbohydrates and should be 4-50 kcal / kg.
If a patient has a significant excess of urea up to 24 mmol / l and potassium up to 7 mmol / l, as well as severe symptoms of uremia, acidosis and overhydration, this is a direct indication for hemodialysis. To date, hemodialysis is due even for prophylactic purposes, to prevent the occurrence of possible complications associated with metabolic disorders.
Renal failure of the acute nature of the course is a severe pathological condition in which the kidneys are disrupted. Due to such malfunctions in functioning, metabolism, urine outflow is disturbed, an imbalance of acid-base and water-electrolyte equilibrium occurs. Pathology has a wide range of complicated conditions, including arrhythmia, pulmonary and cerebral edema, hydrothorax and other pathologies that cause significant damage to the body. To stop the disease, the patient must be placed in the hospital department without fail. Do not self-medicate, as inadequate use medicines can lead to the transition of pathology from an acute form to a chronic one.
Acute renal failure, abbr. ARF is a complex of disorders that develop as a result of impairment of all kidney functions.
Causes of Acute Renal Failure
All causes leading to impaired renal function can be divided into renal and extrarenal. From the definition it is clear that the first group includes those causes that cause changes in the kidneys, by their direct action on them. Vessels include various renal poisons, certain medications, and kidney diseases (inflammatory and non-inflammatory) and kidney injuries.
Extrarenal causes include various pathologies of the blood and circulation, shocks, and some systemic diseases.
The mechanisms of development of acute renal failure and its consequences
Acute renal failure is a secondary disease characterized by manifestations of the underlying pathology, followed by renal symptoms.
The basis of the pathogenesis of the disease is renal ischemia. Its cause is the restructuring of the blood flow of the kidneys: shunting of blood in the vessels of the juxtaglomerular system with a reduced pressure in the arterioles of the glomeruli below sixty millimeters of mercury. This leads to ischemia of the renal cortex.
Then there is a release of catecholamines into the blood, activation of the renin-aldosterone system, the production of antidiuretic hormone, vasoconstriction with ischemia of the epithelium of the renal tubules, an increase in the concentration of calcium and free radicals in it.
Simultaneously with ischemization of the tubules, they are damaged by endotoxins.
Necrosis of the epithelium of the tubules leads to the release of the infiltrate into the tissue with the formation of edema. It also increases renal ischemia and decreases glomerular filtration. Calcium penetrates their cytoplasm into the mitochondria of the cell, this transition requires a lot of energy - amitransferase molecules. Lack of energy, in turn, also leads to tubular cell necrosis, obstruction and anuria.
This is a universal mechanism for the formation of acute renal failure.
But there are also separate forms of renal failure, characteristic of a particular pathology.
For example, DIC syndrome, together with necrotic damage to the cortical layer of the kidneys, occurs in obstetric pathology, sepsis , different forms shock, systemic lupus erythematosus.
With myeloma and hemolysis, renal ischemia develops when the tubular protein binds to myoglobin and hemoglobin.
The pathogenesis of renal dysfunction in gout is explained by the deposition of crystals in the lumen of the tubules. An overdose of sulfa drugs and some other drugs has a similar mechanism for the formation of pathology.
Chronic necrotizing papillitis develops against the background of diabetes mellitus, alcoholism, anemia, nephropathy. In this disease, acute renal failure occurs due to obstruction of the ureters by blood clots and necrotic papillae.
With purulent pyelonephritis, acute renal failure develops against the background of papillitis and leads to uremia. This is often accompanied by renal edema, apostematosis, and bacterial shock.
Often the causes of acute renal failure are diseases of the kidney arteries, accompanied by their inflammation. Necrotizing arteritis is characterized by the appearance of multiple aneurysms, thrombotic microangiopathy of renal vessels, arteriolonecrosis. This occurs in malignant hypertension, sclerodermic kidney, thrombotic thrombocytopenic purpura.
Regardless of the causes of renal failure, the filtration capacity of the nephrons first decreases. This leads to a decrease in daily urine output and an increase in toxins in the blood. Then there is an imbalance of water and electrolytes in the blood. Thus, impaired renal function affects the state of the entire human body. And the malignant course of renal failure leads to the death of the patient.
Stages of acute renal failure and clinic
The initial stage of acute renal failure.
At this stage, when changes in kidney function are minimal, only a slight decrease in the amount of diuresis (the ratio of consumed fluid to excreted fluid) speaks of the threat of developing renal failure. This fact must be taken into account, especially if it appears against the background of any disease.
Oligoanuria stage.
