Acute renal injury opn etiology diagnostics treatment. Renal failure is acute. Emergency care for illness

For citation: Milovanov Yu.S., Nikolaev A.Yu. ACUTE RENAL FAILURE // breast cancer. 1998. No. 19. P. 2

The article is devoted to acute renal failure (ARF), one of the most common critical conditions.

The article deals with the pathogenesis, clinical picture, diagnosis and treatment of three forms of acute renal failure: prerenal, renal and postrenal.
The paper deals with acute renal failure (ARF), A most common critical condition. It considers the pathogenesis, clinical presentation, and treatment of three forms of ARF: prerenal, renal, postrenal.

Yu.S. Milovanov, A. Yu. Nikolaev - Problem Laboratory of Nephrology (Head - Corresponding Member of the Russian Academy of Medical Sciences I.E. THEM. Sechenov
Yu. S. Milovanov, A. Yu. Nikolayev - Problem-Solving Laboratory of Nephrology (Head I.Ye. Tareyevа, Corresponding Member of the Russian Academy of Medical Sciences), I.M. Sechenov Moscow Medical Academy

O The country of renal failure (ARF) is an acute, potentially reversible loss of renal excretory function, manifested by rapidly increasing azotemia and severe water-electrolyte disturbances.

This division of arresters is of great practical importance, as it allows you to outline specific measures for the prevention and control of arresters.
Among the triggers prerenal arrester - a decrease in cardiac output, acute vascular insufficiency, hypovolemia and a sharp decrease in the volume of circulating blood. Violation of general hemodynamics and circulation and a sharp depletion of renal blood circulation induce renal afferent vasoconstriction with redistribution (shunting) of renal blood flow, ischemia of the renal cortex and a decrease in glomerular filtration rate (GFR). With exacerbation of renal ischemia, prerenal ARF can turn into renal due to ischemic necrosis of the epithelium of the renal convoluted tubules.
Renal surge arrester in 75% of cases it is caused by acute tubular necrosis (AIO). Most often it is ischemic AIO complicating shock (cardiogenic, hypovolemic, anaphylactic, septic), coma, dehydration. Among other factors that damage the epithelium of the convoluted renal tubules, an important place is occupied by drugs and chemical compounds that cause nephrotoxic AIO.
In 25% of cases, renal acute renal failure is due to other causes: inflammation in the renal parenchyma and interstitium (acute and rapidly progressive glomerulonephritis - AHN and RPGN), interstitial nephritis, renal vascular disease (thrombosis of the renal arteries, veins, dissecting aortic aneurysm, vasculomitis -uremic syndrome, malignant hypertension), etc.
Nephrotoxic AIO diagnosed in every 10th patient with acute renal failure admitted to the center of acute hemodialysis (HD). Among more than 100 known nephrotoxins, one of the first places is occupied by drugs, mainly aminoglycoside antibiotics, the use of which in 10-15% of cases leads to moderate, and in 1-2% - to severe acute renal failure. Of industrial nephrotoxins, the most dangerous are salts of heavy metals (mercury, copper, gold, lead, barium, arsenic) and organic solvents (glycols, dichloroethane, carbon tetrachloride).
One of the common causes of renal ARF is myorenal syndrome , pigmented myoglobinuric nephrosis caused by massive rhabdomyolysis. Along with traumatic rhabdomyolysis (crash syndrome, convulsions, excessive physical exertion), non-traumatic rhabdomyolysis often develops due to the action of various toxic and physical factors (CO poisoning, zinc, copper, mercury, heroin, electrical trauma, frostbite), viral myositis, muscle ischemia and electrolyte disorders (chronic alcoholism, coma, severe hypokalemia, hypophosphatemia), as well as prolonged fever, eclampsia, prolonged status asthma and paroxysmal myoglobinuria.
Among inflammatory diseases of the renal parenchyma, in the last decade, the proportion of drug (allergic) acute interstitial nephritis in the framework of hemorrhagic fever with renal syndrome (HFRS), as well as interstitial nephritis in leptospirosis, has significantly increased. The increase in the incidence of acute interstitial nephritis (SPE) is explained by the growing allergization of the population and polypharmacy.
Postrenal arrester caused by acute obstruction (occlusion) of the urinary tract: bilateral ureteral obstruction, bladder neck obstruction, adenoma, prostate cancer, tumor, bladder schistosomiasis, urethral stricture. Other causes include necrotizing papillitis, retroperitoneal fibrosis and retroperitoneal tumors, diseases and injuries of the spinal cord. It should be emphasized that unilateral ureteral obstruction is often sufficient for the development of postrenal acute renal failure in a patient with chronic kidney disease. The mechanism of development of postrenal ARF is associated with afferent renal vasoconstriction, which develops in response to a sharp increase in intratubular pressure with release of angiotensin II and thromboxane A 2 .
Highlight ARF developing in the framework of multiple organ failure , due to the extreme severity of the condition and the complexity of treatment. The syndrome of multiple organ failure is manifested by a combination of acute renal failure with respiratory, cardiac, hepatic, endocrine (adrenal) insufficiency. It is found in the practice of resuscitation specialists, surgeons, in the clinic of internal diseases, complicates terminal conditions in cardiological, pulmonological, gastroenterological,gerontological patients, with acute sepsis, with multiple trauma.

Pathogenesis of ARF

The main pathogenetic mechanism for the development of acute renal failure is renal ischemia. Shock restructuring of renal blood flow - intrarenal shunting of blood through the juxtaglomerular system with a decrease in pressure in the glomerular afferent arterioles below 60-70 mm Hg. Art. - is the cause of ischemia of the cortical layer, induces the release of catecholamines, activates the renin-aldosterone system with the production of renin, an antidiuretic hormone and thereby causes renal afferent vasoconstriction with a further decrease in GFR, ischemic damage to the epithelium of convoluted tubules with an increase in the concentration of calcium and free radical epithelium ... Ischemic damage to the renal tubules in acute renal failure is often exacerbated by their simultaneous direct toxic damage caused by endotoxins... Following necrosis (ischemic, toxic) of the convoluted tubule epithelium, glomerular filtrate leaks into the interstitium through damaged tubules, which are blocked by cellular detritus, and also as a result of interstitial edema of the renal tissue. Interstitial edema increases renal ischemia and further decreases glomerular filtration... The degree of increase in the interstitial volume of the kidney, as well as the degree of decrease in the height of the brush border and the area of ​​the basement membrane of the epithelium of the convoluted tubules, correlate with the severity of ARF.
Currently, more and more experimental and clinical data are accumulating indicating that what the effect of constrictive stimuli on blood vessels in acute renal failure is realized through changes in the intracellular calcium concentration... Calcium initially enters the cytoplasm, and then, with the help of a special carrier, into the mitochondria. The energy used by the carrier is also required for the initial synthesis of ATP. Energy deficiency leads to cell necrosis, and the resulting cellular detritus obstructs the tubules, exacerbating anuria. Administration of the calcium channel blocker veropamil simultaneously with ischemia or directly after it prevents the flow of calcium into the cells, which prevents acute renal failure or facilitates its course.
In addition to the universal ones, there are also particular mechanisms of the pathogenesis of certain forms of renal acute renal failure. So, DIC syndrome with bilateral cortical necrosis is characteristic of obstetric acute renal failure, acute sepsis, hemorrhagic and anaphylactic shock, RPGN in systemic lupus erythematosus. Intratubular blockade due to the binding of tubular protein Tamm-Horsfall with Bens-Jones protein, with free hemoglobin, myoglobin determines the pathogenesis of acute renal failure in myeloma, rhabdomyolysis, hemolysis. Crystal deposition in the lumen of the renal tubules is typical for uric acid blockade (primary, secondary gout), ethylene glycol poisoning, overdose of sulfonamides, methotrexate. At necrotizing papillitis (necrosis of the renal papillae), the development of both postrenal and renal acute renal failure is possible. Postrenal ARF is more common, caused by obstruction of the ureters by necrotic papillae and blood clots in chronic necrotizing papillitis (diabetes, analgesic nephropathy, alcoholic nephropathy, sickle cell anemia). Renal acute renal failure due to total necrotizing papillitis develops with purulent pyelonephritis and often leads to irreversible uremia. Renal ARF can develop when acute pyelonephritis as a result of pronounced interstitial edema of the stroma infiltrated by neutrophils, especially with the addition of apostematosis and bacteremic shock. Severe inflammatory changes in the form of diffuse infiltration of the interstitial tissue of the kidneys by eosinophils and lymphocytes are the cause of ARF in SPE medicinal ... ARF in HFRS can be caused by both acute viral interstitial nephritis and others complications of HFRS : hypovolemic shock, hemorrhagic shock and collapse due to subcapsular rupture of the kidney, acute adrenal insufficiency. Heavy inflammatory changes in the renal glomeruli with diffuse extracapillary proliferation, microthrombosis and fibrinoid necrosis of the vascular loops of the glomeruli lead to acute renal failure in RPGN (primary, lupus, with Goodpasture's syndrome) and less often in acute post-streptococcal nephritis. Finally, renal ARF can be caused by severe inflammatory changes in the renal arteries : necrotizing arteritis with multiple aneurysms of the arcuate and interlobular arteries (periarteritis nodosa), thrombotic occlusive microangiopathy of the renal vessels, fibrinoid arteriolonecrosis (malignant hypertension, sclerodermic kidney, hemolytic uremic syndrome and thrombocytophenic thrombocytopathy).

