Symptoms and treatment of acute renal failure. Prerenal acute renal failure Clinical symptoms of acute renal failure
Failure of the functioning of two kidneys, provoked by a weakened blood supply, a delay in glomerular filtration is called acute renal failure (ARF).
The result is an absolute stop in the elimination of toxins, a failure of the acid-base, electrolyte, water balance. Competent therapy prevents painful processes.
Acute renal failure is a failure of two kidneys to function
According to medical statistics, the disease affects 200 people out of 1 million.
Features of renal failure
Acute renal failure - contractions, stopping the work of the kidneys, provoking an increase in metabolites of nitrogen metabolism, metabolic failure. Pathology of the nephron is due to a decrease in blood supply, a decrease in oxygen.
The pathology of acute renal failure requires from a couple of hours to a week for occurrence, lasts more than a day. An early visit to the doctor ensures an absolute resumption of the affected organ. ARF becomes an exacerbation of painful pathologies, subdivided into forms:
- Hemodynamic (perineral), caused by a sharp failure of hemodynamics. It is characterized by a decrease in blood supply, a drop in the rate of glomerular filtration. Failures of this type are caused by a reduction in the amount of pulsating blood. If the blood supply is not restored, then renal tissue death is likely.
- Parenchymal (renal) - arises from a toxic or ischemic effect on the renal parenchyma or acute inflammation. As a result, the integrity of the tubules is damaged, their entrails are ejected into the tissue.
- Obstructive (postrenal) - formed after the resulting obstruction of the urinary tract. This type provides for the preservation of functions, urination will be difficult.
According to the level of preservation of diuresis, the neoliguric, oliguric form is divided.
Causes of Acute Renal Failure
The etiology of the disease is distinguished by its form. Factors in the formation of prerenal ARF include:
- reduced cardiac output;
- blockage of the pulmonary artery;
- surgical interventions, trauma with blood loss;
- tissue damage by high temperatures;
- loss of a lot of water and salts due to loose stools, vomiting;
- taking diuretics;
- drop in vascular tone.
Prerequisites for a renal arrester:
- toxic effect on the kidney tissue of poisonous plants, copper, mercury salts;
- uncontrolled use of drugs (antiblastoma drugs, antimicrobial agents and sulfonamides);
- contrast agents, drugs can cause pathology in people;
- an increased level of myoglobin with prolonged compression of tissues during injury, narcotic, alcoholic coma;
- renal diseases of an inflammatory nature.
There are many reasons for the development of the disease.
Factors in the development of postrenal ARF are:
- pathology of the heart apparatus;
- irregularities in the rhythm of the heartbeat;
- cardiac tamponade, dehydration;
- damage to body tissues by high temperatures;
- ascites, low blood pressure;
- blockage of blood vessels carrying blood to the kidneys;
- the poisonous effect of toxic substances;
- the presence of inflammatory pathologies.
In case of injury and extensive surgery, the formation of acute renal failure is determined by: shock, infection or blood transfusion, therapy with nephrotoxic drugs.
Symptoms of Acute Renal Failure
Distinctive features are characterized by development. There is an aggravation of the patient's well-being, a failure of the functioning of organs. Symptoms of the manifestation of acute renal failure are divided into types according to stages.
The initial stage is accompanied by peripheral edema, weight gain. The primary phase is not detected due to lack of signs. The circulatory crisis that appears at the stage has a duration and proceeds imperceptibly. Nonspecific signs of renal failure (muscle weakness, nausea, headache) are masked by the symptoms of an underlying ailment - shock, injury or poisoning.
The initial stage is accompanied by weight gain
If acute glomerulonephritis is a prerequisite for acute renal failure, there are blood clots in the urine, back pain. The initial phase of ARF is accompanied by low blood pressure, pale skin color, accelerated heart rate, and decreased urine output.
Oligoanuria is considered a severe stage. It poses a threat to the patient's life, accompanied by signs:
- reduction or stop of urine separation;
- poisoning with metabolites of nitrogen metabolism, expressed in the form of nausea, vomiting, loss of appetite;
- increase in blood pressure;
- difficulty concentrating, fainting;
- coma;
- swelling of the connective tissue and internal organs;
- weight gain from an excess of fluid in the body.
The subsequent course of ARF is determined by the effectiveness of treatment in the second phase. A positive result ensures the onset of a special stage. An increase in diuresis is traced, polyuria is formed. Fluid is eliminated from the body, puffiness is reduced, and the blood will be cleansed of toxins.
The polyuria phase carries the danger of dehydration, electrolyte imbalance. A month later, diuresis normalizes, a stage of recovery appears, which lasts up to 12 months.
With ineffective therapy, a terminal phase of ARF is formed with a risk of mortality. It manifests itself in the form of signs:
- difficulty breathing, coughing in the lungs;
- discharge of sputum with blood droplets;
- fainting, coma;
- spasm, convulsions;
- critical failures in the heartbeat.
The disease affects the body, provokes the development of atrophy of the heart muscle, pericarditis, encephalopathy, weakening of the immune system.
Diagnosis of renal failure
The diagnostic process includes the doctor's actions:
- studying the history of pathology, patient complaints;
- a study of the life history (whether the organs were injured, whether the patient had poisoning, blood loss, the presence of chronic renal ailments, diabetes mellitus), the conjugation of working or living conditions with regular intoxication (paints and varnishes, solvents);
- a complete assessment of the patient's general condition (degree of consciousness, color of the skin surface, blood pressure indicators) is carried out, a study of the urinary system using palpation (palpation), light tapping with the edge of the palm in the lumbar region (may be accompanied by pain in the affected side);
- blood tests: the presence of anemia (a decrease in the degree of hemoglobin and the number of erythrocytes, due to the production of a hormone by the kidneys that ensures the production of erythrocytes), the growth of protein breakdown products - creatinine, urea;
- study of urine - a decrease in the volume of its production, the appearance of protein in the urine, an increase in urea, creatinine (eliminate the kidneys);
- study of electrolytes, urinary constituents for probable renal pathologies;
- ultrasound examination of the kidneys;
- examination of urea, urethra with optical equipment;
- radionuclide methods - allow visualizing the functional, anatomical structure of organs, determining the type of tissue damage or urinary tract, inflammatory features, the presence of calculi or tumors;
- according to indications (in case of prolonged course of ARF or its unknown etiology, a kidney biopsy is performed).
The diagnosis of the disease is carried out by a doctor
Information about the size of the organ will not be superfluous. A decrease in size indicates the presence of chronic failure.
Emergency care for illness
With ARF syndrome, emergency care involves calling an ambulance or quickly transporting a patient to a hospital in a medical institution, then the patient must be provided with:
- bed rest;
- warming the body;
- removal from hypovolemia and shock (tachycardia, hypotension, shortness of breath, cyanosis of the skin, mucous tissues, anuria, dehydration);
- jet injection of warm salt solution "Trisol";
- active therapy for sepsis;
- intravenous drip of Dopamine provides improved blood circulation. Heparin is injected intravenously, its drip is carried out.
Treatment is best done in a hospital
Renewal of the kidneys occurs during the compensation of intravascular fluid volume, therapy for blood poisoning, and stopping the intake of nephrotoxic drugs.
