Used as an alternative for AKI 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 IHD or CRRT is not available. PD is indicated for patients with minimal increased catabolism, provided the patient does not have a life-threatening indication for dialysis. This is an ideal option 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. An exchange infusion of 1.5-2.0 liters of standard peritoneal dialysis solution is carried out into the abdominal cavity. Possible complications include bowel perforation during catheter insertion and peritonitis.

Acute PD provides many of the same benefits in pediatric patients that CRRT provides to adult patients with AKI. (See Peritoneal Dialysis Protocol).

In case of toxic AKI, sepsis, liver failure with hyperbilirubinemia, plasma exchange, hemosorption, plasma sorption using a specific sorbent are recommended.

Surgical intervention:

Installation of vascular access;

Carrying out extracorporeal treatment methods;

Elimination of urinary tract obstruction.

Therapy for postrenal acute kidney injury

Treatment of postrenal AKI usually requires the participation of a urologist. The main goal of therapy is to eliminate the disturbance in the outflow of urine as quickly as possible in order to avoid irreversible damage to the kidney. For example, for obstruction due to prostatic hypertrophy, insertion of a Foley catheter is effective. Alpha-blocker therapy or surgical removal of the prostate gland may be necessary. If the obstruction of the urinary system is at the level of the urethra or bladder neck, the installation of a transurethral catheter is usually sufficient. At higher levels of urinary tract obstruction, a percutaneous nephrostomy tube is required. These measures usually lead to complete restoration of diuresis, a decrease in intratubular pressure and restoration of glomerular filtration.

If a patient does not have CKD, it should be kept 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 with close monitoring of creatinine and urine output. It is recommended to divide patients into groups according to the degree of risk of developing AKI. Their management depends on predisposing factors. Patients should be evaluated first to identify reversible causes of AKI so that these factors (eg, postrenal) can be addressed promptly.

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

Republican-level clinic (diagnosed with AKI upon admission or MODS in diagnostically “difficult” patients, or as a complication of RCT, postoperative, etc.)

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

Stabilization of the condition, withdrawal of vasopressors, stabilization of urea, creatinine, acid-base and water-electrolyte balances.

If anuria, edema, moderate azotemia persists, 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 prolonged replacement therapy with the function of hemofiltration, hemodiafiltration).

Observation and RRT regimens in patients with AKI should be carried out separately from patients with ESRD (stage 5 CKD) undergoing program dialysis.

Groups of drugs according to ATC used in treatment

Hospitalization

Indications for hospitalization

Special risk groups of patients on the development of APP:

Information

Sources and literature

Minutes of meetings of the Expert Council of the RCHR of the Ministry of Health of the Republic of Kazakhstan, 2014
1. 1) Acute kidney 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 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 Russian State Enterprise at the PVC “Kazakh National Medical University named after S.D. Asfendiyarov”, head of the nephrology module;

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

4) Nogaibaeva Asem Tolegenovna - JSC “National Scientific Cardiac Surgery Center”, nephrologist in the department of extracorporeal hemocorrection laboratory;

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

Disclosure of no conflict of interest: 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 reviewing the protocol: revision of the protocol after 3 years and/or when new diagnostic/treatment methods with a higher level of evidence become available.

Attached files

Attention!

By self-medicating, you can cause irreparable harm to your health.
The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact a medical facility if you have any illnesses or symptoms that concern you.
The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
The MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are exclusively information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.

Acute renal failure (ARF) is a rapid, but reversible, depression of renal function, sometimes to the point of complete failure of one or both organs. The 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 function increases greatly.

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 fulfill their functional task, doctors provide emergency medical care to the person, diagnosing him with acute renal failure. The somatic pathology code 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 acute renal failure are as follows:

Pathologies of the cardiovascular system that disrupt the blood supply to all organs, including the kidneys:
- arrhythmia;
- atherosclerosis;
- heart failure.
Dehydration against the background of the following ailments, which causes changes in blood parameters, or more precisely, an increase in its prothrombin index, and, as a consequence, difficulty in the functioning of the glomeruli:
- dyspeptic syndrome;
- extensive burns;
- blood loss.
Anaphylactic shock, which is accompanied by a sharp decrease in blood pressure, which negatively affects kidney function.
Acute inflammatory phenomena in the kidneys, which lead to damage to organ tissue:
- pyelonephritis.
A physical obstruction to the outflow of urine during urolithiasis, which first leads to hydronephrosis, and then, due to pressure on the kidney tissue, to damage to the kidney tissue.
Taking nephrotoxic drugs, which include a contrast composition for X-rays, causes poisoning of the body, which the kidneys cannot cope with.