At this stage, kidney dysfunctions become more noticeable. The total urine output is reduced by at least 75%. An increase in toxic substances in the blood causes an increase in the frequency of respiratory movements (tachypnea) and heart rate (tachycardia). A decrease in the amount of urine, and therefore an increase in fluid in the body, leads to the appearance of edema and an increase in blood pressure.
In the absence of treatment, urine output rapidly decreases to 0 and ARF passes into the next stage, which can very often end in death.
Stage of polyuria.
Mass death of nephrons, including tubules, blood plasma begins to pass into the urinary ducts (since the tubule does not absorb it), which leads to a sharp increase in urine output significantly above normal. This is called polyuria, which is the reason for the naming of this stage.
In addition to polyuria, there is tachycardia more than 120-150 beats per minute, tachypnea 30 or more, respiratory movements, dry skin and its increased desquamation, depression of consciousness, up to the development of coma.
Symptoms of Acute Renal Failure
At the beginning of the formation of kidney failure, symptoms of the underlying disease appear, which leads to the development of acute ischemia. These include the following:
- signs of intoxication,
- shock symptoms
- manifestations of the primary disease.
Renal symptoms join the above signs: a decrease in urine output to four hundred milliliters of urine per day, that is, oliguria develops. And then diuresis reaches fifty milliliters per day with the development of anuria.
This is accompanied by the appearance of nausea, lack of appetite, vomiting. Then the symptomatology increases and such clinical manifestations of pathology arise:
- drowsiness,
- lethargy
- disturbances of consciousness,
- convulsions
- hallucinations
- dry skin
- pallor with hemorrhages,
- swelling
- deep, rapid breathing,
- tachycardia,
- arrhythmia,
- hypertension,
- bloating,
- diarrhea.
- Potentially reversible, sudden, severe impairment or cessation of renal function. Characterized by a violation of all renal functions (secretory, excretory and filtration), pronounced changes in the water-electrolyte balance, rapidly increasing azotemia. In the development of acute renal failure, 4 successive phases are distinguished: initial, oligoanuric, diuretic and convalescence. Diagnostics is carried out according to the data of clinical and biochemical analyzes of blood and urine, as well as instrumental studies of the urinary system. Treatment depends on the stage of acute renal failure. It includes symptomatic therapy, methods of extracorporeal hemocorrection, maintenance of optimal blood pressure and urine output.
Acute renal failure is a potentially reversible, sudden onset, severe impairment or cessation of renal function. Characterized by a violation of all renal functions (secretory, excretory and filtration), pronounced changes in the water-electrolyte balance, rapidly increasing azotemia.
The following forms of surge arresters are distinguished:
- Hemodynamic(prerenal). It arises as a result of acute hemodynamic disturbances.
- Parenchymal(renal). The cause is toxic or ischemic damage to the renal parenchyma, less often an acute inflammatory process in the kidneys.
- Obstructive(post-renal). It develops as a result of acute urinary tract obstruction.
Etiology of prerenal ARF
Prerenal ARF can develop in conditions that are accompanied by a decrease in cardiac output (with pulmonary embolism, heart failure, arrhythmias, cardiac tamponade, cardiogenic shock). Often, the cause is a decrease in the amount of extracellular fluid (with diarrhea, dehydration, acute blood loss, burns, ascites caused by liver cirrhosis). May occur due to severe vasodilation that occurs during bacteriotoxic or anaphylactic shock.
Etiology of renal acute renal failure
It arises from toxic effects on the renal parenchyma of fertilizers, poisonous fungi, salts of copper, cadmium, uranium and mercury. It develops with the uncontrolled intake of nephrotoxic drugs (anticancer drugs, a number of antibiotics and sulfonamides). X-ray contrast substances and these drugs, prescribed in the usual dosage, can cause renal acute renal failure in patients with impaired renal function.
In addition, this form of ARF occurs when a large amount of myoglobin and hemoglobin circulates in the blood (with severe macrohemaglobinuria, transfusion of incompatible blood, prolonged compression tissues with trauma, drug and alcohol coma). Less commonly, the development of renal ARF is due to inflammatory kidney disease.
Etiology of postrenal ARF
It develops with a mechanical violation of the passage of urine with bilateral obstruction of the urinary tract with stones. Less commonly, it occurs with tumors of the prostate, bladder and ureters, tuberculous lesions, urethritis and periurethritis, degenerative lesions of the retroperitoneal tissue.
With severe concomitant injuries and extensive surgical interventions Acute renal failure is caused by several factors (shock, sepsis, blood transfusion, treatment with nephrotoxic drugs).