Treatment of acute renal failure
At the first stage of the disease, therapy involves the elimination of the factor that provoked acute renal failure. In the presence of shock, it is required to compensate for the volume of circulating blood, to adjust blood pressure indicators.
The use of innovative methods by urologists, such as extracorporeal hemocorrection, provides cleaning of the body from the poisons that caused the formation of acute renal failure. Hemosorption and plasmapheresis help. If obstructive signs are present, the normal passage of urine is restored. To do this, stones are removed from the kidneys, ureters.
Hemosorption procedure
The oliguric phase is accompanied by the appointment of furosemide, osmotic diuretics that stimulate diuresis. When setting the size of the injected fluid, excluding losses during urination, vomiting, bowel movements, sweating and breathing should be taken into account.
The patient is prescribed protein nutrition, limiting the intake of potassium with food. Drainage of wounds, elimination of areas affected by necrosis is performed. Antibiotic dosage is based on the severity of the kidney damage.
Possible complications of the disease
The initiating and supporting stages of the surge arrester are accompanied by disruptions in the withdrawal of nitrogen metabolism products, water, electrolytes and acids. The manifestation of changes in the chemical structure of blood is due to oliguria, the process of catabolism in the patient.
The degree of glomerular filtration is noted in comparison with patients without oliguria. In the former, more nitrogen metabolism, water, electrolytes are released with urine.
Failures in ARF without oliguria are less pronounced in patients than in patients affected by pathology.
A normal increase in serum potassium concentration in patients without oliguria and catabolism is 0.3-0.5 mmol / day. Large volumes indicate potassium load of the endogenous or exogenous type, as well as the release of potassium from cells due to acidemia.
The disease can cause complications
Severe consequences of pathology can include uremia, as an independent intoxication of the body with products of protein metabolism. There is a failure in the functioning of organs and systems:
- hyperkalemia, provoking changes in the ECG, resulting in cardiac arrest. Pathology affects the development of muscle weakness and tetraparesis;
- changes in blood - suppression of hematopoietic function, production of erythrocytes. The duration of the existence of erythrocytes decreases, anemia begins to develop;
- suppression of the immune system, which leads to the appearance of infectious diseases, the addition of infection aggravates the course of the disease and often leads to death;
- manifestations of neurological failures - weakness, clouding of consciousness, a feeling of disorientation, slowness, alternating with stages of arousal;
- pathologies from the cardiovascular apparatus - arrhythmia, pericarditis, arterial hypertension;
- malfunctions of the gastrointestinal tract - unpleasant sensations in the peritoneal region, nausea, lack of appetite. In acute situations, the development of uremic gastroenterocolitis is likely;
- the last stage in the development of uremia is uremic coma - the patient is immersed in an unconscious state, severe malfunctions of the respiratory and cardiovascular apparatus are formed.
Properly conducted therapy ensures complete reversibility of the disease, except for its most severe cases. The outcome of the disease depends on the patient's age, the level of impaired renal function, and the presence of complications.
In a certain proportion of patients, kidney function is fully restored, 1-3% need hemodialysis.
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, radio-opaque 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 medications - antibiotics (penicillin, morphocyclin, gentamicin, brulomycin, chloramphenicol, rifampicin, etc.), sulfonamides, nitrofurans, salicylates, pyrazolone derivatives, dextrans, barbirurates, anesthetics, ganglionic (rtactic) drugs, 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 nephropathy, hemorrhagic fever with renal syndrome, nephropathy of pregnancy, 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, perinephral blockade, starvation treatment, hyperbaric therapy, the use of radioactive drugs;
- myorenal syndrome: high voltage shock, carbon monoxide poisoning, positional compression syndrome, nontraumatic 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, and 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-excreting kidney function, 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 ARF: 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 intake of fluid or 10-12 ml / kg / day.
Anuria is the presence of urine less than 150 ml / day (60 ml / m 2 / 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 some kidney function 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 lack of restoration of independent diuresis for more than 3 weeks in acute renal failure indicates the development of chronic renal failure (CRF).
The surge arrester is divided 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, recovery- from several months to 1-2 years.
Clinical signs initial stage ARF is completely neutralized 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.
IN oligoanuric stage a progressive decrease in diuresis begins, up to the development of anuria. However, even at this stage, its onset may go unnoticed, because after the correction of hemodynamics, the patients' well-being can slightly improve and a period of imaginary well-being sets in (up to 3-5 days), which makes the timely diagnosis of acute renal failure even more difficult. Only then does the detailed picture of the 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 pathological sediment in it, a sharp deterioration occurs: drowsiness, headache, abdominal pain, constipation, followed by diarrhea. The skin is grayish-pale in color with a jaundice, 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 of the cavity - ascites, hydrothorax, blood thinning, increased blood pressure), and then cell hyperhydration (mental and physical asthenia, nausea , vomiting after eating, headache, mental disorders, cramps, 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 anemia, acidosis and myocardial damage. Signs of myocarditis are noted: deafness of heart sounds, systolic murmur, "gallop" rhythm, congestive heart failure, disturbances of the rhythm and conduction of the heart. In the occurrence of arrhythmias, not only myocarditis is important, but also hyperkalemia, usually associated with acute renal failure during this period. With an increase in potassium levels above 7 mmol / l, bradycardia develops, high-amplitude T waves, ST segment depression, broadening of the initial part of the ventricular complex and flattening of P waves appear. In the event that the arrester 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) can develop, and then cell dehydration (indomitable thirst, weight loss, fever, 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 potassium level to 6.5 mmol / l, magnesium - up to 1.9-2.1 mmol / l. Hyponatremia, hypocalcemia, hyperphosphatemia, hypersulfatemia are noted. All these disorders cause the clinic of uremic intoxication.
In stage restoration of diuresis 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.
Stage of recovery if it occurs, it 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.
Disease treatment
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 doctor, 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;
Apply symptomatic therapy.
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\u003e 60 mm Hg, in the absence of hyperhydration in terms of the 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, 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 re-administered (preferably the introduction of torasemide, taking into account the lower 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 performed 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. Provided that the blood pressure level increases from the initial one against the background of dopamine administration, the dose of pos ice should be titrated down. The duration of 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, dopamine use 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 first choice drug 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, since delaying dialysis worsens the prognosis of ARF. Hyperkalemia is a very dangerous condition that develops in acute renal failure. Emergency measures are determined by the serum potassium level. Hyperkalemia can reach significantly higher values \u200b\u200bwithout 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 acute renal failure and a 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. Modern is the polydisperse glucose polymer icodextrin. In acute renal failure, in contrast to chronic renal failure, peritoneal dialysis is almost always carried out with the help of a cycle, i.e. in automatic mode. Hemodialysis is performed using temporary vascular access (subclavian, jugular or femoral double-stranded catheter). In accordance with modern requirements, the efficiency of dialysis procedures should provide Kt / V over 2.0 (with intensive input - up to 8.0-9.0). Dialysis is performed in the acute kidney or dialysis ward.
When conducting peritoneal dialysis, complications are possible more often occur with catheter patency 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 the high content of urea in the tissue, arterial hyper- and hypotension, hemorrhagic and DIC.