Clinical presentation of acute renal failure

Early clinical signs (precursors) ARF are often minimal and short-lived - renal colic in postrenal ARF, an episode of acute heart failure, circulatory collapse in prerenal ARF. Often, the clinical debut of acute renal failure is masked by extrarenal symptoms (acute gastroenteritis in case of poisoning with heavy metal salts, local and infectious manifestations in multiple trauma, systemic manifestations with medicinal SPE). In addition, many of the early symptoms of ARF (weakness, anorexia, nausea, drowsiness) are nonspecific. Therefore, laboratory methods are of the greatest value for early diagnosis: determination of the level of creatinine, urea and potassium in the blood.
Among signs of clinically advanced acute renal failure - symptoms of loss of homeostatic kidney function - there are acute disorders of water-electrolyte metabolism and acid-base state (CBS), increasing azotemia, damage to the central nervous system (uremic intoxication), lungs, gastrointestinal tract, acute bacterial and fungal infections.
Oliguria (diuresis less than 500 ml) is found in most patients with acute renal failure. Anuric acute renal failure (diuresis less than 50 ml per day) develops in 3-10% of patients. Symptoms of overhydration can quickly join oliguria and especially anuria - first, extracellular (peripheral and cavity edema), then intracellular (pulmonary edema, acute left ventricular failure, cerebral edema). At the same time, almost 30% of patients develop neoliguric ARF in the absence of signs of overhydration.
Azotemia - the cardinal sign of an arrester. The severity of azotemia, as a rule, reflects the severity of ARF. In contrast to chronic renal failure, acute renal failure is characterized by a rapid rate of increase in azotemia. With a daily increase in the level of blood urea by 10-20 mg%, and creatinine by 0.5-1 mg%, one speaks of a non-catabolic form of ARF. The hypercatabolic form of acute renal failure (in acute sepsis, burn disease, multiple trauma with a crash syndrome, surgery on the heart and large vessels) is characterized by a significantly higher daily increase in urea and blood creatinine (30-100 and 2-5 mg%, respectively), as well as more pronounced disorders of potassium metabolism and CBS. In non-oliguric ARF, high azotemia, as a rule, appears with the addition of hypercatabolism.
Hyperkalemia - an increase in the concentration of potassium in serum to a level of more than 5.5 meq / l - is more often detected in oliguric and anuric ARF, especially in hypercatabolic forms, when the accumulation of potassium in the body occurs not only due to a decrease in its renal excretion, but also due to its intake from necrotic muscles, hemolyzed erythrocytes. At the same time, critical, life-threatening hyperkalemia (more than 7 meq / l) can develop on the first day of the disease and determine the rate of increase in uremia. The leading role in the detection of hyperkalemia and control of potassium levels belongs to biochemical monitoring and ECG.
Metabolic acidosis with a decrease in serum bicarbonate levels to 13 mmol / l is found in most patients with acute renal failure. With more pronounced disorders of CBS with a large deficiency of bicarbonates and a decrease in blood pH, which is characteristic of hypercatabolic forms of acute renal failure, large noisy breathing of Kussmaul and other signs of damage to the central nervous system join, heart rhythm disturbances caused by hyperkalemia are aggravated.
Heavy suppression of the immune system typical for surge arresters. With acute renal failure, the phagocytic function and chemotaxis of leukocytes are inhibited, the synthesis of antibodies is suppressed, and cellular immunity is impaired (lymphopenia). Acute infections - bacterial (more often caused by opportunistic gram-positive and gram-negative flora) and fungal (up to candidasepsis) develop in 30-70% of patients with acute renal failure and often determine the patient's prognosis. Typical are acute pneumonia, stomatitis, parotitis, urinary tract infection, etc.
Among pulmonary lesions in acute renal failure one of the most severe is abscess pneumonia. However, other forms of lung damage are also common, which have to be differentiated with pneumonia. Uremic pulmonary edema developing with severe overhydration is manifested by acute respiratory failure, radiographically characterized by multiple cloudy infiltrates in both lungs. Respiratory distress syndrome, often associated with severe acute renal failure, is also manifested by acute respiratory failure with a progressive deterioration in pulmonary gas exchange and diffuse changes in the lungs (interstitial edema, multiple atelectasis)with signs of acute pulmonary hypertension and subsequent addition of bacterial pneumonia. Mortality from distress syndrome is very high.
Arresters are characterized by a cyclical, potentially reversible flow. Allocate a short-term initial stage, oliguric or anuric (2-3 weeks) and recovery polyuric (5-10 days). The irreversible course of acute renal failure should be considered when the duration of anuria has exceeded 4 weeks. This more rare variant of the course of severe acute renal failure is observed in bilateral cortical necrosis, RPGN, severe inflammatory lesions of the renal vessels (systemic vasculitis, malignant hypertension).

ARF diagnosis

At the first stage in the diagnosis of acute renal failure, it is important to distinguish between anuria and acute urinary retention. You should make sure that there is no urine in the bladder (percussion, ultrasound or catheterization) and urgently determine the level of urea, creatinine and serum potassium. The next stage of diagnosis is to establish the form of ARF (prerenal, renal, postrenal)... First of all, obstruction of the urinary tract is excluded using ultrasound, radionuclide, X-ray and endoscopic methods. The study of urine is also important. With prerenal ARF, the content of sodium and chlorine in urine is reduced, and the ratio of urine creatinine / plasma creatinine is increased, which indicates a relatively preserved concentration ability of the kidneys. The opposite relationship is observed with renal ARF. The index of excreted sodium fraction with prerenal ARF is less than 1 and with renal ARF is equal to 2.
After excluding the prerenal arrester, it is necessary to establish the shape of the renal arrester. The presence of erythrocyte and protein casts in the sediment indicates damage to the glomeruli (for example, with OHN and RPGN), abundant cellular detritus and tubular casts indicate AIO, the presence of polymorphonuclear leukocytes and eosinophils is characteristic of acute tubulointerstitial nephritis (ATIN) (detection myoglobin, hemoglobin, myeloma) , and also crystalluria is typical for intratubular blockade.
However, it should be borne in mind that the study of the composition of urine in some cases does not have a decisive diagnostic value. For example, when diuretics are prescribed, the sodium content in urine in prerenal ARF may be increased, and in chronic nephropathies the prerenal component (decreased natriuresis) may not be detected, since even in the initial stage of chronic renal failure (CRF), the kidney's ability to preserve sodium is lost to a greater extent. and water. At the onset of acute nephritis, the electrolyte composition of urine may be similar to that in prerenal ARF, and later on - similar to that in renal ARF. Acute obstruction of the urinary tract leads to changes in the composition of urine, characteristic of prerenal ARF, and chronic causes changes characteristic of renal ARF. Low excreted sodium fraction is found in patients with hemoglobin and myoglobinuric ARF. In the final stages, a kidney biopsy is used. She is shown with prolonged course of the anuric period of acute renal failure, with acute renal failure of unclear etiology, with suspected drug ATIN, with acute renal failure associated with glomerulonephritis or systemic vasculitis.

ARF treatment

the main task treatment of postrenal acute renal failure consists in eliminating the obstruction and restoring the normal passage of urine. After that, the postrenal ARF is quickly eliminated in most cases. Dialysis methods are used for postrenal acute renal failure in cases where, despite the restoration of ureteral patency, anuria persists. This is observed with the addition of apostematous nephritis, urosepsis.
If prerenal ARF is diagnosed, it is important to focus efforts on eliminating the factors that caused acute vascular insufficiency or hypovolemia, to discontinue medications that induce prerenal ARF (nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, sandimmune). To remove from shock and replenish the volume of circulating blood, they resort to intravenous administration of large doses of steroids, large molecular dextrans (polyglucin, rheopolyglucin), plasma, albumin solution. With blood loss, erythrocyte mass is transfused. For hyponatremia and dehydration, saline solutions are administered intravenously. All types of transfusion therapy should be carried out under the control of urine output and the level of central venous pressure. Only after stabilization of blood pressure and replenishment of the intravascular bed is it recommended to switch to intravenous, long-term (6-24 hours) administration of furosemide with dopamine, which makes it possible to reduce renal afferent vasoconstriction.

Renal ARF treatment

With the development of oliguria in patients with myeloma, urate crisis, rhabdomyolysis, hemolysis, continuous (up to 60 hours) infusion alkalizing therapy is recommended, including the administration of mannitol together with isotonic sodium chloride, sodium bicarbonate and glucose solution (on average 400-600 ml / h) and furosemide. Thanks to this therapy, diuresis is maintained at a level of 200-300 ml / h, the alkaline reaction of urine is maintained (pH> 6.5), which prevents intratubular precipitation of the cylinders and ensures the excretion of free myoglobin, hemoglobin, and uric acid.
At an early stage renal arrester, in the first 2-3 days of AIO development, in the absence of complete anuria and hypercatabolism, an attempt at conservative therapy (furosemide, mannitol, fluid infusion) is also justified. The effectiveness of conservative therapy is evidenced by an increase in diuresis with a daily decrease in body weight by 0.25-0.5 kg. A loss of body weight of more than 0.8 kg / day, often combined with an increase in the level of potassium in the blood, is an alarming sign of overhydration, requiring a tightening of the water regime.
In some cases of renal acute renal failure (RPGN, drug SPI, acute pyelonephritis), basic conservative therapy is supplemented with immunosuppressants, antibiotics, plasmapheresis. The latter is also recommended for patients with crash syndrome to remove myoglobin and stop DIC. In case of acute renal failure as a result of sepsis and in case of poisoning, hemosorption is used, which ensures the removal of various toxins from the blood.
In the absence of the effect of conservative therapy, the continuation of this treatment for more than 2-3 days is futile and dangerous due to the increased risk of complications from the use of large doses of furosemide (hearing damage) and mannitol (acute heart failure, hyperosmolarity, hyperkalemia).

Dialysis treatment

The choice of dialysis treatment is determined by the characteristics of ARF. In non-catabolic acute renal failure in the absence of severe overhydration (with residual renal function), acute HD is used. At the same time, acute peritoneal dialysis is effective in case of non-catabolic ARF in children, elderly patients, with severe atherosclerosis, drug ARF (aminoglycoside AIO).
For the treatment of patients with critical overhydration and metabolic disorders, they are successfully used hemofiltration (GF). In patients with acute renal failure without residual renal function, GF is performed continuously throughout the entire period of anuria (constant GF). In the presence of minimal residual renal function, the procedure can be performed in an intermittent mode (intermittent GF). Depending on the type of vascular access, constant GF can be arteriovenous and venovenous. An indispensable condition for conducting arteriovenous GF is hemodynamic stability. In patients with acute renal failure with critical overhydration and unstable hemodynamics (hypotension, decreased cardiac output), veno-venous GF is performed using venous access. Blood is perfused through a hemodialyzer using a blood pump. This pump guarantees adequate blood flow to maintain the required ultrafiltration rate.

Prognosis and outcomes

Despite the improvement of treatment methods, mortality in acute renal failure remains high, reaching 20% ​​in obstetric and gynecological forms, 50% in drug lesions, 70% after trauma and surgical interventions, and 80-100% in multiple organ failure. In general, the prognosis of prerenal and postrenal ARF is better than that of renal. Oliguric and especially anuric renal ARF (compared with neoliguric ARF), as well as ARF with pronounced hypercatabolism, are prognostically unfavorable. The prognosis with acute renal failure is worsening, the addition of infection (sepsis), elderly patients.
Among the outcomes of acute renal failure, the most frequent is recovery: complete (in 35-40% of cases) or partial - with a defect (in 10-15%). Death is almost as often observed: in 40-45% of cases. Chronization with the transfer of the patient to chronic HD is rare (in 1-3% of cases): with such forms of acute renal failure as bilateral cortical necrosis, malignant hypertension syndrome, hemolytic uremic syndrome, necrotic vasculitis. In recent years, there has been an unusually high percentage of chronicity (15-18) after ARF caused by radiopaque contrast agents.
A common complication of previous acute renal failure is urinary tract infection and pyelonephritis, which in the future can also lead to chronic 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 excretion 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.