Classification of surge arresters

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

Prerenal acute renal failure - the cause of the disease is not directly related to the kidneys. The most popular example of a prerenal type of acute renal failure can be called disturbances in the functioning of the heart, which is why the pathology is often called hemodynamic. Less commonly, it occurs due to dehydration.
Renal acute renal failure - the root cause of the pathology can be found precisely in the kidneys themselves, and therefore the second name of the category is parenchymal. Renal functional failure in most cases results from acute glomerulonephritis.
Postrenal acute renal failure (obstructive) is a form that occurs when the urine excretion pathways are blocked by stones and subsequent disruption of urine outflow.

Classification of acute renal failure

Pathogenesis

ARF develops over four periods, which always follow in the specified 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 refers to a decrease in urine volume. Normally, a person should excrete approximately the amount of fluid that he consumed, minus the portion “spent” by the body on sweating and breathing. With oliguria, the volume of urine becomes less than half a liter, without a direct connection with the amount of fluid drunk, which entails an increase in fluid and breakdown products in the body tissues.

Complete disappearance of diuresis occurs only in extremely severe cases. And statistically it rarely happens.

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

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

After completion of the polyuric stage, the person, if the situation develops favorably, recovers. However, it is important to know that this period may last for one year, during which deviations in the interpretation of analyzes will be identified.

Stages of acute renal failure

Clinical picture

The initial stage of acute renal failure does not have specific symptoms by which the disease can be unmistakably recognized; 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:

With oliguric syndrome against the background of acute renal failure, the symptoms become specific, easily recognizable and fit into the overall picture of the pathology:
- decreased diuresis;
- dark, foamy urine;
- dyspepsia;
- lethargy;
- wheezing in the chest due to fluid in the lungs;
- susceptibility to infections due to reduced immunity.
The polyuric (diuretic) stage is characterized by an increase in the amount of urine excreted, so all the patient’s complaints stem from this fact, and the fact that the body loses a large amount of potassium and sodium with urine:
- disturbances in the functioning of the heart are recorded;
- hypotension.
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, red blood cells, protein), blood (total protein, hemoglobin, ESR, urea).

Diagnostics

Diagnosis of acute renal failure is carried out using:

questioning and examining the patient, compiling his anamnesis;
clinical blood test showing low hemoglobin;
biochemical blood test, which detects increased creatinine, potassium, urea;
diuresis monitoring, that is, control over how much liquid (including soups, fruits) a person consumes in 24 hours and how much is excreted;
ultrasound method, in acute renal failure more often shows the physiological size of the kidneys; a decrease in size indicators is a bad sign, indicating tissue damage, which may be irreversible;
nephrobiopsy - taking a piece of an organ using a long needle for microscopic examination; It is performed infrequently due to the high degree of trauma.

Treatment

Treatment of acute renal failure occurs in the intensive care unit of the hospital, less often in the nephrology department of the hospital.

All medical procedures performed by doctors and medical staff can be divided into two stages:

Identification of the root cause of a pathological condition is carried out using diagnostic methods, studying symptoms, and specific complaints of the patient.
Eliminating the cause of acute renal failure is the most important stage of treatment, because without treating the root cause of the disease, any treatment measures will be ineffective:
- when the negative effect of nephrotoxins on the kidneys is detected, extracorporeal hemocorrection is used;
- If an autoimmune factor is detected, glucocorticosteroids (Prednisolone, Metipred, Prenizole) and plasmapheresis are prescribed.
- in case of urolithiasis, drug litholysis or surgery is performed to remove stones;
- For infection, antibiotics are prescribed.

At each stage, the doctor adjusts the prescription 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, and, if necessary, hemodialysis.

Hemodialysis, a procedure for cleansing the blood of waste products and removing excess fluid from the body, has an ambiguous attitude among nephrologists. Some doctors argue that prophylactic hemodialysis for acute renal failure is necessary in order to reduce the risk of complications. Other experts warn of a trend towards 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 missing blood volume, restore the electrolyte balance in the body, continue diet No. 4, and take care of any infection, especially when taking hormonal medications.