A complication of acute renal failure may be the development of sepsis in the case of the microbial debut of renal failure and a stress ulcer that 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 antibiotic treatment, they are prescribed either by extrarenal elimination or in minimal doses, but sepsis is an indication for starting dialysis therapy. Stress ulcer in acute renal failure is treated with proton pump blockers, taking into account the clearance of the drug. Stress ulcer prophylaxis is carried out by the same means in the presence of an adverse patient history.
Syndromic therapy is determined by the causative factor of acute renal failure (vascular disease, glomerular lesions, interstitial process, acute tubular necrosis). It should be noted that corticosteroids are used in the presence of hormone-dependent tumors, such as sarcomas, or the onset of acute renal failure on the background of the nephrotic version of glomerulonephritis. In other cases, the appointment of glucocorticoids is not reasonable. Heparinization (preferably 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 continuously), and after 3 weeks it is possible to determine chronic renal failure as a result of acute renal failure. The restoration 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 restoration of normal hemodynamics using low doses of ACE inhibitors / ARB II1 with an extrarenal route of withdrawal (moexipril, eprosartan, telmisartan) or ticlopedin / clopidogrel.
After restoration of normal diuresis, depending on the functional state of the kidneys, it is possible to develop interstitial nephritis, which ends with chronic renal failure or recovery. Interstitial nephritis as a result of acute renal failure is characterized by a decrease in relative density (specific gravity) in the morning urine analysis (less than 1 018) or in the Zimnitsky analysis, a decrease in GFR of less than 90 ml / min or an increase in blood creatinine of more than about 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. The basis of renoprotection is ACE inhibitors and / or ARB II1 with extrarenal excretion and moxonidine. To ensure the full volume of renoprotection, a protein-restricted diet (with the exception of children) is used in combination with keto acids, erythropoietin-stimulating agents, calcium-phosphorus metabolism regulators, and sorbents.
A normal level of GFR and a urine density of more than 1018 in the absence of urinary syndrome indicate recovery.
RCHR (Republican Center for Health 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 advice
RSE at RVP "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 glomerular filtration rate, leading to the accumulation of nitrogenous (including urea, creatinine) and non-nitrogenous metabolic products (with impaired electrolytes, acid-base balance, fluid volume) excreted by the kidneys.
In 2004 ADQI (Initiative to Improve the Quality of Acute Dialysis) proposed the concept of "acute renal damage" (AKP), replacing the term "acute renal failure" and the classification, called RIFLE by the first letters of each of the consecutive stages of AKI: risk (Risk), damage (Injury), failure (Failure), loss (Loss), terminal chronic renal failure (End stage renal disease) - table 2.
This term and new classifications are introduced with the aim of earlier verification of acute renal damage, early initiation of renal replacement therapy (RRT) with the ineffectiveness of conservative methods and preventing the development of severe forms of renal failure with adverse outcomes.
I. INTRODUCTION:
Protocol Name:Acute renal failure (acute renal damage)
Protocol Code:
Code (codes) according to ICD-10:
Acute renal failure (N17)
N17.0 Acute renal failure with tubular necrosis
Tubular necrosis: NOS. acute
N17.1 Acute renal failure with acute cortical necrosis
Cortical necrosis: NOS. acute. renal
N17.2 Acute renal failure with medullary necrosis
Medullary (papillary) necrosis: NOS. acute. renal
N17.8 Other acute renal failure
N17.9 Acute renal failure, unspecified
Abbreviations used in the protocol:
ANCA Antineutrophil Antibodies
ANA Antinuclear Antibodies
Blood pressure
ADQI Acute Dialysis Quality Improvement Initiative
AKIN Acute Kidney Injury Network - Acute Renal Damage Study Group
LVAD Left Ventricular Assist Device
KDIGO Kidney Disease Improving Global Outcomes - Global Kidney Disease Outcome Initiative
MDRD Modification Diet of Renal Disease
RVAD Right Ventricular Assist Device
BDU Without further elaboration
ARB-II Angiotensin-II receptor blockers
GDS hepatorenal syndrome
HUS Hemolytic uremic syndrome
GLC Gastrointestinal bleeding
RRT Renal replacement therapy
IHD Intermittent (periodic) hemodialysis
Mechanical ventilation
I-ACE Angiotensin-Converting Enzyme Inhibitors
KI-OPP Contrast - induced OPP
KShchS Acid-base state
NSAIDs Nonsteroidal anti-inflammatory drugs
Acute renal failure acute renal failure
AKI Acute renal damage
OTH Acute tubular necrosis
OTIN Acute tubulointerstitial nephritis
Bcc circulating blood volume
ICU Intensive Care Unit
PZPT Continued renal replacement therapy
PHF Continued veno-venous hemofiltration
PVVGD 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, doctor of the hemodialysis department, resuscitation anesthetist, general practitioner, general practitioner, toxicologist, urologist.
Classification
Classification
Causes and classifications of AKI
According to the main development mechanismOPP 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 Renal Damage
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 diuresis values2 forms are distinguished:
Oliguric (diuresis less than 500 ml / day);
Neoliguric (diuresis of 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 the majority of patients with suspected acute renal failure / AKI do not have information about the initial state of renal function, the basal creatinine level, related to the patient’s age and gender, is calculated at a given level of GFR (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, micromol / 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 |
Classification of OPP by RIFLE (2004) - table 2
|
Classes |
Glomerular Filtration Criteria | Criteria for urine output |
| Risk | Scr * 1.5 times or ↓ KF ** 25% | <0,5 мл/кг/час ≥6 часов |
| Damage | Scr 2 times or ↓ CF at 50% | <0,5 мл/кг/час ≥12 часов |
| Failure | 3 times Scr 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\u003e 4 weeks | |
| Terminal renal failure | TKHP\u003e 3months | |
Serum Scr * -creatinin, CF ** - glomerular filtration
Table 4. Stages of OPP (KDIGO, 2012)
Diagnostics
II. DIAGNOSTIC AND TREATMENT METHODS, APPROACHES AND PROCEDURES
The list of the main diagnostic measures
The main (mandatory) diagnostic examinations conducted on an outpatient basis:
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 tests performed on an outpatient basis:
Blood biochemical analysis (protein fractions, M-gradient, total and ionized calcium, phosphorus, lipid spectrum);
Rheumatoid factor;
Ultrasound of the vessels of the kidneys;
Ultrasound of the abdominal cavity.
The minimum list of examinations that must be carried out when sent to a planned hospitalization:
Due to the urgency of emergency emergency hospitalization, enough data on the volume of urine excreted (oliguria, anuria) and / or an increase in creatinine, according to the diagnostic criteria of paragraph 12.3.
The main (mandatory) diagnostic examinations carried out at the stationary level:
Biochemical analysis of blood (serum creatinine, serum urea, potassium, sodium, total serum protein and protein fractions, ALT, AST, total and direct bilirubin, CRP);
HSV blood;
Coagulogram (PV-INR, APTT, fibrinogen);
Urinalysis (in the presence of diuresis!);
Ultrasound of the kidneys;
Notes:
All urgent patient receipts, planned x-ray contrast studies, as well as surgical interventions, should be assessed for the risk of AKI;
All urgent receipts 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, indications for PST, prognosis determined, and the patient should be referred to a multidisciplinary hospital with the presence of an extracorporeal hemocorrection department.