Antibiotics, sulfonamides, aminoglycosides, antineoplastic agents, have a toxic effect on the kidneys

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. In the clinical picture of acute renal failure, stages are distinguished, 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 an infectious kidney disease, fever, headache, muscle weakness are noted. In the case of an 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 products of nitrogen metabolism, 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. First, there is a gradual increase in urine output, 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.

Urinalysis detects renal dysfunction

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

In acute renal failure, emergency 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. It is best to call an ambulance, since in this case qualified doctors will be able to take all the necessary measures right on the spot.

In severe condition in case of acute renal failure, the patient must be taken to the hospital

In acute renal failure, treatment is carried out taking into account the stage of the disease and the cause of it. After elimination of the 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, ARF has a favorable prognosis.

RCHRH (Republican Center for Healthcare Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2014

Nephrology

general information

Short description

Expert Council
RSE on REM "Republican Center
health development "

Ministry of Health
and social development

Acute renal failure (ARF)- a syndrome that develops as a result of a rapid (hours-days) decrease in the glomerular filtration rate, leading to the accumulation of nitrogenous (including urea, creatinine) and non-nitrogenous metabolic products (with disturbances in electrolyte levels, acid-base balance, fluid volume) excreted by the kidneys.

In 2004, ADQI (Acute Dialysis Quality Improvement Initiative) proposed the concept of acute renal injury (AKI), replacing the term acute renal failure and a classification called RIFLE for the first letters of each of the sequentially identified stages of AKI: risk (Risk), Injury, Failure, Loss, End stage renal disease - Table 2.

This term and new classifications have been introduced with the aim of earlier verification of acute renal injury, early initiation of renal replacement therapy (RRT) when conservative methods are ineffective, and to prevent the development of severe forms of renal failure with unfavorable outcomes.

I. INTRODUCTORY PART:

Protocol name: Acute renal failure (acute kidney injury)

Protocol code:

Code (codes) for ICD-10:

Acute renal failure (N17)

N17.0 Acute renal failure with tubular necrosis

Tubular necrosis: NOS. spicy

N17.1 Acute renal failure with acute cortical necrosis

Cortical necrosis: NOS. spicy. renal

N17.2 Acute renal failure with medullary necrosis

Medullary (papillary) necrosis: NOS. spicy. renal

N17.8 Other acute renal failure

N17.9 Acute renal failure, unspecified

Abbreviations used in the protocol:

ANCA Antineutrophil antibodies

ANA Antinuclear antibodies

BP Blood pressure

ADQI Acute Dialysis Quality Improvement Initiative

AKIN Acute Kidney Injury Network - Acute Kidney Injury Research Group

LVAD Left Ventricular Assist Device

KDIGO Kidney Disease Improving Global Outcomes - Initiative to Improve Global Kidney Disease Outcomes

MDRD Modification Diet of Renal Disease

RVAD Right Ventricular Assist Device

NOS No additional specification

ARB-II Angiotensin II receptor blockers

HRS Hepatorenal Syndrome

HUS Hemolytic uremic syndrome

GCC Gastrointestinal bleeding

RRT Renal Replacement Therapy

IHD Intermittent (periodic) hemodialysis

Ventilation Artificial lung ventilation

ACE I Angiotensin converting enzyme inhibitors

CI-AKI Contrast - Induced AKI

Acid-base balance acid-base state

NSAIDs Non-steroidal anti-inflammatory drugs

ARF Acute renal failure

AKI Acute renal injury

OTN Acute tubular necrosis

ATIN Acute tubulointerstitial nephritis

BCC Circulating blood volume

ICU Intensive care unit

CRRT Continued renal replacement therapy

PGF Continued veno-venous hemofiltration

CVVHD Continued veno-venous hemodialysis

PVVGDF Continued veno-venous hemodiafiltration

GFR Glomerular filtration rate

RIFLE Risk, damage, failure, loss, ESRD

ESRD Terminal Chronic Renal Failure

CRF Chronic renal failure

CKD Chronic Kidney Disease

CVP Central venous pressure

ECMO Extracorporeal Membrane Oxygenation

Protocol development date: year 2014.

Protocol users: nephrologist, hemodialysis department doctor, anesthesiologist-resuscitator, general practitioner, therapist, toxicologist, urologist.

Classification

Classification

Causes and classifications of AKI

By the main mechanism of development OPP is divided into 3 groups:

Prerenal;

Renal;

Postrenal.

Picture 1. Classification of the main causes of AKI

Prerenal causes

Figure 2. Causes of prerenal acute kidney injury

Morphological classification based on the nature of morphological changes and localization of the process:

Acute tubular necrosis;

Acute cortical necrosis;

Acute tubulointerstitial nephritis.

Depending on the urine output there are 2 forms:

Oliguric (urine output less than 500 ml / day);

Non-oliguric (diuresis more than 500 ml / day).

Additionally distinguish:

Non-catabolic form (daily increase in blood urea less than 20 mg / dl, 3.33 mmol / l);

Hypercatabolic form (daily increase in blood urea more than 20 mg / dl, 3.33 mmol / l).

Since most patients with suspected ARF / AKI do not have information about the initial state of renal function, the basal creatinine level, correlated with the patient's age and sex, is calculated at a given GFR level (75 ml / min) using the MDRD formula using the ADQI proposed by experts (tab. 1) .

Estimated Basal Creatinine (ADQI abbreviated) - Table 1

Age, years	Men, μmol / l	Women, μmol / l
20-24	115	88
25-29	106	88
30-39	106	80
40-54	97	80
55-65	97	71
Over 65	88	71

RIFLE classification of PPE (2004) - table 2

Classes	Glomerular filtration criteria	Diuresis criteria
Risk	Scr * by 1.5 times or ↓ KF ** by 25%	<0,5 мл/кг/час ≥6 часов
Damage	Scr 2 times or ↓ CF by 50%	<0,5 мл/кг/час ≥12 часов
Failure	Scr 3 times or ↓ CF by 75% or Scr≥354 μmol / L with an increase of at least 44.2 μmol / L	<0,3 мл/кг/час ≥24 часов или анурия ≥12 часов
Loss of renal function	Persistent OPP; complete loss of renal function> 4 weeks
Terminal renal failure	ESRD> 3 months

Scr * - serum creatinine, CF ** - glomerular filtration

Table 4... Stages of AKI (KDIGO, 2012)

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES OF DIAGNOSTICS AND TREATMENT

List of basic diagnostic measures

Basic (mandatory) diagnostic examinations carried out at the outpatient stage:

After discharge from the hospital:

General blood analysis;

General urine analysis;

Biochemical blood test (creatinine, urea, potassium, sodium, calcium);

Determination of protein in urine (quantitative test);

Ultrasound of the kidneys.

Additional diagnostic examinations carried out at the outpatient stage:

Biochemical blood test (protein fractions, M-gradient, total and ionized calcium, phosphorus, lipid spectrum);

Rheumatoid factor;

Doppler ultrasonography of the vessels of the kidneys;

Ultrasound of the abdominal organs.

The minimum list of examinations that must be carried out when referring to planned hospitalization:

Due to the need for urgent emergency hospitalization, there is enough data on the volume of urine excreted (oliguria, anuria) and / or an increase in creatinine, according to the diagnostic criteria of clause 12.3.

Basic (mandatory) diagnostic examinations carried out at the inpatient level:

Biochemical blood test (serum creatinine, serum urea, potassium, sodium, total serum protein and protein fractions, ALT, AST, total and direct bilirubin, CRP);

Blood acid base balance;

Coagulogram (PV-INR, APTT, fibrinogen);

General urine analysis (in the presence of diuresis!);

Ultrasound of the kidneys;

Notes:

All urgent admissions of patients, planned X-ray contrast studies, as well as surgical interventions, should be assessed for the risk of developing AKI;

All urgent admissions should be accompanied by an analysis of urea, creatinine and electrolyte levels;

With the expected development of AKI, the patient should be examined by a nephrologist within the first 12 hours, the indications for RRT and the prognosis should be determined, and the patient should be referred to a multidisciplinary hospital with an extracorporeal hemocorrection department.

Additional diagnostic examinations carried out at the stationary level:

Urine analysis according to Zimnitsky;

Rehberg's test (daily);

24-hour albuminuria / proteinuria or albumin / creatinine ratio, protein / creatinine ratio;

Electrophoresis of urine proteins + urine M-gradient;

Excretion of potassium, sodium, calcium in the urine;

Daily excretion of uric acid;

Urinalysis for Bens-Jones Protein;

Bacteriological examination of urine to determine the sensitivity of the pathogen to antibiotics;

Biochemical blood test (total and ionized calcium, phosphorus, lactate dehydrogenase, creatine phosphokinase, lipid spectrum);

Rheumatoid factor;

Immunological analyzes: ANA, ENA, a-DNA, ANCA, antiphospholipid antibodies, antibodies to cardiolipin antigen, complement fractions C3, C4, CH50;

Parathyroid hormone;

Free hemoglobin in blood and urine;

Schizocytes;

Blood procalcitonin;

Ultrasound of the bladder;

Doppler ultrasonography of renal vessels;

Chest x-ray;

Fundus examination;

TRUS of the prostate;

Ultrasound of the pleural cavities;

Ultrasound of the pelvic organs;

CT scan of the thoracic segment, abdominal segment, pelvic organs (if a systemic disease with multiple organ lesions is suspected, if paraneoplastic nephropathy is suspected to exclude neoplasms, metastatic lesions; in case of sepsis, to search for the primary source of infection);

Osmolarity of urine, osmolality of urine;

Puncture biopsy of the kidney (used for AKI in difficult diagnostic cases, indicated for renal AKI of unclear etiology, AKI with a prolonged more than 4 weeks period of anuria, AKI associated with nephrotic syndrome, acute nephritic syndrome, diffuse lung lesions like necrotizing vasculitis);

Biopsy of the skin, muscles, rectal mucosa, gums - for the diagnosis of amyloidosis, as well as for the verification of a systemic disease;

Electroencephalography - in the presence of neurological symptoms;

ELISA for markers of viral hepatitis B, C;

PCR for HBV-DNA and HCV-RNA - to exclude virus-associated nephropathy;

Coagulogram 2 (RFMK, ethanol test, antithrombin III, platelet function);

CT / MRI of the brain;

MRI of the thoracic segment, abdominal segment, pelvic organs (if a systemic disease with multiple organ lesions is suspected, if paraneoplastic nephropathy is suspected to exclude neoplasms, metastatic lesions; in case of sepsis - to search for the primary source of infection) ;;

Blood culture three times for sterility from both hands;

Sowing blood for blood culture;

Crops from wounds, catheters, tracheostomy, pharynx;

Fibroesophagogastroduodenoscopy - to exclude the presence of erosive and ulcerative lesions, due to the high risk of gastrointestinal bleeding when using anticoagulants during RRT; exclude neoplasm if a paraneoplastic process is suspected;

Colonoscopy - to exclude the presence of erosive and ulcerative lesions, due to the high risk of intestinal bleeding when using anticoagulants during RRT; exclude neoplasm if a paraneoplastic process is suspected.