ARF symptoms
There are four phases of acute renal failure:
The patient's condition is determined by the underlying disease causing ARF. Clinically, the initial phase is usually not detected due to the lack of characteristic symptoms... The circulatory collapse that occurs in this phase has a very short duration, therefore it passes unnoticed. Non-specific symptoms of acute renal failure (drowsiness, nausea, lack of appetite, weakness) are masked by manifestations of the underlying disease, injury or poisoning.
Anuria is rare. The amount of urine to be separated is less than 500 ml per day. Characterized by severe proteinuria, azotemia, hyperphosphatemia, hyperkalemia, hypernatasia, metabolic acidosis. Diarrhea, nausea, vomiting are noted. At pulmonary edema due to overhydration, shortness of breath and wet wheezing appear. The patient is inhibited, drowsy, may fall into a coma. Pericarditis, uremic gastroenterocolitis, complicated by bleeding often develop. The patient is susceptible to infection due to decreased immunity. Possible pancreatitis, stomatitis, mumps, pneumonia, sepsis.
The oligoanuric phase of ARF develops within the first three days after exposure. Late development of the oligoanuric phase is considered a prognostically unfavorable sign. The average duration of this stage is 10-14 days. The period of oliguria can be shortened up to several hours or lengthened up to 6-8 weeks. Prolonged oliguria often occurs in elderly patients with concomitant vascular pathology. With the oliguric stage of ARF, lasting more than a month, it is necessary to conduct an additional differential diagnosis to exclude progressive glomerulonephritis, renal vasculitis, occlusion renal artery, diffuse necrosis of the renal cortex.
The duration of the diuretic phase is about two weeks. Daily urine output gradually increases and reaches 2-5 liters. There is a gradual restoration of the water-electrolyte balance. Possible hypokalemia due to significant loss of potassium in the urine.
Further recovery of renal functions occurs, which takes from 6 months to 1 year.
Arrester complications
The severity of disorders characteristic of renal failure (fluid retention, azotemia, imbalance in water and electrolyte balance) depends on the state of catabolism and the presence of oliguria. With pronounced oliguria, there is a decrease in the level of glomerular filtration, the release of electrolytes, water and nitrogen metabolism products significantly decreases, which leads to more pronounced changes in the composition of the blood.
With oliguria, the risk of developing water and salt overload increases. Hyperkalemia in acute renal failure is caused by insufficient excretion of potassium while maintaining the level of its release from tissues. In patients who do not suffer from oliguria, the level of potassium is 0.3-0.5 mmol / day. More pronounced hyperkalemia in such patients may indicate exogenous (blood transfusion, medications, the presence of potassium-rich foods in the diet) or endogenous (hemolysis, tissue destruction) potassium load.
The first symptoms of hyperkalemia appear when the potassium level exceeds 6.0-6.5 mmol / L. Patients complain of muscle weakness. In some cases, flaccid tetraparesis develops. ECG changes are noted. The amplitude of the P waves decreases, the P-R interval increases, and bradycardia develops. A significant increase in potassium concentration can cause cardiac arrest.
In the first two stages of acute renal failure, hypocalcemia, hyperphosphatemia, and mild hypermagnesemia are observed.
The consequence of severe azotemia is the inhibition of erythropoiesis. The life span of erythrocytes is reduced. Normocytic normochromic anemia develops.
Suppression of immunity contributes to the emergence infectious diseases in 30-70% of patients with acute renal failure. The addition of an infection aggravates the course of the disease and often becomes the cause of the patient's death. Inflammation develops in the area postoperative wounds, the oral cavity, respiratory system, urinary tract suffers. A common complication of acute renal failure is sepsis, which can be caused by both gram-positive and gram-negative flora.
Drowsiness, confusion, disorientation, lethargy, alternating with periods of excitement are noted. Peripheral neuropathy is more common in older patients.
- Complications from the cardiovascular system
With acute renal failure, congestive heart failure, arrhythmia, pericarditis, and arterial hypertension may develop.
Patients are worried about the feeling of discomfort in the abdominal cavity, nausea, vomiting, loss of appetite. In severe cases, uremic gastroenterocolitis develops, often complicated by bleeding.
Arrester diagnostics
The main marker of acute renal failure is an increase in potassium and nitrogenous compounds in the blood against the background of a significant decrease in the amount of urine excreted by the body up to the state of anuria. The amount of daily urine and the concentration capacity of the kidneys are assessed according to the results of the Zimnitsky test. Monitoring of such indicators of blood biochemistry as urea, creatinine and electrolytes is important. It is these indicators that make it possible to judge the severity of acute renal failure and the effectiveness of the treatment.