Additional diagnostic examinations carried out at the stationary level:
Urinalysis according to Zimnitsky;
Reberg test (daily);
Daily albuminuria / proteinuria or albumin / creatinine, protein / creatinine ratio;
Urine protein electrophoresis + M-gradient of urine;
Excretion of potassium, sodium, calcium with urine;
Daily uric acid excretion;
Urine analysis for Bens-Jones Protein;
Bacteriological examination of urine with determination of the sensitivity of the pathogen to antibiotics;
Blood biochemical analysis (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 the blood and urine;
Schizocytes;
Blood procalcitonin;
Ultrasound of the bladder;
Dopplerography of the vessels of the kidneys;
Chest x-ray;
Fundus examination;
TRACT OF THE PROSTATE;
Ultrasound of the pleural cavities;
Ultrasound of the pelvic organs;
CT scan of the thoracic segment, abdominal segment, pelvic organs (with suspected systemic disease with multiple organ damage, with suspected paraneoplastic nephropathy to exclude neoplasms, metastatic lesions; with sepsis, in order to search for the primary source of infection);
Urine osmolarity, urine osmolality;
Puncture biopsy of the kidney (used in AKI in complex diagnostic cases, indicated for renal AKI of unclear etiology, AKI with a period of anuria lasting more than 4 weeks, AKI associated with nephrotic syndrome, acute nephritic syndrome, diffuse lung lesion, such as necrotizing vasculitis);
Biopsy of the skin, muscles, rectal mucosa, gums - for the diagnosis of amyloidosis, as well as for the verification of systemic disease;
Electroencephalography - in the presence of neurological symptoms;
ELISA for markers of viral hepatitis B, C;
PCR on HBV-DNA and HCV-RNA - to exclude virus-associated nephropathy;
Coagulogram 2 (RFMC, ethanol test, antithrombin III, platelet function);
CT / MRI of the brain;
MRI of the thoracic segment, abdominal segment, pelvic organs (with suspected systemic disease with multiple organ damage, with suspected paraneoplastic nephropathy to exclude neoplasms, metastatic lesions; with sepsis - in order to search for the primary source of infection) ;;
Blood culture three times for sterility from both hands;
Blood culture for blood culture;
Crops from wounds, catheters, tracheostomy, pharynx;
Fibroesophagogastroduodenoscopy - eliminate the presence of erosive and ulcerative lesions, due to the high risk of gastrointestinal bleeding when using anticoagulants during PST; exclude neoplasm in cases of suspected paraneoplastic process;
Colonoscopy - eliminate the presence of erosive and ulcerative lesions, due to the high risk of intestinal bleeding when using anticoagulants during PST; exclude neoplasm in cases of suspected paraneoplastic process.
Diagnostic measures carried out at the stage of emergency ambulance:
Collection of complaints and anamnesis, data regarding 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."
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 must remember 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-infection glomerulonephritis;
The presence of arterial hypertension, diabetes mellitus or malignant neoplasms (the likelihood of hypercalcemia);
Rapid urging, weakening of the urine stream in men are signs of postrenal obstruction caused by prostate disease. Renal colic with nephrolithiasis may be accompanied by a decrease in diuresis;
Establish which medicines the patient was taking, if there were any cases of intolerance to these drugs. Of particular note is the admission: ACE inhibitors, ARB-II, NSAIDs, aminoglycosides, the introduction of radiopaque substances. Find out contact with toxic, toxic substances;
Symptoms of muscle damage (pain, muscle swelling, increased creatine kinase, myoglobinuria in the past), the presence of metabolic diseases may indicate rhabdomyolysis;
Information about diseases of the kidneys and arterial hypertension and cases of increased creatinine and urea in the past.
The main points necessary for diagnosis, in emergency conditions with AKI:
Presence of impaired renal function: AKI or CKD?
Impaired renal blood flow - arterial or venous.
Are there any abnormalities in urine outflow?
A history of kidney disease, an accurate diagnosis?
Physical examination
The main areas of physical examination are as follows:
Assessing the degree of hydration of the body is of paramount importance for determining the tactics of patient management (thirst, dry skin, mucous membranes or the presence of edema; loss or weight gain; level of CVP; shortness of breath).
Skin color, rashes. Thermometry.
Assessment of the central nervous system
Assessment of the condition of the lungs (edema, wheezing, bleeding, etc.).
Assessment of the cardiovascular system (hemodynamics, blood pressure, pulse. Ripple on large vessels). Ocular fundus.
The presence of hepatosplenomegaly, a decrease in the size of the liver.
Palpation can reveal enlarged kidneys with polycystosis, an enlarged bladder with tumors, and urethral obstruction.
Evaluation of diuresis (oliguria, anuria, polyuria, nocturia).
Start period: at the onset of the disease, the clinical manifestations of AKI are non-specific. The symptoms of the underlying disease prevail.
The period of development of oliguria:
Oliguria, anuria;
Peripheral and abdominal edema;
Rapidly increasing hyponatremia with nausea, seizures with headache and disorientation is a harbinger of cerebral edema;
Clinical manifestations of azotemia - anorexia, uremic pericarditis, smell of ammonia from the mouth;
Hyperkalemia
Acute adrenal insufficiency;
Metabolic acidosis, severe alkalosis,
Non-cardiogenic pulmonary edema,
Adult respiratory distress syndrome
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 DIC)
Activation of opportunistic flora (bacterial or fungal, against the background of uremic immunodeficiency, develops in more than 50% of patients with renal AKI. Typically, damage to the lungs, urinary tract, stomatitis, mumps, infection of surgical wounds);
Generalized infections with septicemia, infectious endocarditis, peritonitis, candididasepsis.
The period of recovery of diuresis:
Normalization of nitrogen excretory function of the kidneys;
Polyuria (5-8 liters per day);
Phenomena of dehydration;
Hyponatremia;
Hypokalemia (risk of arrhythmia);
Hypocalcemia (risk of tetany and bronchospasm).
Laboratory research:
Jab: increased ESR, anemia.
OAM: proteinuria from moderate 0.5 g / day to severe - more than 3.0 g / day, macro / microhematuria, cylindruria, decreased relative density of urine
Blood chemistry: hypercreatininemia, decreased GFR, electrolyte disturbances (hyperkalemia, hyponatremia, hypocalcemia).
HSV blood: acidosis, a decrease in the level of bicarbonates.