Diagnostic measures carried out at the stage of an ambulance emergency:

Collection of complaints and anamnesis, data in relation to contact with a toxic substance;

Data on hydrobalance, diuresis;

Physical examination;

Measurement of blood pressure, correction of blood pressure, according to the clinical protocol "Arterial hypertension".

Providing emergency care for pulmonary edema according to the clinical protocol.

Diagnostic criteria***:

General complaints:

Decreased urine output or lack of urine;

Peripheral edema;

Dyspnea;

Dry mouth;

Weakness;

Nausea, vomiting;

Lack of appetite.

Specific complaints- depending on the etiology of AKI.

Anamnesis:

Find out the conditions leading to hypovolemia (bleeding, diarrhea, heart failure, surgery, trauma, blood transfusion). With recent gastroenteritis, bloody diarrhea, one should remember about HUS, especially in children;

Pay attention to the presence of systemic diseases, vascular diseases (possible stenosis of the renal arteries), episodes of fever, the possibility of post-infectious glomerulonephritis;

The presence of arterial hypertension, diabetes mellitus or malignant neoplasms (the likelihood of hypercalcemia);

Increased urge, weakening of the urine stream in men are signs of postrenal obstruction caused by a disease of the prostate gland. Renal colic with nephrolithiasis may be accompanied by a decrease in urine output;

Establish what drugs the patient was taking, whether there were any cases of intolerance to these drugs. Special attention should be paid to the reception: ACE inhibitors, ARB-II, NSAIDs, aminoglycosides, the introduction of X-ray contrast agents. Find out contact with toxic, poisonous substances;

Symptoms of muscle damage (pain, muscle swelling, increased creatine kinase, past myoglobinuria), metabolic disease may indicate rhabdomyolysis;

Information about kidney disease and arterial hypertension and cases of increased creatinine and urea in the past.

The main points required for diagnosis in emergencies with AKI:

Kidney dysfunction: AKI or CKD?

Violation of renal blood flow - arterial or venous.

Is there a disturbance in urine flow due to obstruction?

History of kidney disease, accurate diagnosis?

Physical examination

The main directions for physical examination are as follows:

Assessment of the degree of hydration of the body is of paramount importance to determine the tactics of patient management (thirst, dry skin, mucous membranes, or the presence of edema; loss or weight gain; CVP level; shortness of breath).

Skin color, rashes. Thermometry.

Assessment of the state of the central nervous system

Assessment of the condition of the lungs (edema, wheezing, bleeding, etc.).

Evaluation of the cardiovascular system (hemodynamics, blood pressure, pulse. Pulsation on large vessels). Ocular fundus.

The presence of hepatosplenomegaly, a decrease in the size of the liver.

Palpation can reveal enlarged kidneys with polycystic disease, an enlarged bladder with tumors, and obstruction of the urethra.

Diuresis assessment (oliguria, anuria, polyuria, nocturia).

Initial period: at the onset of the disease, the clinical manifestations of AKI are nonspecific. Symptoms of the underlying disease prevail.

The period of development of oliguria:

Oliguria, anuria;

Peripheral and cavity edema;

Rapidly increasing hyponatremia with nausea, seizures with headache, and disorientation is a precursor to cerebral edema;

Clinical manifestations of azotemia - anorexia, uremic pericarditis, odor of ammonia from the mouth;

Hyperkalemia;

Acute adrenal insufficiency;

Metabolic acidosis, severe alkalosis,

Noncardiogenic pulmonary edema

Respiratory distress syndrome in adults,

Moderate anemia

Profuse gastrointestinal bleeding (in 10-30% of patients, caused by ischemia of the mucous membrane, erosive gastritis, enterocolitis against the background of platelet dysfunction and disseminated intravascular coagulation syndrome),

Activation of opportunistic flora (bacterial or fungal, against the background of uremic immunodeficiency develops in more than 50% of patients with renal AKI. Typical damage to the lungs, urinary tract, characterized by stomatitis, parotitis, infection of surgical wounds);

Generalized infections with septicemia, infective endocarditis, peritonitis, candidasepsis.

Diuresis recovery period:

Normalization of the nitrogen excretory function of the kidneys;

Polyuria (5-8 liters per day);

Dehydration phenomena;

Hyponatremia;

Hypokalemia (risk of arrhythmia);

Hypocalcemia (risk of tetany and bronchospasm).

Laboratory research:

UAC: increased ESR, anemia.

OAM: proteinuria from moderate 0.5 g / day to severe - more than 3.0 g / day, macro / microhematuria, cylindruria, decrease in the relative density of urine

Blood chemistry: hypercreatininemia, decreased GFR, electrolyte disturbances (hyperkalemia, hyponatremia, hypocalcemia).

Blood acid base balance: acidosis, decreased bicarbonate levels.

Differential diagnostic laboratory signs.

Research	Characteristic	Reasons for AKI
Urine	Erythrocyte casts, dysmorphic erythrocytes Proteinuria ≥ 1 g / L	Glomerular diseases Vasculitis TMA
	... Leukocytes, leukocyte casts	Otin
	Proteinuria ≤ 1g / L Low molecular weight proteins Eosinophiluria	Otin Atheroembolic disease
	... Visible hematuria	Post-renal causes Acute GBV Injury
	Hemoglobinuria Myoglobinuria	Diseases with pigmenturia
	... Granular or epithelial casts	OTN Acute GN, vasculitis
Blood	... Anemia	Bleeding, hemolysis CKD
	... Schizocytes, thrombocytopenia	GUS
	... Leukocytosis	Sepsis
Biochemical blood tests	Urea Creatinine Changes in K +, Na +, Ca 2+, PO 4 3-, Cl -, HCO 3 -	AKI, CKD
	... Hypoproteinemia, hypoalbuminemia	Nephrotic syndrome, liver cirrhosis
	... Hyperproteinemia	Multiple myeloma and other paraproteinemia
	... uric acid	Tumor lysis syndrome
	... LDH	GUS
	... Creatine kinase	Injuries and metabolic diseases
Biochemical	... Na +, creatinine for calculating the excreted fraction of Na (FENa)	Prerenal and renal OPP
	... Bens Jones squirrels	Multiple myeloma
Specific immunological studies	... ANA, antibodies to double-stranded DNA	SLE
	... p- and s-ANCA	Small vessel vasculitis
	... anti-GBM antibodies	Anti-GBM nephritis (Goodpasture syndrome)
	... ASL-O titer	Post-streptococcal GN
	... Cryoglobulinemia, sometimes + rheumatoid factor	Cryoglobulinemia (essential or for various diseases)
	... Antiphospholipid antibodies (anticardiolipin antibodies, lupus anticoagulant)	APS syndrome
	... ↓ С 3, ↓ С 4, СН50	SLE, infective endocarditis, shunt nephritis
	... ↓ C 3, CH50	Post-streptococcal GN
	... ↓ C 4, CH50	Essential mixed cryoglobulinemia
	... ↓ C 3, CH50	MPGN type II
	... Procalcitonin test	Sepsis
Urine examination	... NGAL urine	Early diagnosis of AKI

Instrumental research:

... ECG: rhythm and cardiac conduction disturbances.

... Chest X-ray: accumulation of fluid in the pleural cavities, pulmonary edema.

... Angiography: to exclude vascular causes of AKI (stenosis of the renal artery, dissecting aneurysm of the abdominal aorta, ascending thrombosis of the inferior vena cava).

... Ultrasound of the kidneys, abdominal cavity: an increase in the volume of the kidneys, the presence of calculi in the renal pelvis or urinary tract, the diagnosis of various tumors.

... Radioisotope kidney scan: assessment of renal perfusion, diagnosis of obstructive pathology.

... Computer and magnetic resonance imaging.

... Kidney biopsy according to indications: used for AKI in difficult diagnostic cases, indicated for renal AKI of unclear etiology, AKI with a prolonged more than 4 weeks period of anuria, AKI associated with nephrotic syndrome, acute nephritic syndrome, diffuse lung lesions of the type of necrotizing vasculitis.

Indications for specialist consultation:

Consultation with a rheumatologist - when new symptoms or signs of a systemic disease appear;

Hematologist's consultation - to exclude blood diseases;

Consultation with a toxicologist - in case of poisoning;

Consultation with a resuscitator - postoperative complications, AKI due to shock, emergency conditions;

Consultation with an otolaryngologist - to identify the focus of infection with subsequent sanitation;

Consultation with a surgeon - if a surgical pathology is suspected;

Urologist's consultation - in the diagnosis and treatment of postrenal AKI;

Traumatologist's consultation - in case of injuries;

Dentist consultation - to identify foci of chronic infection with subsequent sanitation;

Obstetrician-gynecologist's consultation - for pregnant women; with suspicion of gynecological pathology; in order to identify foci of infection, and their subsequent sanitation;

Ophthalmologist consultation - to assess fundus changes;

Consultation with a cardiologist - in case of severe arterial hypertension, ECG abnormalities;

Consultation with a neurologist - in the presence of neurological symptoms;

Consultation of an infectious disease specialist - in the presence of viral hepatitis, zoonotic and other infections

Consultation with a psychotherapist is a mandatory consultation of patients in consciousness, since the patient's "attachment" to the artificial kidney apparatus and the fear of "dependence" on it can negatively affect the patient's mental state and lead to a deliberate refusal of treatment.

Consultation with a clinical pharmacologist - for adjusting the dosage and combination of drugs, taking into account creatinine clearance, when prescribing drugs with a narrow therapeutic index.

Differential diagnosis

Differential diagnosis

In case of violations corresponding to stages 2-3 of AKI, it is necessary to exclude CKD, and then specify the form. Morphology and etiology of AKI.

Differential diagnosis of AKI and CKD .

Signs	OPP	CKD
Diuresis	Oligo-, anuria → polyuria	Polyuria → Anuria
Urine	Plain, bloody	Colorless
Arterial hypertension	In 30% of cases, without LVH and retinopathy	in 95% of cases with LVH and retinopathy
Peripheral edema	often	Not typical
Kidney size (ultrasound)	normal	Reduced
Increase in creatinine	More than 0.5 mg / dl / day	0.3-0.5 mg / dl / day
Renal history	absent	Often perennial

Differential diagnosis of AKI, AKI for CKD and CKD.