The main task in the diagnosis of ARF is to determine its shape. For this, an ultrasound of the kidneys and bladder is performed, which allows you to identify or exclude obstruction of the urinary tract. In some cases, bilateral pelvic catheterization is performed. If, at the same time, both catheters freely passed into the pelvis, but urine flow through them is not observed, the postrenal form of acute renal failure can be excluded with confidence.
If necessary, renal blood flow is assessed by ultrasonography of the renal vessels. Suspected tubular necrosis, acute glomerulonephritis, or systemic disease is an indication for a kidney biopsy.
ARF treatment
Initial treatment
Therapy is aimed primarily at eliminating the cause that caused the impaired renal function. In case of shock, it is necessary to replenish the circulating blood volume and normalize blood pressure. In case of poisoning with nephrotoxins, the patient is washed the stomach and intestines. Application in urology of such modern methods treatment as extracorporeal hemocorrection allows you to quickly cleanse the body of toxins that have caused the development of acute renal failure. For this purpose, hemosorption and plasmapheresis are performed. In the presence of obstruction, the normal passage of urine is restored. To do this, they remove stones from the kidneys and ureters, promptly remove ureteral strictures and remove tumors.
Treatment in the phase of oliguria
To stimulate diuresis, the patient is prescribed furosemide and osmotic diuretics. Dopamine is administered to reduce renal vasoconstriction. When determining the volume of injected fluid, in addition to losses during urination, vomiting and bowel movement, it is necessary to take into account losses during sweating and breathing. The patient is transferred to a protein-free diet, the intake of potassium from food is limited. Drainage of wounds, removal of areas of necrosis is carried out. When choosing a dose of antibiotics, the severity of kidney damage should be considered.
Indications for hemodialysis
Hemodialysis is performed with an increase in the level of urea to 24 mmol / l, potassium - up to 7 mmol / l. Indications for hemodialysis are symptoms of uremia, acidosis and overhydration. Currently, to prevent complications arising from metabolic disorders, nephrologists are increasingly conducting early and prophylactic hemodialysis.
Mortality primarily depends on the severity of the pathological condition that caused the development of acute renal failure. The outcome of the disease is influenced by the patient's age, the degree of renal dysfunction, and the presence of complications. In surviving patients, renal functions are fully restored in 35-40% of cases, partially in 10-15% of cases. 1-3% of patients require constant hemodialysis.
Acute renal failure (ARF) develops as a complication of many diseases and pathological processes. Acute renal failure is a syndrome that develops as a result of impaired renal processes (renal blood flow, glomerular filtration, tubular secretion, tubular reabsorption, renal concentrating ability) and is characterized by azotemia, impaired water-electrolyte balance and acid-base state.
Acute renal failure can be caused by prerenal, renal, and postrenal disorders. Prerenal ARF develops in connection with impaired renal blood flow, renal ARF - with damage to the renal parenchyma, postrenal ARF is associated with impaired urine outflow.
The morphological substrate of ARF is acute tubulonecrosis, manifested by a decrease in the height of the brush border, a decrease in the folding of the basolateral membranes, and epithelial necrosis.
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 kidney function is preserved.
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);
a decrease in the volume of circulating blood (blood loss, plasma loss, indomitable vomiting, diarrhea);
an increase in intravascular capacity, accompanied by a decrease peripheral resistance(septicemia, endotoxinemia, anaphylaxis);
decrease in cardiac output (myocardial infarction, heart failure, pulmonary embolism).
The key link in the pathogenesis of prerenal ARF 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 prolonged decrease in renal blood flow (more 3 days), the prerenal arrester passes into the renal arrester.
The degree of renal ischemia correlates with structural changes epithelium of the proximal tubules (a decrease in the height of the brush border and the area of the basolateral membranes). Initial ischemia increases the permeability of tubular epithelial cell membranes for ions, which enters the cytoplasm, is actively transported by a special carrier to the inner surface of mitochondrial membranes or to the sarcoplasmic reticulum. The energy deficit developing in the cells due to ischemia and energy consumption during the movement of ions leads to cell necrosis, and the resulting cellular detritus obstructs the tubules, thereby aggravating anuria. The volume of tubular fluid in ischemic conditions is reduced.