Differential diagnostic laboratory signs.
|
Research |
Characteristic | Causes of AKI |
| Urine |
Erythrocyte cylinders, dysmorphic red blood cells Proteinuria ≥ 1g / L |
Glomerular diseases Vasculitis TMA |
| . White blood cells, white blood cells | OTIN | |
|
Proteinuria ≤ 1g / L Low molecular weight proteins Eosinophiluria |
OTIN Atheroembolic disease |
|
| . Visible hematuria |
Postrenal causes Acute GN Injury |
|
|
Hemoglobinuria Myoglobinuria |
Pigmenturia diseases | |
| . Granular or epithelial cylinders |
OTH 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 - |
OPP, CKD |
| . Hypoproteinemia, hypoalbuminemia | Nephrotic syndrome, cirrhosis | |
| . Hyperproteinemia | Myeloma and other paraproteinemias | |
| . uric acid | Tumor Lysis Syndrome | |
| . LDH | Gus | |
| . Creatine kinase | Injuries and metabolic diseases | |
| Biochemical | . Na +, creatinine for calculating the excreted Na fraction (FENa) | Prerenal and renal AKI |
| . Squirrels of Bens Jones | Multiple myeloma | |
| Specific immunological studies | . ANA, antibodies to double-stranded DNA | Hard currency |
| . p- and s-ANCA | Vasculitis of small vessels | |
| . anti-GBM antibodies | Anti-GBM Nephritis (Goodpasture Syndrome) | |
| . ASL-O titer | Post Streptococcal GN | |
| . Cryoglobulinemia, sometimes + rheumatoid factor | Cryoglobulinemia (essential or in various diseases) | |
| . Antiphospholipid antibodies (anticardiolipin antibodies, lupus anticoagulant) | APS syndrome | |
| . ↓ C 3, ↓ C 4, CH50 | SLE, infectious endocarditis, shunt nephritis | |
| . ↓ C 3, CH50 | Post Streptococcal GN | |
| . ↓ C 4, CH50 | Essential mixed cryoglobulinemia | |
| . ↓ C 3, CH50 | MPGN type II | |
| . Procalcitonin test | Sepsis | |
| Urinalysis | . NGAL urine | Early diagnosis of AKI |
Instrumental research:
. ECG: disturbances in rhythm and cardiac conduction.
. Chest x-ray: accumulation of fluid in the pleural cavities, pulmonary edema.
. Angiography: to exclude vascular causes of AKI (renal artery stenosis, stratified abdominal aortic aneurysms, ascending thrombosis of the inferior vena cava).
. Ultrasound of the kidneys, abdomen:an increase in kidney volume, the presence of calculi in the renal pelvis or urinary tract, the diagnosis of various tumors.
. Kidney Radioisotope Scan: assessment of renal perfusion, diagnosis of obstructive pathology.
. Computed and magnetic resonance imaging.
. Kidney biopsy according to indications: it is used for AKI in complex diagnostic cases, it is indicated for renal AKI of unclear etiology, AKI with a period of anuria lasting more than 4 weeks, AKI associated with nephrotic syndrome, acute nephritic syndrome, diffuse lung lesion, such as necrotizing vasculitis.
Indications for expert advice:
Consultation of a rheumatologist - with the appearance of new symptoms or signs of a systemic disease;
Hematologist consultation - to exclude blood diseases;
Toxicologist consultation - in case of poisoning;
Resuscitation consultation - postoperative complications, AKI, due to shock, emergency conditions;
Consultation of an otolaryngologist - to identify a foci of infection with subsequent rehabilitation;
Surgeon consultation - if you suspect a surgical pathology;
Consultation of a urologist - in the diagnosis and treatment of postrenal AKI;
Consultation of a traumatologist - for injuries;
Dental consultation - to identify foci of chronic infection with subsequent rehabilitation;
Consultation with an obstetrician-gynecologist - in pregnant women; with suspected gynecological pathology; in order to identify foci of infection, and their subsequent rehabilitation;
Consultation with an ophthalmologist - to assess changes in the fundus;
Cardiologist consultation - in case of severe arterial hypertension, ECG disorders;
Neurologist consultation - in the presence of neurological symptoms;
Infectionist consultation - in the presence of viral hepatitis, zoonotic and other infections
Consultation of a psychotherapist is a compulsory consultation of patients in consciousness, since the patient’s “attachment” to the artificial kidney apparatus and the fear of “dependence” on him can negatively affect the patient’s mental state and lead to a conscious refusal of treatment.
Consultation of a clinical pharmacologist - to adjust 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 the 2-3 stages 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 characteristic |
| Kidney Size (Ultrasound) | normal | Reduced |
| Creatinine gain | More than 0.5 mg / dl / day | 0.3-0.5 mg / dl / day |
| Renal history | is absent | Often perennial |
Differential diagnosis of AKI, AKI on CKD and CKD.
|
Signs |
OPP | AKI on CKD | CKD |
| History of kidney disease | No or short | Long | Long |
| Blood creatinine before AKI | Normal | Promoted | Promoted |
| Blood creatinine in the background of AKI | Promoted | Significantly upgraded | Promoted |
| Polyuria | seldom | not | Almost always |
| A history of polyuria before AKI | not | Long | Long |
| Ag | seldom | Often | Often |
| SD | seldom | Often | Often |
| History of nocturia | not | there is | there is |
| Causing factor (shock, trauma ..) | Often | Often | Seldom |
| An acute increase in creatinine\u003e 44 μmol / L | is always | is always | Never |
| Ultrasound kidney sizes | Normal or Enlarged | Normal or reduced | Reduced |
To confirm the diagnosis of AKI, its postrenal form is primarily excluded. To identify 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, ultrasound scan, renal radiopaque angiography are indicated.
Differential diagnosis of prerenal and renal AKI .
|
Indicators |
OPP | |
| prerenal | Renal | |
| The relative density of urine | > 1020 | < 1010 |
| Urine osmolarity (mosm / kg) | > 500 | < 350 |
| The ratio of osmolarity of urine to plasma osmolarity | > 1,5 | < 1,1 |
| Urine Sodium Concentration (mmol \\ L) | < 20 | > 40 |
| Excreted Na (FE Na) 1 fraction | < 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 loss |
Decreased fluid intake | Urine exit through unnatural paths |
|
Hot climate Fever Diarrhea Gastrostomy Mechanical ventilation |
Psychogenic oligodipsia Water shortage Tumors of the esophagus Rumination Esophagus Achalasia Esophageal strictures Nausea iatrogenic |
Cloaca (urinary-rectal anastomosis) Urinary tract injuries The flow of urine with a nephrostomy |
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Treatment
The goals of treatment:
Conclusion from an acute condition (elimination of shock, stabilization of hemodynamics, restoration of heart rate, etc.);
Restoration of diuresis;
Elimination of azotemia, dyselectrolytemia;
Correction of the acid-base state;
Relief of edema, seizures;
Normalization of blood pressure;
Prevention of CKD formation, AKI transformation in CKD.
Tactics of treatment:
Treatment is divided into conservative (etiological, pathogenetic, symptomatic), surgical (urological, vascular) and active - renal replacement therapy - dialysis methods (RRT).
The principles of treatment of AKI
|
OPP form |
Treatment | Treatment methods |
| Prerenal | Conservative | Infusion and antishock therapy |
| Acute urate nephropathy | Conservative | Alkaline infusion therapy, allopurinol, |
| BPGN, allergic OTIN | Conservative | Immunosuppressive therapy, plasmapheresis |
| Postrenal | Surgical (Urological) | Elimination of acute urinary obstruction |
| Ups | Surgical | Renal Artery Angioplasty |
| OKN, 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 |
Methods of treatment and prevention |
| Preclinical stage with identification of exonephrotoxin | Intermittent GF, PFF, PA, GS |
|
Early hyperkalemia (rhabdomyolysis, hemolysis) Early decompensated acidosis (methanol) Hypervolemic hyperhydration (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 first day, then ward, general.