Signs	OPP	AKI for CKD	CKD
History of renal disease	No or short	Long	Long
Blood creatinine before AKI	Normal	Promoted	Promoted
Blood creatinine in the presence of AKI	Promoted	Significantly increased	Promoted
Polyuria	rarely	No	Almost always
History of polyuria before AKI	No	Long	Long
AG	rarely	Often	Often
SD	rarely	Often	Often
History of nocturia	No	There is	There is
Causing factor (shock, trauma ..)	Often	Often	Rarely
Acute increase in creatinine> 44 μmol / L	always	always	Never
Kidney size ultrasound	Normal or enlarged	Normal or reduced	Reduced

To confirm the diagnosis of AKI, first of all, its postrenal form is excluded. To detect obstruction (upper urinary tract, infravesical) at the first stage of the examination, ultrasound and dynamic nephroscintigraphy are used. In the hospital, chromocystoscopy, digital intravenous urography, CT and MRI, antegrade pyelography are used to verify obstruction. For the diagnosis of renal artery occlusion, USG, renal radiopaque angiography are shown.

Differential diagnosis of prerenal and renal AKI .

Indicators	OPP
	prerenal	Renal
Relative density of urine	> 1020	< 1010
Osmolarity of urine (mosm / kg)	> 500	< 350
The ratio of urine osmolarity to plasma osmolarity	> 1,5	< 1,1
Urine sodium concentration (mmol / l)	< 20	> 40
Excreted fraction Na (FE Na) 1	< 1	> 2
Plasma urea / creatinine ratio	> 10	< 15
The ratio of urine urea to plasma urea	> 8	< 3
The ratio of urine creatinine to plasma creatinine	> 40	< 20
Renal failure index 2	< 1	> 1

1 * (Na + urine / Na + plasma) / (urine creatinine / plasma creatinine) x 100

2 * (Na + urine / urine creatinine) / (plasma creatinine) x 100

It is also necessary to exclude the causes of false oliguria, anuria.

High extrarenal losses	Decreased fluid intake	Exiting urine through unnatural pathways
Hot climate Fever Diarrhea Gastrostomy Mechanical ventilation	Psychogenic oligodipsia Water scarcity Tumors of the esophagus Rumination Achalasia of the esophagus Esophageal strictures Nausea iatrogenic	Cloaca (urinary-rectal fistula) Urinary tract injury Urine leakage with nephrostomy

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Treatment

Treatment goals:

Withdrawal from an acute condition (elimination of shock, stabilization of hemodynamics, restoration of heart rate, etc.);

Restoration of diuresis;

Elimination of azotemia, dyselectrolythemia;

Correction of the acid-base state;

Relief of edema, seizures;

Blood pressure normalization;

Prevention of the formation of CKD, transformation of AKI into CKD.

Treatment tactics:

Treatment is divided into conservative (etiological, pathogenetic, symptomatic), surgical (urological, vascular) and active - renal replacement therapy - dialysis methods (RRT).

Principles of AKI treatment

OPP form	Treatment	Treatment methods
Prerenal	Conservative	Infusion and anti-shock therapy
Acute urate nephropathy	Conservative	Infusion alkalizing therapy, allopurinol,
RPGN, allergic ATIN	Conservative	Immunosuppressive therapy, plasmapheresis
Post-renal	Surgical (urological)	Elimination of acute urinary tract obstruction
UPS	Surgical	Renal artery angioplasty
AIO, myorenal syndrome, PON	Active (dialysis)	Acute HD, hemodiafiltration (HDF), acute PD

The use of dialysis techniques in different stages of AKI(indicative diagram)

Manifestations and stages of renal AKI	Treatment and prevention methods
Preclinical stage with exonephrotoxin identification	Intermittent GF, PGF, PA, GS
Early hyperkalemia (rhabdomyolysis, hemolysis) Early decompensated acidosis (methanol) Hypervolemic overhydration (diabetes) Hypercalcemia (vitamin D poisoning, multiple myeloma)	Intermittent GF PGF Intermittent ultrafiltration Intermittent HD, acute PD
OPP	Intermittent HD, acute PD, PHF
OPPN	Plasma sorption, hemofiltration, hemodiafiltration, Albumin dialysis

Non-drug treatment

Mode bed for the first day, then ward, general.

Diet: restriction of table salt (mainly sodium) and liquid (the volume of liquid obtained is calculated taking into account the urine output for the previous day + 300 ml) with sufficient calorie intake and the content of vitamins. In the presence of edema, especially during the period of their growth, the content of table salt in food is limited to 0.2-0.3 g per day, the protein content in the daily diet is limited to 0.5-0.6 g / kg of body weight, mainly for account of proteins of animal origin.

Drug treatment

Outpatient drug treatment

(having a 100% chance of being applied:

In the prehospital stage, without specifying the reasons that led to AKI, it is impossible to prescribe this or that drug.

(less than 100% likely to be used)

Furosemide 40 mg 1 tablet in the morning, under the control of urine output 2-3 times a week;

Adsorbix 1 capsules x 3 times a day - under the control of creatinine levels.

Inpatient drug treatment

Essential Medicines List(having a 100% chance of being applied):

Potassium antagonist - calcium gluconate or chloride 10% 20 ml IV for 2-3 minutes No. 1 (in the absence of changes in the ECG, repeated administration at the same dose, in the absence of effect - hemodialysis);

20% glucose 500 ml + 50 IU of soluble human short-acting insulin intravenous cap 15-30 U every 3 hours 1-3 days, until the level of potassium in the blood is normalized;

Sodium bicarbonate 4-5% w / w cap. Dose calculation according to the formula: X = BE * weight (kg) / 2;

Sodium bicarbonate 8.4% w / w cap Dose calculation according to the formula: X = BE * 0.3 * weight (kg);

Sodium chloride 0.9% intravenous drip 500 ml or 10% 20 ml intravenously 1-2 times a day - until the BCC deficiency is replenished;

Furosemide 200-400 mg IV through a perfuser, under the control of hourly urine output;

Dopamine 3 μg / kg / min IV cap for 6-24 hours, under the control of blood pressure, heart rate -2-3 days;

Adsorbix 1 capsule x 3 times a day - under the control of creatinine levels.

List of additional medicines(less than 100% likelihood of use):

Norepinephrine, mesoton, refortan, infesol, albumin, colloidal and crystalloid solutions, fresh frozen plasma, antibiotics, blood transfusion drugs, and others;

Methylprednisolone, tablets 4mg, 16mg, powder for solution for injection complete with solvent 250mg, 500mg;

Cyclophosphamide powder for solution for intravenous administration 200 mg;

Torasemide tablets 5, 10, 20mg;

Rituximab, 100 mg, 500 mg IV bottle;

Normal human immunoglobulin, 10% solution for infusion, 100 ml.

Medical treatment provided at the stage of emergency emergency care:

Relief of pulmonary edema, hypertensive crisis, convulsive syndrome.

Other treatments

Dialysis therapy

If RRT is required for AKI, the patient is dialyzed for 2 to 6 weeks until renal function is restored.

When treating AKI patients who require renal replacement therapy, the following questions should be answered:

When is the best time to start treatment with RRT?

What type of RRT should you use?

Which access is better?

What level of clearance of soluble substances should be observed?

Initiation of RRT

Absolute indications for sessions of substitution therapy with AKI are:

Increasing level of azotemia and impaired diuresis according to the recommendations of RIFLE, AKIN, KDIGO.

Clinical manifestations of uremic intoxication: asterixis, pericardial effusion, or encephalopathy.

Uncorrectable metabolic acidosis (pH<7,1, дефицит оснований -20 и более ммоль/л, НСОЗ<10 ммоль/л).

Hyperkalemia> 6.5 mmol / L and / or marked changes on the ECG (bradyarrhythmia, rhythm dissociation, severe deceleration of electrical conduction).

Hyperhydration (anasarca), resistant to drug therapy (diuretics).

Relative indications for sessions of substitution therapy include a sharp and progressive increase in the level of urea nitrogen and blood creatinine without obvious signs of convalescence, when there is a real threat of the development of clinical manifestations of uremic intoxication.

Indications for Renal Support methods of substitution therapy are: providing adequate nutrition, removing fluid in congestive heart failure, and maintaining an adequate hydrobalance in a patient with multiple organ failure.

By the duration of therapy there are the following types of OST:

Intermittent (intermittent) RRT techniques lasting no more than 8 hours with a break longer than the duration of the next session (on average 4 hours) (see MES stationary hemodialysis)

Extended methods of RRT (CRRT), designed to replace kidney function for a long time (24 hours or more). CRPT are conditionally divided into:

Semi-extended 8-12 hours (see MES semi-extended hemo (dia) filtration)

Extended 12-24 hours (see MES extended hemo (dia) filtration)

Permanent for more than a day (see MES permanent hemo (dia) filtration)

CRRT selection criteria:

1) Renal:

AKI / MOI in patients with severe cardiorespiratory failure (AMI, high-dose inotropic support, recurrent interstitial pulmonary edema, acute pulmonary injury)

AKI / PON against the background of high hypercatabolism (sepsis, pancreatitis, mesenteric thrombosis, etc.)

2) Extrarenal indications for CRRT

Volume overload, providing fluid therapy

Septic shock

ARDS or risk of ARDS

Severe pancreatitis

Massive rhabdomyolysis, burn disease

Hyperosmolar coma, preeclampsia of pregnancy

RRT methods:

Hemodialysis intermittent and prolonged

Slow low-flow hemodialysis (SLED) in the treatment of AKI is the ability to control the patient's hydrobalance without hemodynamic fluctuations in a shorter period of time (6-8 hours - 16-24 hours).

Prolonged veno-venous hemofiltration (PHF),

Extended veno-venous hemodiafiltration (PVVHDF).

According to the recommendations of KDIGO (2012), in CRRT, it is suggested to use, unlike IHD, regional anticoagulation with citrate instead of heparin (if there are no contraindications). This type of anticoagulation is very useful in patients with heparin-induced thrombocytopenia and / or at high risk of bleeding (disseminated intravascular coagulation syndrome, coagulopathy) when systemic anticoagulation is absolutely contraindicated.

Continuous veno-venous hemofiltration (PHF) is an extracorporeal circuit with a blood pump, high-flow or high-porosity dialyzer, and replacement fluid.

Continued veno-venous hemodiafiltration (PVVHDF) is an extracorporeal circuit with a blood pump, high-flow or highly porous dialyzer, as well as replacement and dialysis fluids.