Damage to nephrocytes is accompanied by impaired sodium reabsorption in the proximal tubules and excess sodium intake into the distal sections. Sodium stimulates in macula densa renin production, in patients with acute renal failure, its content, as a rule, is 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 the components of the renin-apgiotensin-aldosterone system and catecholamines, afferent vasoconstriction and renal ischemia are maintained. In the capillaries of the glomeruli, the pressure drops and, accordingly, the effective filtration pressure decreases.
With a sharp restriction of the 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 most sensitive distal tubules is manifested by necrosis of tubular epithelium and basement membrane up to tubular necrosis. The tubules are obturated with fragments of necrotic epithelial cells, cylinders, etc.
Under conditions of hypoxia in the medulla, a change in the activity of enzymes of the arachidonic cascade is accompanied by a decrease in the formation of prostaglandins, which have a vasodilatory effect, and the release of biologically active substances (histamine, serotonin, bradykinin), which directly affect the vessels of the kidneys and disrupt renal hemodynamics. This, in turn, promotes secondary damage to the renal tubules.
After the restoration of renal blood flow, the formation of reactive oxygen species, free radicals and the activation of phospholipase occur, which maintains impaired membrane permeability for ions and prolongs the oliguric phase of ARF. V last years 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, calcium channel blockers (nifedipine, verapamil) are used. 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 renal ischemia correlates with structural changes in the epithelium of the tubules, possibly the development of vacuolar degeneration or necrosis of individual nephrocytes. Vacuolar dystrophy is eliminated within 15 days after the termination of the damaging factor.
Renal acute renal failure develops as a result of renal ischemia, that is, it occurs a second time with a primary impaired renal perfusion or under the influence of the following reasons:
inflammatory process in the kidneys (glomerulonephritis, interstitial nephritis, vasculitis);
endo- and exotoxins (drugs, radiopaque substances, salts of heavy metals - compounds of mercury, lead, arsenic, cadmium, etc., organic solvents, ethylene glycol, carbon tetrachloride, animal and vegetable poisons;
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);
This type of ARF is characterized by acute tubular necrosis caused by ischemia or nephrotoxins that are fixed on the cells of the renal tubules. First of all, the proximal tubules are damaged, dystrophy and necrosis of the epithelium occurs, followed by moderate changes in the renal interstitium. Glomerular damage is usually minor.
To date, more than 100 nephrotoxins have been described that have a direct damaging effect on the cells of the renal tubules (acute tubular necrosis, nephrosis of the lower nephron, vasomotor vasopathy). Acute renal failure caused by nephrotoxins accounts for about 10% of all patients admitted to acute hemodialysis centers.
Nephrotoxins cause damage to tubuloepithelial structures of varying degrees of severity - from dystrophies (hydropic, vacuolar, balloon, fatty, hyaline droplet) to partial or massive coagulation necrosis of nephrocytes. These changes occur as a result of reabsorption and deposition of macro- and microparticles in the cytoplasm, as well as fixation on the cell membrane and in the cytoplasm of nephrotoxins filtered through the glomerular filter. The emergence of one or another dystrophy is determined by the acting factor.
Nephrotoxicity of poisons " thiol group "(compounds of mercury, chromium, copper, gold, cobalt, zinc, lead, bismuth, lithium, uranium, cadmium and arsenic) is manifested by the blockade of sulfhydryl (thiol) groups of enzymatic and structural proteins and a plasma-coagulating effect, which causes massive coagulation necrosis of the tubules. Sublimate causes selective kidney damage - " sublimate nephrosis ". Other substances of this group do not differ in selectivity of action and damage the tissue of the kidneys, liver and erythrocytes. For example, a feature of poisoning with copper sulfate, dichromates, arsenous hydrogen is a combination of coagulation necrosis of the epithelium of the proximal tubules with acute hemoglobinuric nephrosis. In case of poisoning with bichromates and arsenous hydrogen, centrilobular necrosis of the liver with cholemia and chelation is observed.
Poisoning ethylene glycol and its derivatives are characterized by irreversible destruction of intracellular structures, called balloon dystrophy. Ethylene glycol and its decay products are reabsorbed by the epithelial cells of the renal tubules, a large vacuole is formed in them, which displaces the cell organelles, along with the nucleus, to the basal sections. Such dystrophy, as a rule, ends with colliquation necrosis and complete loss of function of the affected tubules. The sequestration of the damaged part of the cell together 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) of the 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-drop dystrophy. Pigment proteins filtered through the glomerular filter move along the tubule and gradually settle on the brush border in the proximal tubules, 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 casts are formed. The process unfolds over 3-7 days. During this period, unreabsorbed pigment masses in the lumen of the tubules are compacted, move into the loop of Henle and the distal tubules. Partial necrosis occurs in the apical sections of epithelial cells overloaded with pigment granules. 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. Filtered aminoglycosides are fixed on the apical membrane of cells of the proximal tubules and 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 with aminoglycosides is characterized by an increase in the membranes of anionic phospholipids, in particular, phosphatidylinositol, damage to mitochondrial membranes, accompanied by the loss of intracellular potassium and magnesium, impaired oxidative phosphorylation and energy deficiency. The combination of these changes leads to tubular epithelium necrosis.