General principles of treatment of acute renal failure

Prognosis and complications

Acute renal failure with proper treatment has a favorable prognosis: after suffering the disease, only 2% of patients require 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 during oliguria or when the rate of blood filtration by glomeruli is low.

Pathology leads to:

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

It is important to note that with acute nephrological failure, unlike chronic failure, complications rarely occur.

Prevention

Prevention of acute renal failure is as follows:

Avoid taking nephrotoxic medications.
Treat chronic diseases of the urinary and vascular system in a timely manner.
Monitor blood pressure readings, and if signs of chronic hypertension are detected, immediately consult a specialist.

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

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Archive - Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2010 (Order No. 239)

Acute renal failure, unspecified (N17.9)

general information

Short description

Acute renal failure(AKI) is a nonspecific syndrome that develops as a result of acute transient or irreversible loss of homeostatic functions of the kidneys caused by hypoxia of the renal tissue with subsequent primary damage to the tubules and edema of the interstitial tissue. The syndrome is manifested by increasing azotemia, electrolyte imbalance, decompensated metabolic acidosis and impaired ability to excrete water. The severity of the clinical picture of acute renal failure is determined by the relationship between the degrees of involvement of tubules, interstitial tissue and glomeruli in the pathological process.

Protocol"Acute renal failure"

ICD-10:

N17 Acute renal failure

N17.0 Acute renal failure with tubular necrosis

N17.1 Acute renal failure with acute cortical necrosis

N17.2 Acute renal failure with medullary necrosis

N17.8 Other acute renal failure

N17.9 Acute renal failure, unspecified

Classification

1. Prerenal causes.

2. Renal reasons.

3. Postrenal causes.

During acute renal failure, there are 4 stages: pre-nuric, oligoanuric, polyuric and recovery.

Diagnostics

Diagnostic criteria

Complaints and anamnesis: acute intestinal infection, hypovolemia, loose stools, vomiting, decreased diuresis.

Physical examination: pallor of the skin and mucous membranes, oligoanuria, edema syndrome, arterial hypertension.

Laboratory research: hyperazotemia, hyperkalemia, decreased red blood counts.

Instrumental studies: Ultrasound of the abdominal organs and kidneys - enlarged kidneys, hepatomegaly, ascites. X-ray of the chest organs - pleurisy, signs of cardiopathy.

Indications for consultation with specialists:

Gastroenterologist - dyspeptic disorders;

Cardiologist - ECG abnormalities, arterial hypertension;

Ophthalmologist - to assess changes in retinal vessels;

Neurologist - uremic encephalopathy;

ENT doctor - stopping nosebleeds, sanitation of infections of the nasopharynx and oral cavity;

Infectious disease specialist - viral hepatitis, zoonoses.

List of main additional diagnostic measures:

3. Blood biochemistry (detailed).

4. Coagulogram.

6. Urine culture tank 3 times.

7. HBsAg, RW, HIV.

8. ELISA for markers of viral hepatitis.

9. Blood testing for all types of zoonoses.

10. Coprogram.

11. Bacterial culture of stool 3 times.

12. Computed tomography of the kidneys.

13. Urinalysis according to Zimnitsky.

14. Ultrasound of the abdominal organs and kidneys.

16. X-ray of the chest organs.

17. Blood type, Rh affiliation.

Before emergency hospitalization: OBC, OAM, blood biochemistry, kidney ultrasound.

Differential diagnosis

Differential diagnosis of functional and organic acute renal failure, differential diagnosis of acute renal failure with acute decompensation of latent chronic renal failure.

Treatment abroad

Get treatment in Korea, Israel, Germany, USA

Get advice on medical tourism

Treatment

Treatment tactics

Treatment goals: elimination of symptoms of acute renal failure, restoration of diuresis, acidosis, electrolyte disturbances, correction of renal anemia and arterial hypertension.

Non-drug treatment: gentle regimen, table 16, 7, hemodialysis, hemosorption, plasmapheresis.