Recent evidence suggests the use of bicarbonate (not lactate) as a buffer in dialysate and replacement fluid for RRT in patients with AKI, especially in patients with AKI and circulatory shock, also with hepatic impairment and / or lactate acidosis.

Table 8.

Stable

Unstable

IGD

CRPT

Severe hyperphosphatemia Stable / unstable CRPT Cerebral edema Unstable CRPT

When AKI is used as an alternative peritoneal dialysis (PD)... The technique of the procedure is quite simple and does not require highly qualified personnel. It can also be used in situations where it is not possible to conduct a DGD or CRRT. PD is indicated for patients with minimal increased catabolism, provided that the patient does not have a life-threatening indication for dialysis. It is ideal for patients with unstable hemodynamics. For short-term dialysis, a rigid dialysis catheter is inserted into the abdominal cavity through the anterior abdominal wall at a level of 5-10 cm below the navel. Exchange infusion is carried out into the abdominal cavity of 1.5-2.0 liters of standard peritoneal dialysis solution. Possible complications include bowel perforation during catheter insertion and peritonitis.

Acute PD offers a number of pediatric benefits that CRRT provides to adult AKI patients. (see Protocol "Peritoneal dialysis").

In case of toxic AKI, sepsis, liver failure with hyperbilirubinemia, it is recommended to carry out plasma exchange, hemosorption, plasma adsorption using a specific sorbent.

Surgical intervention:

Installation of vascular access;

Conducting extracorporeal treatment methods;

Elimination of urinary tract obstruction.

Therapy for postrenal acute renal injury

Treatment of postrenal AKI usually requires the involvement of a urologist. The main task of therapy is to eliminate the violation of the outflow of urine as soon as possible in order to avoid irreversible damage to the kidney. For example, in case of obstruction due to prostatic hypertrophy, the introduction of a Foley catheter is effective. You may need alpha-blocker therapy or surgical removal of the prostate gland. If the urinary obstruction is at the level of the urethra or bladder neck, a transurethral catheter is usually sufficient. At a higher level of urinary tract obstruction, a percutaneous nephrostomy is required. These measures usually lead to a complete restoration of diuresis, a decrease in intratubular pressure and restoration of glomerular filtration.

If the patient does not have CKD, it should be borne in mind that the patient is at increased risk of developing CKD and should be managed in accordance with the KDOQI Practice Guidelines. ”

Patients at risk of developing AKI (AKI) should be monitored closely with creatinine and urine volume. Patients are recommended to be divided into groups according to the degree of risk of developing AKI. Their maintenance depends on the predisposing factors. First of all, patients should be examined to identify reversible causes of AKI, which will immediately eliminate these factors (for example, postrenal).

At the outpatient stage after discharge from the hospital: compliance with the regimen (elimination of hypothermia, stress, physical overload), diet; completion of treatment (sanitation of foci of infection, antihypertensive therapy) dispensary observation for 5 years (in the first year - measurement of blood pressure on a quarterly basis, blood and urine tests, determination of serum creatinine content and calculation of GFR by creatinine - Cockcroft-Gault formula). If extrarenal signs persist for more than 1 month (arterial hypertension, edema), severe urinary syndrome or their aggravation, a kidney biopsy is necessary, since unfavorable morphological variants of GN, requiring immunosuppressive therapy, are likely.

Clinic of the republican level (diagnosed AKI on admission or SPON in diagnostic "difficult" patients, or as a complication of RCT, postoperative, etc.)

The use of prolonged hemofiltration, hemodiafiltration, hemodialysis. Plasma exchange, plasma sorption - according to indications.

Stabilization of the state, abolition of vasopressors, stabilization of the level of urea, creatinine, acid-base and water-electrolyte balances.

With persisting anuria, edema, moderate azotemia, transfer to a regional or city level hospital, with the presence of an artificial kidney apparatus in the clinic (not only simple dialysis machines, but also devices for prolonged replacement therapy with the function of hemofiltration, hemodiafiltration).

Monitoring and RRT regimens in patients with AKI should be carried out separately from patients with ESRD (CKD stage 5) who are on programmed dialysis.

Short-acting human insulin Calcium gluconate Calcium chloride Methylprednisolone (Methylprednisolone) Sodium hydrocarbonate Sodium chloride Norepinephrine Plasma, fresh frozen Rituximab Torasemide Phenylephrine Furosemide (Furosemide) Cyclophosphamide (Cyclophosphamide)

Groups of drugs according to ATC used in treatment

Hospitalization

Indications for hospitalization

Special risk groups of patients on the development of PPE:

Information

Sources and Literature

1. Minutes of the meetings of the Expert Council of the RCHRH MHSD RK, 2014
   1. 1) Acute renal injury. Tutorial. A.B.Kanatbaeva, K.A.Kabulbaev, E.A. Karibaev. Almaty 2012.2) Bellomo, Rinaldo, et al. "Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group." Critical care 8.4 (2004): R204. 3) KDIGO, AKI. "Work Group: KDIGO clinical practice guideline for acute kidney injury." Kidney Int Suppl 2.1 (2012): 1-138. 4) Lewington, Andrew, and Suren Kanagasundaram. "Renal association clinical practice guidelines on acute kidney injury." Nephron Clinical Practice 118.Suppl. 1 (2011): c349-c390. 5) Cerdá, Jorge, and Claudio Ronco. "THE CLINICAL APPLICATION OF CRRT-CURRENT STATUS: Modalities of Continuous Renal Replacement Therapy: Technical and Clinical Considerations." Seminars in dialysis. Vol. 22. No. 2. Blackwell Publishing Ltd, 2009. 6) Chionh, Chang Yin, et al. "Acute peritoneal dialysis: what is the‘ adequate’dose for acute kidney injury ?. ” Nephrology Dialysis Transplantation (2010): gfq178.

Information

III. ORGANIZATIONAL ASPECTS OF THE PROTOCOL IMPLEMENTATION

List of protocol developers:

1) Tuganbekova Saltanat Kenesovna - Doctor of Medical Sciences, Professor of JSC National Scientific Medical Center, Deputy General Director for Science, Chief Freelance Nephrologist of the Ministry of Health and Social Development of the Republic of Kazakhstan;

2) Kabulbaev Kairat Abdullaevich - Doctor of Medical Sciences, Professor of the RSE at the REM “Kazakh National Medical University named after S.D. Asfendiyarova ", head of the nephrology module;

3) Gaipov Abduzhappar Erkinovich - Candidate of Medical Sciences, JSC National Scientific Medical Center, head of the department of extracorporeal hemocorrection, nephrologist;

4) Nogaybaeva Asem Tolegenovna - JSC "National Scientific Cardiac Surgery Center", nephrologist of the department of the laboratory of extracorporeal hemocorrection;

5) Zhusupova Gulnar Darigerovna - Candidate of Medical Sciences of JSC "Astana Medical University", clinical pharmacologist, assistant of the Department of General and Clinical Pharmacology.

No Conflict of Interest Statement: absent.

Reviewers:
Sultanova Bagdat Gazizovna - Doctor of Medical Sciences, Professor of JSC Kazakh Medical University of Continuing Education, Head of the Department of Nephrology and Hemodialysis.

Indication of the conditions for revision of the protocol: revision of the protocol after 3 years and / or when new diagnostic / treatment methods with a higher level of evidence appear.

Attached files

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Acute renal failure (ARF) is a rapid, but reversible, depression of renal function, sometimes to the stage of complete failure of one or both organs. Pathology is deservedly characterized as a critical condition that requires immediate medical intervention. Otherwise, the risk of an unfavorable outcome in the form of loss of organ performance increases dramatically.

Acute renal failure

The kidneys are the main "filters" of the human body, the nephrons of which continuously pass blood through their membranes, removing excess fluid and toxins with urine, sending the necessary substances back into the bloodstream.

Kidneys are organs without which human life is impossible. Therefore, in a situation where, under the influence of provoking factors, they cease to perform their functional task, doctors provide emergency medical assistance to a person, diagnosing him with acute renal failure. The code of somatic pathology according to ICD-10 is N17.

Today, statistical information makes it clear that the number of people facing this pathology is growing every year.

Etiology

The causes of djpybryjdtybz acute renal failure are as follows:

1. Pathologies of the cardiovascular system that disrupt the process of blood supply to all organs, including the kidneys:
   • arrhythmia;
   • atherosclerosis;
   • heart failure.
2. Dehydration against the background of the following ailments, which is the cause of changes in blood counts, or rather, an increase in its prothrombin index, and, as a result, difficult work of the glomeruli:
   • dyspeptic syndrome;
   • extensive burns;
   • blood loss.
3. Anaphylactic shock, which is accompanied by a sharp drop in blood pressure, which negatively affects the functioning of the kidneys.
4. Acute inflammation in the kidney that leads to tissue damage in organs:
   • pyelonephritis.
5. A physical obstruction to the outflow of urine in urolithiasis, which first leads to hydronephrosis, and then, due to pressure on the kidney tissue, damage to their tissues.
6. Taking nephrotoxic drugs, which include a contrast composition for conducting an X-ray, becomes the cause of poisoning in the body, which the kidneys cannot cope with.

Arrester classification

The process of acute kidney failure is divided into three types:

1. Prerenal ARF - the cause of the disease is not directly related to the kidneys. The most popular example of the prerenal type of acute renal failure can be called cardiac abnormalities, because the pathology is often called hemodynamic. Less commonly, it occurs against the background of dehydration.
2. Renal acute renal failure - the root cause of the pathology can be found in the kidneys themselves, and therefore the second name of the category is parenchymal. Renal functional failure in most cases results from acute glomerulonephritis.
3. Postrenal ARF (obstructive) is a form that occurs when the pathways for urine excretion are blocked by calculi and the subsequent violation of the outflow of urine.

Classification of acute renal failure

Pathogenesis

ARF develops over four periods, which always follow in the indicated order:

• initial stage;
• oliguric stage;
• polyuric stage;
• recovery.

The duration of the first stage can last from several hours to several days, depending on what is the root cause of the disease.

Oliguria is a term that briefly denotes a decrease in the volume of urine. Normally, a person should excrete approximately the amount of liquid that he consumed, minus the part “spent” by the body on sweating and breathing. With oliguria, the volume of urine becomes less than half a liter, out of direct relation to the amount of fluid drunk, which entails an increase in fluid and decay products in the tissues of the body.

The complete disappearance of diuresis - occurs only in extremely severe cases. And it rarely happens statistically.

The duration of the first stage depends on how quickly adequate treatment was started.

Polyuria, on the contrary, means an increase in urine output, in other words, the amount of urine can reach five liters, although 2 liters of urine per day is already a reason for diagnosing polyuric syndrome. This stage lasts about 10 days, and its main danger is the loss by the body of the substances it needs along with urine, as well as dehydration.