It is characteristic that the ions prevent the fixation of aminoglycosides on the brush border and thus reduce their nephrotoxicity. It is 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.) can be complicated by hydropic and vacuolar degeneration of nephrocytes. In this case, the osmotic gradient of fluids changes in the proximal tubules on both sides of the tubular cell - the blood that washes the tubules and provisional urine. Therefore, it is possible to move water into the cells of the tubular epithelium from the peritubular capillaries or from the provisional urine. Hydropy of epithelial cells with the use of osmotic diuretins is preserved long time and, as a rule, is associated with partial reabsorption of osmotically active substances and their retention in the cytoplasm. Retention of water in the cell drastically 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 the 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 the urine is increased due to the 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 with calculi or blood clots;
obstruction of the ureters or ureter by a tumor located outside the urinary tract;
Violation of the outflow of urine is accompanied by overstretching of the urinary tract (ureters, pelvis, cups, collecting tubes, 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 glomeruli is very moderate, and filtration is slightly reduced. There are no pronounced disorders of peri-tubular blood flow and, despite anuria, renal function is preserved. After removing the obstacle to the outflow of urine, diuresis is restored. If the duration of the occlusion does not exceed three days, the symptoms of acute renal failure after the restoration of the patency of the urinary tract quickly disappear.
With prolonged occlusion and high hydrostatic pressure, filtration and peri-tubular blood flow are impaired. 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 regularity and stages, regardless of the reason that caused it.
1st stage- short in duration and ends after the termination of the factor;
2nd stage - the period of oligoanuria (the volume of excreted urine does not exceed 500 ml / day), azotemia; in the case of prolonged oliguria (up to 4 weeks), the likelihood of developing cortical necrosis increases sharply;
3rd stage- period of polyuria - restoration of diuresis with a phase of polyuria (the volume of excreted urine exceeds 1800 ml / day);
4th stage- restoration of kidney function. Clinically, the 2nd stage is the most difficult.
Extracellular and intracellular hyperhydration, non-gaseous excretory renal acidosis develops (depending on the localization of tubular damage, acidosis of the 1st, 2nd, 3rd types is possible). The first sign of overhydration is shortness of breath due to interstitial or cardiogenic pulmonary edema. A little later, the fluid begins to accumulate in the cavities, hydrothorax, ascites, edema occur lower limbs and in the lumbar region. This is accompanied by pronounced changes in blood biochemical parameters: azotemia (the content of creatinine, urea, uric acid is increased), hyperkalemia, hyponatremia, hypochloremia, hypermagnesemia, hyperphosphatemia.
The level of creatinine in the blood rises regardless of the nature of the patient's diet and the intensity of protein breakdown. Therefore, the degree of creatinemia gives an idea of the severity of the course and prognosis in acute renal failure. The degree of catabolism and necrosis of muscle tissue reflects hyperuricemia.
Hyperkalemia occurs as a result of a decrease in potassium excretion, increased release of potassium from cells, and developing renal acidosis. Hyperkalemia of 7.6 mmol / l is clinically manifested by cardiac arrhythmias up to complete cardiac arrest; hyporeflexia occurs, muscle excitability decreases with subsequent development of muscle paralysis.
Electrocardiographic indicators for hyperkalemia: T wave - high, narrow, the ST line merges with the T wave; the disappearance of the P wave; widening of the QRS complex.
Hyperphosphatemia is caused by impaired excretion of phosphates. The genesis of hypocalcemia remains unclear. As a rule, shifts in calcium-phosphorus homeostasis are asymptomatic. But with a quick correction of acidosis in patients with hypocalcemia, tetany and seizures may occur. Hyponatremia is associated with water retention or overdosing. There is no absolute sodium deficiency in the body. Hypersulfatemia, hypermagnesemia, as a rule, are asymptomatic.
Within a few days, anemia develops, the genesis of which is explained by overhydration, hemolysis of erythrocytes, bleeding, inhibition of erythropoietin production by toxins circulating in the blood. Usually, anemia is associated with thrombocytopenia.