Diet: restriction of sodium chloride (mainly sodium) and liquid (the volume of liquid obtained is calculated taking into account the urine output of the previous day + 300 ml) with sufficient calorie content and vitamin content. 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 count of animal proteins, origin.
Drug treatment
Outpatient drug treatment
(having a 100% probability of use:
In the prehospital phase, without specifying the reasons leading to AKI, it is impossible to prescribe one or another drug.
(less than 100% probability of use)
Furosemide 40 mg 1 tablet in the morning, under the control of diuresis 2-3 times a week;
Adsorbix 1 capsule x 3 times a day - under the control of creatinine level.
Inpatient drug treatment
Essential Medicines List (having a 100% probability of use):
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 in the same dose, in the absence of effect - hemodialysis);
20% glucose 500 ml + 50 IU of insulin of soluble human short-acting intravenous cap 15-30 IU every 3 hours 1-3 days, until the normal level of potassium in the blood;
Sodium bicarbonate 4-5% in \\ in cap. Calculation of the dose according to the formula: X \u003d BE * weight (kg) / 2;
Sodium bicarbonate 8.4% in \\ in cap. Calculation of the dose according to the formula: X \u003d BE * 0.3 * weight (kg);
Sodium chloride 0.9% i.v. in a cap of 500 ml or 10% 20 ml i.v. 1-2 times a day - until the deficiency of bcc is filled
Furosemide 200-400 mg iv through perfusion, under the control of hourly urine output;
Dopamine 3 μg / kg / min in / in 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 level.
List of Additional Medicines (less than 100% probability of use):
Norepinephrine, mesotone, reftan, infezol, albumin, colloidal and crystalloid solutions, freshly frozen plasma, antibiotics, blood transfusion drugs, and others;
Methylprednisolone, tablets 4 mg, 16 mg, powder for solution for injection complete with a solvent 250 mg, 500 mg;
Cyclophosphamide, powder for the preparation of a solution for intravenous administration of 200 mg;
Torasemide, tablets 5, 10, 20 mg;
Rituximab, intravenous infusion vial 100 mg, 500 mg;
Human immunoglobulin is normal, 10% solution for infusion of 100 ml.
Drug treatment provided at the stage of emergency ambulance:
Relief of pulmonary edema, hypertensive crisis, convulsive syndrome.
Other treatments
Dialysis therapy
If it is necessary to conduct PST during AKI, the patient is dialyzed from 2 to 6 weeks, until kidney function is restored.
In the treatment of patients with AKI who require renal replacement therapy, the following questions should be answered:
When is the best time to start treatment for HRT?
What type of PTA should be used?
Which access is better?
What is the clearance level of soluble substances?
The beginning of PTA
Absolute readings to conduct PTA sessions with AKI are:
Increasing levels 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\u003e 6.5 mmol / L and / or pronounced ECG changes (bradyarrhythmia, rhythm dissociation, severe slowdown of electrical conductivity).
Hyperhydration (anasarca), resistant to drug therapy (diuretics).
To relative indications for conducting PTA sessions 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 pTA methods are: providing good nutrition, removing fluid with congestive heart failure, and maintaining adequate hydrobalance in a patient with multiple organ failure.
According to the duration of therapy The following types of RFP exist:
Intermittent (intermittent) RRT techniques lasting no more than 8 hours with a break longer than the duration of the next session (average 4 hours) (see MES stationary hemodialysis)
Extended PST methods (PST) designed to replace renal function for a long time (24 hours or more). PZPT conditionally divided into:
Half-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 constant hemo (dia) filtration)
Criteria for the selection of PZPT:
1) Renal:
AKI / PON in patients with severe cardiorespiratory insufficiency (AMI, high doses of 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 PZPT
Volume overload, providing infusion therapy
Septic shock
ARDS or ARDS risk
Severe pancreatitis
Massive rhabdomyolysis, burn disease
Hyperosmolar coma, preeclampsia of pregnant women
RFP Methods:
Intermittent and extended hemodialysis
Slow low effective hemodialysis (MNGD) (slow low effective dialysis - SLED) in the treatment of AKI - the ability to control the patient’s hydrobalance without hemodynamic fluctuations for a shorter period of time (6-8 hours - 16-24 hours).
Prolonged veno-venous hemofiltration (PHF),
Prolonged veno-venous hemodiafiltration (PVVGDF).
According to the recommendations of KDIGO (2012), in case of PZPT it is proposed to use, in contrast to 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 with a high risk of bleeding (DIC, coagulopathy), when systemic anticoagulation is absolutely contraindicated.
Continued veno-venous hemofiltration (PHF) is an extracorporeal circuit with a blood pump, a high-flux or highly porous dialyzer and a replacement fluid.
Continued veno-venous hemodiafiltration (PVVHDF) is an extracorporeal circuit with a blood pump, high-flux or highly porous dialyzer, as well as with replacement and dialysis fluids.
According to the latest data, it is recommended to use bicarbonate (not lactate) as a buffer in dialysate and a replacement fluid for RRT in patients with AKI, especially in patients with AKI and circulatory shock, also with liver failure and / or lactate acidosis.
Table 8.
Stable
Unstable
IGD
PZPT
When AKI is used as an alternative peritoneal dialysis (PD). The technique of the procedure is quite simple and its implementation does not require highly qualified personnel. It can also be used in situations where it is not possible to carry out IHD or PZPT. PD is indicated for patients with a minimal increase in catabolism, provided that the patient has no life-threatening indications for dialysis. This is ideal for patients with unstable hemodynamics. For short-term dialysis, a rigid dialysis catheter at a level of 5-10 cm below the navel is inserted into the abdominal cavity through the anterior abdominal wall. Conduct exchange infusion into the abdominal cavity of 1.5-2.0 liters of standard peritoneal dialysis solution. Possible complications include intestinal perforation during catheter insertion and peritonitis.
Acute PD provides a number of advantages in pediatric practice, which adult patients with AKI give PZPT. (see Protocol "Peritoneal dialysis").
In case of toxic AKI, sepsis, liver failure with hyperbilirubinemia, plasma exchange, hemosorption, plasma absorption using a specific sorbent is recommended.
Surgical intervention:
Installation of vascular access;
Carrying out extracorporeal treatment methods;
Elimination of urinary tract obstruction.
Therapy of postrenal acute renal injury
Treatment of postrenal AKI usually requires the participation of a urologist. The main goal 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, with obstruction due to prostatic hypertrophy, the introduction of a Foley catheter is effective. Alpha-blockers or surgical removal of the prostate may be needed. If obstruction of the urinary system is at the level of the urethra or bladder neck, a transurethral catheter is usually sufficient. At a higher level of urinary tract obstruction, the application of percutaneous nephrostomy is required. These measures usually lead to a complete restoration of diuresis, a decrease in intra-tubular pressure and restoration of glomerular filtration.