After the completion of the polyuric stage, a person, with a favorable development of the situation, recovers. However, it is important to know that this period can drag on for one year, during which deviations in the interpretation of analyzes will be revealed.

Arrester stages

Clinical picture

The initial stage of acute renal failure does not have specific symptoms by which it was possible to accurately recognize the ailment, the main complaints during this period are:

• loss of strength;
• headache.

The symptomatic picture is complemented by signs of the pathology that caused acute renal failure:

1. With oliguric syndrome against the background of acute renal failure, the symptoms become specific, easily recognizable and fit into the overall picture of pathology:
   • decrease in urine output;
   • dark, frothy urine;
   • dyspepsia;
   • lethargy;
   • wheezing in the chest due to fluid in the lungs;
   • susceptibility to infections due to reduced immunity.
2. The polyuric (diuretic) stage is characterized by an increase in the amount of urine excreted, therefore, all the patient's complaints follow from this fact, and the fact that with urine the body loses a large amount of potassium and sodium:
   • violations in the work of the heart are recorded;
   • hypotension.
3. The recovery period, which takes from 6 months to one year, is characterized by fatigue, changes in the results of laboratory tests of urine (specific gravity, erythrocytes, protein), blood (total protein, hemoglobin, ESR, urea,).

Diagnostics

Arrester diagnostics is carried out using:

• questioning and examining the patient, makes up his anamnesis;
• a clinical blood test showing low hemoglobin;
• biochemical blood test, which detects increased creatinine, potassium, urea;
• monitoring diuresis, that is, control over how much liquid (including soups, fruits) a person consumes in 24 hours, and how much he excretes;
• ultrasound method, with ARF more often showing the physiological size of the kidneys, a decrease in size indicators is a bad sign, indicating tissue damage that can be irreversible;
• nephrobiopsym - taking a piece of an organ using a long needle for microscopic examination; it is carried out infrequently due to the high degree of trauma.

Treatment

ARF therapy occurs in the intensive care unit of the hospital, less often in the nephrology unit of the hospital.

All medical manipulations carried out by a doctor and medical staff can be divided into two stages:

1. Revealing the root cause of the pathological condition is carried out using diagnostic methods, studying the symptoms, specific complaints of the patient.
2. Elimination of the cause of acute renal failure is the most important stage of treatment, because without treatment of the root cause of the disease, any therapy measures will be ineffective:
   • when detecting the negative effect of nephrotoxins on the kidneys, extracorporeal hemocorrection is used;
   • when an autoimmune factor is detected, glucocorticosteroids (Prednisolone, Metipred, Prenizol) and plasmapheresis are prescribed.
   • with urolithiasis, medical litholysis or surgery is performed to remove calculi;
   • antibiotics are prescribed for infection.

At each stage, the doctor adjusts the appointment, based on the symptomatic picture at the moment.

During oliguria, it is necessary to prescribe diuretics, a strict diet with a minimum amount of protein and potassium, if necessary, hemodialysis.

Hemodialysis - a procedure for cleansing the blood from decay products and removing excess fluid from the body, has an ambiguous attitude of nephrologists. Some doctors argue that preventive hemodialysis for acute renal failure is necessary in order to reduce the risk of complications. Other experts warn of the tendency of complete loss of kidney function since the start of artificial blood purification.

During the period of polyuria, it is important to replenish the patient's lack of blood volume, restore the electrolyte balance in the body, continue diet No. 4, and guard against any infection, especially when taking hormonal drugs.

General principles of ARF treatment

Predictions and complications

ARF against the background of proper treatment has a favorable prognosis: after suffering an illness, only 2% of patients need lifelong hemodialysis.

Complications from acute kidney failure are associated with, that is, with the process of poisoning the body with its own decay products. As a result, the latter are not excreted by the kidneys with oliguria or with a low rate of blood filtration by glomeruli.

Pathology leads to:

• violation of cardiovascular activity;
• anemia;
• increased risk of infections;
• neurological disorders;
• dyspeptic disorders;
• uremic coma.

It is important to note that in acute nephrological failure, in contrast to chronic, complications rarely occur.

Prophylaxis

ARF prevention is as follows:

1. Avoid taking nephrotoxic medications.
2. Timely treat chronic ailments of the urinary and vascular system.
3. Monitor blood pressure indicators, if signs of chronic hypertension are detected, immediately consult a specialist.

In the video about the causes, symptoms and treatment of acute renal failure:

Causes of the disease

Acute renal failure is divided into prerenal, caused by general circulation disorders (shock), renal, caused by damage to the renal parenchyma, and postrenal, caused by impaired urination (urinary tract stricture).

Prerenal causes of acute renal failure include shock states of various etiologies and various disorders of water and electrolyte metabolism (profuse diarrhea, vomiting, etc.). Renal causes of acute renal failure include nephrotic effects (mercuric chloride, lead, carbon tetrachloride, etc.), toxic-allergic reactions (antibiotics, radiopaque substances), primary kidney disease (glomerulonephritis, pyelonephritis, etc.). Postrenal causes include blockage of the ureters (stone, tumor), acute urinary retention (prostate adenoma, stone or bladder tumor).

Relatively rare causes of arresters include the following:

- exposure to toxic substances (antifreeze, gasoline, hydroquinone, glycerin, alcohol and its surrogates, freon, Lokon liquid, Crystal lotion, BF glue, carbon tetrachloride, ursol, pesticides);

- taking a number of drugs - antibiotics (penicillin, morphocyclin, gentamicin, brulomycin, chloramphenicol, rifampicin, etc.), sulfonamides, nitrofurans, salicylates, pyrazolone derivatives, dextrans, barbirurates, anesthetics, ganglionic blockers, diuretics, diuretics , hypoglycemic agents, quinine, indirect anticoagulants, preparations containing salts of heavy metals, antineoplastic agents, etc.;

- kidney diseases: acute, subacute and exacerbation of chronic pyelonephritis, amyloidosis, collagen nephropathies, hemorrhagic fever with renal syndrome, nephropathy of pregnant women, thrombosis and embolism of renal vessels;

- diseases of internal organs: dissecting aortic aneurysm, tuberculous aortitis, pulmonary embolism, pancreatitis, toxic hepatitis, salmonellosis;

- blood diseases and malignant tumors: leukemia, thrombocytopenic purpura, hemolytic anemia, multiple myeloma, lymphosarcomatosis, sarcoidosis, metastases of malignant tumors;

- poisoning with poisons of animal and plant origin: snake, mushroom and bee, intoxication with helminthic invasion;

- the consequences of diagnostic and therapeutic measures: X-ray contrast studies, kidney biopsy, electroshock therapy, perirenal blockade, starvation treatment, hyperbaric therapy, the use of radioactive drugs;

- myorenal syndrome: high voltage shock, carbon monoxide poisoning, positional compression syndrome, non-traumatic myoglobinuria;

- diseases of the central nervous system: TBI, tumor, meningitis, viral encephalitis, psychotrauma;

- malaria, foreign body of the bladder, alcohol withdrawal.

Mechanisms of the onset and development of the disease (pathogenesis)

ARF is characterized by a sudden and prolonged decrease in the glomerular filtration rate, leading to the accumulation of urea and other chemicals in the blood.

The reason for the development of prerenal ARF is a decrease in renal blood flow resulting from damage to the renal artery, systemic arterial hypotension, or redistribution of blood flow in the body. Intrarenal ARF occurs when the renal parenchyma is affected (against the background of acute renal tubular necrosis, interstitial nephritis, renal artery embolism, glomerulonephritis, vasculitis, or small vessel disease). Postrenal ARF develops due to obstruction of the urinary tract. In most critically ill patients, ARF is prerenal, but in such cases ARF is usually only a component of multiple organ or polysystemic failure, and renal tubular necrosis is due to ischemic and / or toxic renal damage.

Prerenal ARF is characterized by a urea to creatinine ratio of more than 20: 1, urine osmolarity of more than 500 mOsm / L, fractional sodium excretion of less than 1%, and no or minor urinary syndrome; conversely, in the presence of renal ARF, the urea to creatinine ratio does not exceed 20: 1. urine osmolality is in the range of 250-300 mosmol / l, fractional sodium excretion is more than 3% in the presence of urinary syndrome.

The following phases of acute renal failure are distinguished:

1) initial (signs of the pathological process that caused acute renal failure dominate: shock, infection, sepsis, hemolysis, intoxication, disseminated intravascular coagulation);

2) oliguria and anuria, impaired concentration and nitrogen excretion function of the kidneys, symptoms of uremia;

3) the phase of early polyuria;

4) restoration of kidney function.

The clinical picture of the disease (symptoms and syndromes)

Criteria for the diagnosis of acute renal failure: oligoanuria, decreased glomerular filtration rate (GFR), relative urine density (osmolality), increased concentration of creatinine, urea, serum potassium, acid-base imbalance, anemia, hypertension.

Oliguria is characterized by a decrease in urine output to 500 ml / day (less than 300 ml / m 2 / day) with a physiological fluid intake or 10-12 ml / kg / day.

Anuria is the presence of urine less than 150 ml / day (60 ml / m2 / day) or 2-3 ml / kg of the patient's weight.

Violation of nitrogen excretory function is documented in the presence of a simultaneous increase in blood creatinine (CC) more than 0.125 mmol / L and urea - more than 10 mmol / L or a decrease in GFR less than 90 ml / min. Decrease in relative density less than 1018, hemoglobin less than 110 g / l, BE less than 2 (indicator indicates an excess or deficiency of alkalis (norm - 2.0 mol / l)), blood pH less than 7.32, increase in potassium over 5.5 mmol / L and blood pressure (BP) more than 140/90 mm Hg. indicate impaired renal function.

The principal in acute renal failure is the degree of renal dysfunction and the duration of this condition. Therefore, in practice, a distinction is made between functional and organic arresters. Functional ARF is a temporary impairment of certain renal functions that reverses during conservative therapy. Organic ARF does not reverse development without the use of extracorporeal methods of treatment and is characterized by a wider spectrum of impairment of various renal functions.

It should be noted that the absence of restoration of independent diuresis for more than 3 weeks with acute renal failure indicates the development of chronic renal failure (CRF).

The surge arrester is subdivided into four stages : initial ( shock) - lasting from several hours to 3 days, oligoanuric- from 2-3 weeks to 72 days, restoration of urine output ( polyuric) - up to 20-75 days, convalescence- from several months to 1-2 years.

Clinical signs initial stage ARF is completely leveled by the symptoms of the main aggressive factor (shock, intestinal obstruction, exogenous poisoning, etc.). This stage, regardless of the initial cause, is characterized by general hemodynamic disorders and impaired microcirculation. ARF symptoms go unnoticed due to the severity of the underlying disease.