The second stage is characterized by the appearance of signs of uremia, while symptoms from the gastrointestinal tract prevail (lack of appetite, nausea, vomiting, flatulence, diarrhea).
When antibiotics are prescribed early, the symptoms of diarrhea increase. Subsequently, diarrhea is replaced by constipation due to severe intestinal hypokinesia. In 10% of cases, gastrointestinal bleeding(erosion, ulcers of the gastrointestinal tract, blood clotting disorders).
Timely prescribed therapy prevents the development of coma, uremic pericarditis.
During the oliguric stage (9-11 days), urine is dark in color, proteinuria and cylindruria are expressed, natriuria does not exceed 50 mmol / l, urine osmolarity corresponds to plasma osmolarity. In 10% of patients with acute medicinal interstitial nephritis, diuresis is preserved.
3rd stage characterized by the restoration of diuresis by the 12-15th day from the onset of the disease and polyuria (more than 2 l / day), which persists for 3-4 weeks. The genesis of polyuria is explained by the restoration of the filtration function of the kidneys and the insufficient concentration function of the tubules. In the polyuric stage, the body is unloaded from the fluid accumulated during the oliguria period. Secondary dehydration, hypokalemia and hyponatremia are possible. The severity of proteinuria is reduced.
Differential diagnosis of prerenal and renal acute renal failure
Acute renal failure (ARF) is a sudden dysfunction of both kidneys caused by a decrease in renal blood flow and a slowdown in glomerular filtration and tubular reabsorption. As a result, there is a delay or complete cessation of the elimination of toxic substances from the body and a disorder of the acid-base, electrolyte and water balance.
With proper and timely treatment, these pathological changes are reversible. According to medical statistics, about 200 people per 1 million people have ARF annually.
Forms and causes of arresters
Depending on what processes led to the onset of acute renal failure, prerenal, renal and postrenal forms are distinguished.
Prerenal form of arrester
The prerenal form of ARF is characterized by a significant reduction in renal blood flow and a decrease in the glomerular filtration rate. Such disorders in the work of the kidneys are associated with a general decrease in the volume of circulating blood in the body. If the normal blood supply to the organ is not restored as soon as possible, ischemia or necrosis of the renal tissue is possible. The main reasons for the development of prerenal ARF are:
- decreased cardiac output;
- pulmonary embolism;
- operations and injuries accompanied by significant blood loss;
- extensive burns;
- dehydration caused by diarrhea, vomiting;
- taking diuretics;
- a sudden decrease in vascular tone.
Renal arrester
In the renal form of acute renal failure, damage to the renal parenchyma is observed. It can be caused by inflammatory processes, toxic effects or pathologies of the vessels of the kidneys, which lead to insufficient blood supply to the organ. Renal ARF is a consequence of renal tubular epithelial cell necrosis. As a result, there is a violation of the integrity of the tubules and the release of their contents into the surrounding kidney tissue. The following factors can lead to the development of the renal form of ARF:
- intoxication with various poisons, drugs, radiopaque compounds, heavy metals, snake or insect bites, etc.;
- kidney disease: interstitial nephritis, acute pyelonephritis and glomerulonephritis;
- damage to the renal vessels (thrombosis, aneurysm, atherosclerosis, vasculitis, etc.);
- kidney injury.
Important: Long-term use of drugs that have a nephrotoxic effect, without first consulting a doctor, can cause acute renal failure.
Postrenal arrester
Postrenal ARF develops as a result of acute disturbance of the passage of urine. In this form of acute renal failure, kidney function is preserved, but the process of urine excretion is difficult. The occurrence of ischemia of the renal tissue is possible, since the renal pelvis overflowing with urine begin to squeeze the surrounding kidney tissue. The causes of postrenal ARF include:
- spasm of the sphincter of the bladder;
- blockage of the ureters due to urolithiasis;
- tumors of the bladder, prostate, urinary tract, pelvic organs;
- trauma and hematoma;
- inflammatory diseases of the ureters or bladder.
Stages and symptoms of ARF
The characteristic symptoms of ARF develop very quickly. There is a sharp deterioration in the general condition of the patient and impaired renal function. V clinical picture Acute renal failure is divided into stages, each of which is characterized by certain signs:
- initial stage;
- stage of oligoanuria;
- stage of polyuria;
- stage of recovery.