If a patient does not have CKD, it should be borne in mind that such a patient has an increased risk of developing CKD and should be managed in accordance with KDOQI Practical Recommendations. ”
Patients at risk of developing AKI (AKI) should be observed with careful monitoring of creatinine and urine volume. It is recommended that patients be divided into groups according to the degree of risk of AKI. Their management depends on 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 regime (elimination of hypothermia, stress, physical overload), diet; completion of treatment (sanitation of foci of infection, antihypertensive therapy) follow-up for 5 years (in the first year - measurement of blood pressure on a quarterly basis, blood and urine tests, determination of serum creatinine 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 worsen them, a kidney biopsy is necessary, since unfavorable morphological GN variants that require immunosuppressive therapy are likely.
Clinic of the republican level (diagnosed with AKI upon admission or SPON in diagnostic "complex" patients, or as a complication of RCT, postoperative, etc.)
The use of prolonged hemofiltration, hemodiafiltration, hemodialysis. Plasma exchange, plasma sorption - according to indications.
Stabilization, cancellation of vasopressors, stabilization of the level of urea, creatinine, acid-base and water-electrolyte balances.
With persistent anuria, edema, moderate azotemia, transfer to a hospital at the regional or city level, with the presence of an artificial kidney apparatus in the clinic (not only simple dialysis machines, but also devices for extended replacement therapy with the function of hemofiltration, hemodiafiltration).
Monitoring and regimen of PST in patients with AKI should be carried out separately from patients with ESRD (stage 5 CKD) who are on program dialysis.
ATX groups of drugs used in treatment
Hospitalization
Indications for hospitalization
Special risk groups for patients for the development of OPP:
Information
Sources and literature
- Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health and Social Development of the Republic of Kazakhstan, 2014
- 1) Acute renal damage. Tutorial. A.B.Kanatbaev, 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 Director General 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 Republican State Pedagogical University at the Perm State Pedagogical University Kazakh National Medical University Asfendiyarova ”, head of the nephrology module;
3) Gaypov Abduzhappar Erkinovich - candidate of medical sciences of JSC National Scientific Medical Center, head of the department of extracorporeal hemocorrection, nephrologist;
4) Nogaybaeva Asem Tolegenovna - JSC "National Scientific Cardiac Surgery Center" doctor nephrologist, department of the laboratory of extracorporeal hemocorrection;
5) Zhusupova Gulnar Darigerovna - candidate of medical sciences of Astana Medical University JSC, Clinical Pharmacologist, assistant at the Department of General and Clinical Pharmacology.
Indication of no conflict of interest:is absent.
Reviewers:
Sultanova Bagdat Gazizovna - Doctor of Medical Sciences, Professor of Kazakh Medical University of Continuing Education JSC, Head of the Department of Nephrology and Hemodialysis.
Indication of the conditions for revising the protocol: revision of the protocol after 3 years and / or with the advent of new methods of diagnosis / treatment with a higher level of evidence.
Attached files
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The clinic of acute renal failure includes four periods (stages):
1) the period of action of the etiological factor;
2) the period of oliguria - anuria, in which the daily diuresis is less than 500 ml (duration up to 3 weeks);
3) the recovery period of diuresis with the initial diuresis phase (when the amount of urine exceeds 500 ml per day) and with the polyuria phase (urine amount of 2-3 liters or more per day), up to 75 days;
4) the recovery period starting from the moment of normalization of azotemia.
About 10% of patients have neoliguric arrester, i.e., changes in blood biochemical parameters occur against the background of normal or even increased diuresis. The most common cause of neoliguric acute renal failure is acute interstitial nephritis.
Acute Interstitial Nephritis (SPE) - multifactorial diffuse kidney disease with a primary lesion of tubulointerstitial tissue. Morphologically, SPE is characterized by interstitial edema, more pronounced in the cerebral layer, by uneven focal infiltration by mono- and polynuclear cells. Plasma cell infiltration, dystrophy or atrophy of the tubular epithelium is characteristic. In the glomeruli, moderate segmental mesangial proliferation, an increase in the mesangial matrix, and glomerular sclerosis develop.
The most common cause of acute SPE is exposure to drugs, primarily antibiotics, as well as a number of chemicals. SPE often develops after administration of sera and vaccines. It is still not clear - why among a huge number of patients taking various drugs, SPE develops in a relatively small number of individuals. The acute onset of the disease in the first hours or days of taking the drug is considered typical for SPEs. Characteristic: fever, eosinophilia, decreased renal function, short-term allergic rash. With an expanded clinical picture, urinary syndrome is typical: hematuria, leukacituria, moderate proteinuria, eosinophilia, red blood cells are possible.
The following symptoms are characteristic of the clinical picture and course of SPE:
against the background of polyuria, an increase in plasma creatinine levels begins from the first day;
a combination of creatinemia, polyuria with proteinuria and hematuria;
lack of hyperkalemia;
develop oliguria with SPE, can quickly be replaced by polyuria, however, an increase in the level of cretinin continues.
Clinical picture
The early clinical signs (precursors) of acute renal failure are often minimal and short-lived - renal colic in postrenal acute renal failure, an episode of acute heart failure, circulatory collapse in prerenal acute renal failure. 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 in drug-induced arthritis). In addition, many early symptoms of acute renal failure (weakness, anorexia, nausea, drowsiness) are nonspecific. Therefore, laboratory methods have the greatest value for early diagnosis: determining the level of creatinine, urea and potassium in the blood.
Clinical manifestations appear in the oligoanuric period. In this period, there is a phase of “imaginary” well-being, which can last up to several days and a phase of intoxication, due to water-electrolyte disturbances, changes in acid-base balance and nitrogen-excreting kidney function. Polymorphism of signs of acute renal failure is due to clinical manifestations of disorders of 5 basic renal functions that provide homeostasis: isovolumia, isoionia, isoosmia, isohydria, azotemia. For acute renal failure, the most characteristic manifestations are:
Anuria (diuresis less than 50 ml).
Oliguria (diuresis of less than 500 ml) 400-500 mosm should be excreted daily with urine. substances (urea, creatinine, uric acid, ammonia, electrolytes), which are products of normal metabolism. With physical exertion and pathological conditions, accompanied by an increase in catabolism, this load increases. The maximum osmolarity of urine in a healthy person reaches 1200 mosm./kg, for the excretion of daily osmotic load, the volume of urine should be at least 400-500 ml. Accordingly, with a daily amount of urine less than 500 ml, the final products of nitrogen metabolism accumulate in the body.
Azotemiaincreased blood urea and creatinine.
Hyperkalemia - increasing the concentration of potassium in serum to a level of more than 5.5 meq / l
Metabolic acidosis -with a decrease in serum bicarbonates to 13 mmol / l
Heavy violationfunctions of the immune system -phagocytic function and chemotaxis of leukocytes are inhibited, antibody synthesis is suppressed, cellular immunity (lymphopenia) is disturbed. Therefore, acute infections, bacterial and fungal, develop in 30-70% of patients with acute renal failure and often determine the prognosis of the patient.