V oligoanuric stage a progressive decrease in diuresis begins, up to the development of anuria. However, even at this stage, its onset may remain unnoticed, because after the correction of hemodynamics, the patient's well-being may slightly improve and a period of imaginary well-being begins (up to 3-5 days), which further complicates the timely diagnosis of acute renal failure. Only then does the detailed picture of the surge arrester appear. During this period, along with a decrease in urine output and a decrease in the relative density of urine (up to 1007-1010), the presence of a pathological sediment in it, a sharp deterioration occurs: drowsiness, headache, abdominal pain, constipation, followed by diarrhea. The skin is grayish-pale in color with an icteric tinge, the skin is dry, with hemorrhagic rashes and bruising, especially if the patient has concomitant liver failure. An increase in the size of the liver and spleen, a violation of water metabolism in this stage of acute renal failure are manifested by symptoms of extracellular (the appearance of edema of the subcutaneous base, and subsequently cavity - ascites, hydrothorax, blood thinning, increased blood pressure), and then cellular overhydration (mental and physical asthenia, nausea , vomiting after meals, headache, mental disorders, seizures, cerebral edema and coma). With hyperhydration, shortness of breath and a clinic of pulmonary edema develop. Shortness of breath is caused not only by pulmonary edema, but also by anemization, acidosis and myocardial damage. Signs of myocarditis are noted: deafness of heart sounds, systolic murmur, gallop rhythm, congestive heart failure, arrhythmias and cardiac conduction disturbances. In the occurrence of arrhythmia, not only myocarditis is important, but also hyperkalemia, usually accompanying acute renal failure during this period. With an increase in the level of potassium above 7 mmol / L, bradycardia develops, high-amplitude T waves appear, depression of the ST segment, widening of the initial part of the ventricular complex and flattening of the P waves. In the case when ARF develops due to loss of water and electrolytes (pyloric stenosis, diarrhea) or with excessive administration of sodium chloride, extracellular (hypovolemia, decreased skin turgor and blood pressure, dry mucous membranes in the absence of thirst, nausea, vomiting), and then cellular dehydration (indomitable thirst, weight loss, increased body temperature, stupor, alternating excitement, hallucinations). However, symptoms of dehydration in acute renal failure during this period are relatively rare. Violation of nitrogen metabolism is manifested by an increase in the level of urea in the blood to 119-159 mmol / l, creatinine - up to 0.3-0.5 mmol / l. Electrolyte metabolism is disturbed: an increase in the level of potassium up to 6.5 mmol / l, magnesium - up to 1.9-2.1 mmol / l. Hyponatremia, hypocalcemia, hyperphosphatemia, hypersulfatemia are noted. All these disorders determine the clinic of uremic intoxication.

In stage restoration of urine output there is a gradual increase in it to 2-3 liters per day with a low relative density of urine (1001-1002), an improvement in the general condition, a decrease in azotemic intoxication. During this period, the development of dehydration, hypokalemia, hypomagnesemia and hypochloremia is possible, which aggravates the patient's condition and requires appropriate correction.

Recovery stage , if it occurs, is characterized by the normalization of renal function, the reverse development of dystrophic changes in internal organs and the restoration of the patient's working capacity.

Despite the absence of generally accepted biochemical criteria for acute renal failure, in most studies this diagnosis is made at a serum creatinine level of 2-3 mg / dL (200-500 mmol / L), an increase in this indicator by 0.5 mg / dL (by 45 mmol / l) at the initial value<2 мг/дл (<170 ммоль/л) или при повышении уровня креатинина по сравнению с исходным в 2 раза. Тяжелая ОПН характеризуется уровнем креатинина в сыворотке крови >5.5 mg / dL (500 mmol / L) or the need for hemodialysis.

Diagnosis of the disease

Patients undergo: Clinical analysis of urine, biochemical blood test (determination of urea, blood creatinine, creatinine clearance, blood electrolytes (K +, Na +), blood pH. Ultrasound of the kidneys.

Treatment of the disease

Treatment of acute renal failure in oligoanuric and subsequent stages should be carried out in intensive care units or renal centers, where it is possible to control and correct water and electrolyte metabolism, CBS, nitrogen balance and other parameters of acute renal failure, as well as hemodialysis, which can significantly improve the prognosis in severe disease. For a prehospital physician, forecasting, diagnostics, prevention and treatment of acute renal failure in the initial (shock) period are relevant. The fate of the patient largely depends on the timeliness, correctness and completeness of emergency care at this stage.

Conservative treatment

From the moment the diagnosis of acute renal failure is established, the patient is carried out the following actions:

Eliminate the factor that led to the development of arresters;

Prescribe a carbohydrate-free diet and special foods;

A test is carried out to restore urine output;

Determine the indications for dialysis;

Symptomatic therapy is used.

Elimination of the factor that led to the development of acute renal failure makes it possible to slow down its progressive development. For example, removal of ureteral stones often prevents the onset of dialysis ARF.

Diuresis recovery test. The test is carried out at BP> 60 mm Hg, in the absence of hyperhydration in terms of BCC and hematocrit (a type of kidney hypoperfusion "moisture-wet" and no urine in the bladder according to ultrasound data. First, in the presence of increased hematocrit, an infusion is performed 20 ml / kg of saline or 5% albumin for 30-60 minutes Then a 2.4% solution of aminophylline is injected at the rate of 1 ml / 10 kg of body weight and sequentially 2-7 mg / kg of furosemide (torasemide). within 1.5-2 hours, furosemide is reintroduced (preferably the introduction of torasemide, taking into account the lesser toxic effect on the kidneys) until the total dose for two injections is not more than 15 mg / kg.In the absence of a diuretic effect, titrated administration of dopamine (dobutamine) is carried out in renal dose of 1.5-3.5 mcg / kg / min around the clock.The criterion for the adequacy of the selected dose is the absence of hypertension. ice should be titrated down. The duration of the administration of this drug is determined by the timing of the initiation of dialysis. In the absence of such an opportunity for social or medical reasons, the use of dopamine can be successfully continued continuously. In some cases, to restore diuresis, it is possible to use angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB II1) with an extrarenal route of excretion and bosentan. In the case of heart failure on the background of acute renal failure, the drug of first choice may be a natriuretic peptide (for example, nesiritide).

In case of impossibility of pharmacological recovery of diuresis, the indications for dialysis are determined. It should be noted that dialysis initiation should not be delayed as delaying dialysis worsens the prognosis of ARF. A very dangerous condition that develops with acute renal failure is hyperkalemia. Emergency measures are determined by the serum potassium level. Hyperkalemia can reach significantly higher values ​​without the development of pronounced changes on the ECG in patients with diabetes mellitus with high glycemia.

The first dialysis is mainly peritoneal. It is the method of choice in the treatment of children and adults in order to determine the cause of ARF and the possible prognosis. There are practically no contraindications for peritoneal dialysis. This method is indicated in the presence of hypotension and increased bleeding. For peritoneal dialysis, polyglucose, amino acid or bicarbonate solutions are used. Polydisperse glucose polymer icodextrin is modern. In acute renal failure, in contrast to chronic renal failure, peritoneal dialysis is almost always performed using a Cycler, i.e. in automatic mode. Hemodialysis is performed using a temporary vascular access (subclavian, jugular or femoral double-sheath catheter). In accordance with modern requirements, the effectiveness of dialysis procedures should provide Kt / V above 2.0 (with intensive input - up to 8.0-9.0). Dialysis is performed in an acute kidney or dialysis unit.

During peritoneal dialysis, complications are possible more often with the patency of the catheter and microbial contamination, which leads to the development of peritonitis. The most common complications of hemodialysis include: fluid redistribution syndrome with cerebral edema due to a high content of urea in the tissue, arterial hyper- and hypotension, hemorrhagic and disseminated intravascular coagulation.

A complication of acute renal failure can be the development of sepsis in the case of microbial onset of renal failure and a stress ulcer, which can develop in the second week of the disease. In the treatment of septic conditions against the background of acute renal failure in the case of dialysis, antibacterial drugs are prescribed taking into account their clearance. At the pre-dialysis stage of treatment, antibiotics are prescribed either by the extrarenal elimination route or in minimal doses, but sepsis is an indication for initiating dialysis therapy. Stress ulcers in acute renal failure are treated with proton pump blockers based on drug clearance. Prevention of stress ulcers is carried out by the same means in the presence of an unfavorable patient history.

Syndrome therapy is determined by the causative factor of ARF (vascular disease, glomerular lesions, interstitial process, acute tubular necrosis). It should be noted that corticosteroids are used in the presence of hormone-dependent tumors, for example, sarcoma, or the onset of acute renal failure in the presence of a nephrotic variant of glomerulonephritis. In other cases, the appointment of glucocorticoids is not justified. Heparinization (preferably with low molecular weight heparins) is carried out only during hemodialysis procedures.

In the absence of restoration of diuresis in the case of dialysis (the latter continues constantly), and after 3 weeks it is possible to determine chronic renal failure as a consequence of acute renal failure. Recovery of diuresis indicates a favorable prognosis and the transition to the polyuric stage of acute renal failure, which lasts from 1 to 6 weeks.

At the polyuric stage of acute renal failure, minimal pharmacological treatment is used with increased attention to electrolyte compensation and the restoration of normal hemodynamics using low doses of an ACE inhibitor / ARB II1 with an extrarenal route of excretion (moexipril, eprosartan, telmisartan) or ticlopedina / clopidogrel.

After the restoration of normal diuresis, depending on the functional state of the kidneys, interstitial nephritis may develop, which ends with chronic renal failure or recovery. Interstitial nephritis as a consequence of ARF is characterized by a decrease in the relative density (specific gravity) in the morning urine analysis (less than 1,018) or in the analysis according to Zimnitsky, a decrease in GFR less than 90 ml / min or an increase in blood creatinine of approximately more than 0.125 mmol / L in adults and over 0.104 mmol / l in children, the presence of urinary syndrome, which is more often represented by microalbuminuria / proteinuria and anemia.

Given the progressive course of interstitial nephritis, which is classified as chronic kidney disease, and the subsequent development of chronic renal failure, patients are prescribed a renoprotective agent. Renoprotection is based on an ACE inhibitor and / or ARB II1 with an extrarenal route of excretion and moxonidine. To ensure the full volume of renoprotection, a protein-restricted diet is used (with the exception of children) in combination with keto acids, erythropoietin-stimulating agents, regulators of calcium-phosphorus metabolism, sorbents.

Recovery is evidenced by a normal GFR level and a urine density of more than 1018 in the absence of urinary syndrome.