In the first stage of ARF, symptoms are determined by the cause of the disease. These may be signs of intoxication, shock, or the manifestation of some kind of disease. So, with infectious kidney disease, fever is noted, headache, muscle weakness. When intestinal infection vomiting and diarrhea are present. For toxic kidney damage, manifestations of jaundice, anemia, and convulsions are possible. If acute glomerulonephritis is the cause of acute renal failure, then there is an excretion of urine mixed with blood and pain in the lumbar region. The first stage of acute renal failure is characterized by a decrease in blood pressure, pallor, rapid pulse, a slight decrease in urine output (up to 10%).
The stage of oligoanuria in acute renal failure is the most severe and poses the greatest danger to the patient's life. It is characterized by the following symptoms:
- a sharp decrease or cessation of urine output;
- intoxication with nitrogen metabolism products, manifested in the form of nausea, vomiting, itching of the skin, increased breathing, loss of appetite, tachycardia;
- increased blood pressure;
- confusion and loss of consciousness, coma;
- swelling of the subcutaneous tissue, internal organs and cavities;
- increase in body weight due to the presence of excess fluid in the body;
- general serious condition.
The further course of acute renal failure is determined by the success of the therapy performed at the second stage. With a favorable outcome, the stage of polyuria and subsequent recovery begins. At first, a gradual increase in urine output is observed, and then polyuria develops. Excess fluid is excreted from the body, edema decreases, the blood is cleared of toxic products. The stage of polyuria can be dangerous due to the occurrence of dehydration and electrolyte imbalances (for example, hypokalemia). After about a month, the urine output returns to normal and the recovery period begins, which can last up to 1 year.
If the treatment was chosen incorrectly or carried out too late and proved to be ineffective, then the terminal stage of ARF develops with a high probability of death. It is characterized by:
- shortness of breath, cough due to the accumulation of fluid in the lungs;
- secretion of sputum mixed with blood;
- subcutaneous hemorrhage and internal bleeding;
- loss of consciousness, coma;
- muscle spasms and cramps;
- severe heart rhythm disturbances.
Tip: If you find even a slight decrease in urine output, especially if there are kidney diseases or other pathologies, you should immediately contact a nephrologist. Such violations can be the beginning of the development of acute renal failure.
Arrester diagnostics
In acute renal failure, the diagnosis of the disease is carried out using both laboratory and instrumental methods... In laboratory tests, the following deviations from the norm are present:
- a general blood test is characterized by a decrease in the level of hemoglobin, an increase in the concentration of leukocytes, an increase in ESR;
- in the general analysis of urine, protein, cylinders, a decrease in density, an increased content of erythrocytes and leukocytes, a decrease in platelet levels are found;
- daily urine analysis is characterized by a significant decrease in urine output;
- in the biochemical analysis of blood, an increased level of creatinine and urea is found, as well as an increase in the concentration of potassium and a decrease in the concentration of sodium and calcium.
Of the instrumental diagnostic methods used:
- ECG, used to monitor the work of the heart, which may be impaired due to hyperkalemia;
- Ultrasound, allows you to assess the size of the kidneys, the level of blood supply and the presence of obstruction;
- kidney biopsy;
- radiography of the lungs and heart.
Treatment and emergency care for acute renal failure
For acute renal failure urgent care consists in the quick delivery of a person to a hospital hospital. In this case, the patient needs to be provided with a state of rest, warmth and a horizontal position of the body. Best to call ambulance, since in this case qualified doctors will be able to take all the necessary measures right on the spot.
In acute renal failure, treatment is carried out taking into account the stage of the disease and the cause of it. After elimination etiological factor, it is necessary to restore homeostasis and renal excretory function. Given the reason for the arrester, you may need to:
- taking antibiotics for infectious diseases;
- replenishment of the volume of fluid (with a decrease in the volume of circulating blood);
- using diuretics and fluid restriction to reduce swelling and increase urine production;
- taking heart medications for cardiac dysfunction;
- taking medications to lower blood pressure if it rises;
- surgery to restore kidney tissue damaged as a result of injury or to remove obstacles that interfere with the outflow of urine;
- taking medications to improve blood supply and blood flow in the nephrons;
- detoxification of the body in case of poisoning (gastric lavage, administration of antidotes, etc.).
To remove toxic products from the blood, hemodialysis, plasmapheresis, peritoneal dialysis, hemosorption are used. The acid-base and water-electrolyte balance is restored by introducing saline solutions of potassium, sodium, calcium, etc. These procedures are used temporarily until renal function is restored. With timely treatment, acute renal failure has a favorable prognosis.
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But perhaps it is more correct to treat not the effect, but the cause?
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