Drug treatment:

6. Activated carbon, tablets 250 mg No. 50.

7. Calcium gluconate 10% - 5.0 No. 10.

15. Epoetin, powder 1000 IU 100-150 IU/kg/week (Recormon).

16. Etamsylate, solution for injection 12.5% -2.0 No. 10 (dicinone).

21. Polyhydroxyethyl starch, solution for intravenous administration 60 mg/ml - 250.0 No. 3 (refortan, stabizol).

27. Papaverine, solution for injection 2% -1.0 No. 10.

28. Drotaverine, injection solution 40 mg/2 ml in ampoules No. 10 (no-spa).

29. Platyphylline hydrotartrate, solution for injection 0.2% -1.0 in ampoules No. 10.

30. Korglykon solution for injection 0.06% -1.0 No. 10.

38. Aminophylline, injection solution 2.4% -5.0 No. 10 (aminophylline).

46. Ascorbic acid, injection solution 10% -2.0 No. 10 (vitamin C).

47. Pyridoxine, injection solution 1% -1.0 No. 10 (pyridoxine hydrochloride).

49. Tocopherol acetate, oil solution in ampoules 10% -1.0 No. 10 (vitamin E, etovite).

Preventive actions: eliminating the causes of acute renal failure.

Further management: observation for 3-6-12 months by a pediatric nephrologist, exemption from preventive vaccinations for 3 years.

List of basic and additional medications:

1. Diazepam, solution 10 mg/day. (Valium, Seduxen, Relanium, Bruzepam, Sibazon).

2. Oxygen, for inhalation (medical gas).

3. Ketoprofen solution 100 mg/day. (ketonal, ketoprofen).

4. Paracetamol, tablets 500 mg/day.

5. Prednisolone, solution 30 mg/ml/day.

6. Activated carbon, tablets 250 mg, No. 50.

7. Calcium gluconate 10% - 5.0 No. 10.

8. Amoxicillin + clavulanic acid, tablets 375 mg No. 30 (amoxiclav, augmentin).

9. Cefazolin, powder for preparations. injection solution 1000 mg/day. (kefzol, cefzol).

10. Cefuroxime, powder for preparations. injection solution 750 mg (zinacef).

11. Ceftriaxone, powder for preparation. injection solution 1000 mg/day. (rocephin).

12. Co-trimoxazole, tab. 480 mg/day. (bactrim, biseptol).

13. Pipemidic acid, tab. 400 mg No. 30 (palin, urotractin, pipemidine, pimidel).

14. Fluconazole, capsules 50 mg/day. (Diflucan, Mikosist).

15. Epoetin, powder 1000 IU, 100-150 IU/kg/week (Recormon).

16. Etamsylate, solution for injection 12.5% -2.0 No. 10 (dicinone).

17. Dipyridamole, tab. 25 mg No. 90 (chimes, persantine).

18. Nadroparin calcium, injection solution 0.3 No. 10 (fraxiparin).

19. Polividone, solution in bottles 6% -200.0 No. 3 (hemodez).

21. Polyhydroxyethyl starch, solution for intravenous administration 60 mg/ml-250.0 No. 3 (refortan, stabizol).

22. Albumin, solution 5%, 10%, 20%, No. 3.

23. Atenolol, tab. 50 mg/day. (atenova, atenol, atenolan).

24. Nifedipine, tab. 10 mg/day. (adalat, cordafen, cordipine, nifecard).

25. Amlodipine, tab. 5 mg/day. (norvask, stamlo).

26. Enalapril, tab. 10 mg/day. (enap, enam, ednit, renitek, berlipril).

27. Papaverine, injection solution 2% - 1.0 No. 10.

28. Drotaverine, injection solution 40 mg/2 ml in ampoules, No. 10 (no-spa).

29. Platyphylline hydrotartrate, injection solution 0.2% - 1.0 in ampoules, No. 10.

30. Korglykon injection solution 0.06% -1.0 No. 10.

31. Digoxin, tab. 62.5 mcg/day. (lanicor).

32. Dopamine, solution for injection in ampoules 0.5% -5.0/day. (dopamine).

33. Furosemide, tab. 40 mg/day. (Lasix).

34. Famotidine, tab. 20 mg/day. (famosan, gastrosidin, kvamatel).

35. Oral rehydration salts, powder in sachets/day. (rehydron).

36. Lyophilized bacteria, lyophilized powder in bottles of 3 and 5 doses, capsules (Linex, Bifidumbacterin, Lactobacterin, Bificol, Biosporin).