CLINICAL SYMPTOMATOLOGY OF THE BASIC WATER-ELECTROLYTIC DISORDERS AT OPN.
|
1. Extracellular dehydration |
Hypovolemia, dry, pale skin, turgor reduced, icteric sclera decreased blood pressure, pulsed pulse, shortness of breath |
|
2. Cellular dehydration |
Thirst, fever, headaches, psychomotor disorders, cramps |
|
3. Hyperhydration |
Dyspnea, edema, increased blood pressure, pulmonary edema |
|
4. Hypokalemia |
Sharp drowsiness (or coma), adynamia, speech slowed down, deep reflexes absent, paralytic intestinal obstruction, enlargement of the borders of the heart, tachycardia, arrhythmia, ECG symptoms (decreased voltage, depression of the ST segment, P wave inversion) |
|
5. Hyperkalemia |
Apathy, drowsiness, convulsions, hypotension, bradycardia, shortness of breath, arrhythmia; ECG symptoms (an increase in the T wave, a decrease in the ST interval below the isoelectric line, broadening of the QRS complex, flattening of the T wave, conduction disturbances). |
|
6. Hyponatremia |
Apathy, hypotension, tachycardia, muscle pain, orthostatic collapses, pathological respiratory rhythms. |
|
7. Hypocalcemia |
Aetania, increased neuromuscular irritability, spasm of the larynx, asphyxia. |
|
8. Hypermagnesemia |
Damage to the central nervous system (depression, mental disorders, coma). |
The duration of the oliguric phase depends on:
identifying and eliminating the causes of its development,
from the severity of kidney damage,
the effectiveness of specialized treatment.
The average duration of oliguria is 7 to 12 days. In case of poisoning with ethylene glycol, crash syndrome, obstetric and gynecological pathology, the duration of oliguria is up to 4 weeks, and with their complicated course - up to 6 weeks. When after 4 weeks of treatment there is no recovery of diuresis, then we need to think about the possible development of cortical necrosis and the formation of “primary” CRF.
Acute renal failure is a disease accompanied by a decrease in excretory function of the kidneys.
In this condition, blood azotemia and pronounced electrolyte disturbances gradually increase.
In such cases, round-the-clock monitoring of the patient's condition is necessary.
All causes of acute renal failure can be divided into 3 groups:
- Prerenal.
- Renal.
- Postrenal.
Preferred causes of acute failure:
- arterial hypotension;
- willemia;
- decentralization of blood supply;
- violation of peripheral microcirculation.
The following types of shock - posthemorrhagic, infectious, traumatic. Each of them is capable of causing rapid death of renal nephrons.
Similar pathogenetic changes also develop against the background of rapid and abundant fluid loss during burns, vomiting and an overdose of diuretics (hypochlorothiazide, furosemide).
Renal renal failure occurs under the influence of the following nosological forms:
- sepsis;
- uremic hemolytic syndrome;
- renal dysplasia;
- systemic vasculitis;
- lupus erythematosus;
- nephropathy.
Acute death of renal nephrons develops when toxins enter the bloodstream, as well as when taking medications. In some patients, acute renal failure is observed after x-ray studies (excretory radiography), the use of chemicals, anemia.
Postrenal failure occurs in the following diseases:
- Ureter stenosis.
- Foreign body of the urinary tract.
- Tumors of the urethra and pelvis.
- Inflammation of the pyelocaliceal system.
- Bacterial and viral infections.
With this type of disease, a urinary block is formed, leading to an expansion of the urinary tract above the narrowing area.
A similar situation occurs with urolithiasis, when the decrease in the lumen of the ureter is due to calculus.
The clinical picture (symptoms classification and stage)
The clinical picture of the disease depends on the pathogenetic stage of acute renal failure:
- initial;
- oligoanuria;
- polyuria;
- recovery (convalescence).
At the initial stage of the disease, the clinical picture is not accompanied by severe symptoms. They are formed gradually. The only manifestation of the initial stage of acute renal failure may be oliguria (a 10% decrease in daily urine output). Additional signs of the disease are nausea, pallor, abdominal pain, ictericity (yellowness of the skin and sclera).
The oliguric stage is characterized by a decrease in the level of urine output by 25% and is combined with a decrease in the specific gravity of urine to 1005. At the same time, the heart rate decreases in order to normalize the total blood volume. With an increase in the concentration of potassium in the blood, convulsive muscle contractions appear.
Examination of the fundus of the patient in the oliguric stage of insufficiency reveals swelling of the optic nerve head.
Such changes are quite dangerous, as they are evidence of the presence of small hemorrhages in the brain and other internal organs.
The polyuric degree of pathology is characterized by an increase in the level of urine output, against the background of which there is an increase in the level of potassium and uric acid in the blood. After its occurrence, the symptoms of blood intoxication disappear.
Pathogenetic classification
At the prerenal stage of acute renal failure, the following pathogenetic links of the pathological process can be observed:- Decrease in cardiac output;
- Impaired circulation;
- Narrowing of the peripheral vessels;
- The formation of shunts between the capillaries.
All of the above pathogenetic changes without adequate treatment lead to the appearance of a renal form of failure.
With such symptoms of acute renal failure, it is necessary to call emergency care and undergo a full examination by specialists.
What types of shock are combined with renal renal failure:
- Septic.
- Anaphylactic.
- Hypovolemic.
- Cardiogenic shock.
- Dehydration.
- Coma.
In 25% of cases, the renal form of the disease is caused by inflammatory causes (glomerulo- and pyelonephritis), interstitial nephritis, vasculitis.
With this form of the disease, additional syndromes arise:
- Hemorrhagic - small petechiae on the skin and in the vessels of the brain;
- Hypertensive - increased blood pressure due to the activation of the renin-angiotensin-aldosterone system;
- Nephrotoxic - a significant increase in urea and blood creatinine;
- Myorenal syndrome - damage to the muscles, leading to an increase in blood levels of myoglobin;
- Violation of electrolyte metabolism (hypophosphatemia, hypokalemia);
- Intoxication - an increase in temperature, the appearance of c-reactive protein in the blood;
- Allergic - an increase in the concentration of immunoglobulins in the blood.
The postrenal form of the disease occurs in the following diseases:
Retroperitoneal fibrosis
- Urinary tract obstruction;
- Tumors
- Schistosomiasis of the ureter and bladder;
- Narrowing of the urethra;
- Papillitis necrotic;
- Spinal cord injuries;
- Retroperitoneal fibrosis;
- The narrowing of the vessels of the nephron.
Diagnostics
Diagnosis of acute renal failure is based on the use of the following methods:
- Clinical examination;
- Urine and blood tests
- Clinical and instrumental methods.
It is important to begin treatment of the disease in the early stages in order to prevent the death of a functional renal unit - nephron.
The main task of the doctor in case of suspected presence of this pathology in the patient is to determine the level of urine in the bladder (using ultrasound), to analyze the concentration of potassium and creatinine in serum.
The next step in the diagnostic procedures is to determine the form of the disease (prerenal, renal or postrenal). First, obstruction of the pelvis and urethra (ultrasound, excretory urography, endoscopy, and radionuclide diagnosis) should be excluded.
You may not have guessed that the causes of the same kidney disease in children, adults and the elderly may be different. Read more - as well as various methods of treatment - folk and conservative methods.
Read about the proper diet for dialysis patients.
And here is a detailed classification of the stages of chronic renal failure. The clinical picture and prevalence of the disease.
What urine tests show
In renal failure, urine and blood tests are an important diagnostic method that allows not only to identify the disease, but also to monitor the effectiveness of its treatment.
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Treatment of acute renal failure
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