37. Sterile concentrate of metabolic products of intestinal microflora, drops for oral administration (hilak forte).

38. Aminophylline, injection solution 2.4% - 5.0 No. 10 (aminophylline).

39. Complex of amino acids for parenteral nutrition, solution for infusion 250.0 No. 3 (infezol).

40. Aprotinin, solution for injections and infusions 100 EIC in ampoules of 5 ml No. 20 (Gordox, Contrical).

41. Sodium chloride, solution for injection 0.9% -500.0/day.

42. Water for injection, solution for injection 1 ml, 2 ml, 5 ml/day.

44. Potassium chloride, injection solution 4% -10.0/day.

45. Sodium bicarbonate, powder/day.

46. Ascorbic acid, injection solution 10% - 2.0 No. 10 (vitamin C).

47. Pyridoxine, injection solution 1% - 1.0 No. 10 (pyridoxine hydrochloride).

48. Thiamine, injection solution 5% - 1.0 No. 10 (thiamine chloride).

49. Tocopherol acetate, oil solution in ampoules 10% - 1.0 No. 10 (vitamin E, etovite).

50. Folic acid, tab. 1 mg, No. 90.

51. Cyanocobalamin, injection solution 200 mcg, No. 10.

Indicators of treatment effectiveness:

No signs of acute renal failure;

Restoration of spontaneous diuresis;

Normalization of the concentration of nitrogenous wastes in the blood;

No acidosis;

Normalization of blood pressure;

Target hemoglobin and hematocrit levels.

Hospitalization

Indications for hospitalization: hyperazotemia, hyperkalemia, metabolic acidosis. Emergency hospitalization.

Information

Sources and literature

Protocols for diagnosis and treatment of diseases of the Ministry of Health of the Republic of Kazakhstan (Order No. 239 of 04/07/2010)
1. 1. Naumova V.I., Papayan A.V. Kidney failure in children. - L.: Medicine, 1991. - 288 p.: ill. - (a practical doctor). 2. Papayan A.V., Savenkova N.D. Clinical nephrology of childhood. - Guide for doctors. - SOTIS, St. Petersburg. - 1997.

Information

List of developers:

Attached files

Attention!

By self-medicating, you can cause irreparable harm to your health.
The information posted on the MedElement website and in the mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Guide" cannot and should not replace a face-to-face consultation with a doctor. Be sure to contact a medical facility if you have any illnesses or symptoms that concern you.
The choice of medications and their dosage must be discussed with a specialist. Only a doctor can prescribe the right medicine and its dosage, taking into account the disease and condition of the patient’s body.
The MedElement website and mobile applications "MedElement", "Lekar Pro", "Dariger Pro", "Diseases: Therapist's Directory" are exclusively information and reference resources. The information posted on this site should not be used to unauthorizedly change doctor's orders.
The editors of MedElement are not responsible for any personal injury or property damage resulting from the use of this site.

Acute renal failure code ICD. Acute kidney failure (acute kidney injury)

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 the RVC "Republican Center"
healthcare development"

Ministry of Health
and social development

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

In 2004, ADQI (Acute Dialysis Quality Initiative) proposed the concept of “acute kidney injury” (AKI), replacing the term “acute kidney failure” and a classification called RIFLE according to the first letters of each of the sequentially identified stages of AKI: Risk, damage (Injury), failure (Failure), loss (Loss), end-stage chronic renal disease (End stage renal disease) - table 2.

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

I. INTRODUCTORY PART:

Protocol name: Acute kidney failure (acute kidney injury)

Protocol code:

ICD-10 code(s):

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 Study Group

LVAD Left Ventricular Assist Device

KDIGO Kidney Disease Improving Global Outcomes - Initiative to improve global outcomes in kidney disease

MDRD Modification Diet of Renal Disease

RVAD Right Ventricular Assist Device

NOS Not otherwise specified

ARB-II Angiotensin-II receptor blockers

HRS Hepatorenal syndrome

HUS Hemolytic-uremic syndrome

Gastrointestinal bleeding

RRT Renal replacement therapy

IHD Intermittent (periodic) hemodialysis

Mechanical ventilation

ACEI Angiotensin-converting enzyme inhibitors

CI- AKI Contrast - induced AKI

acid alkaline state

NSAIDs Nonsteroidal anti-inflammatory drugs

AKI Acute renal failure

AKI Acute kidney injury

ATN Acute tubular necrosis

OTIN Acute tubulointerstitial nephritis

BCC Volume of circulating blood

ICU Intensive Care Unit

CRRT Continuous renal replacement therapy

PHF Continuous venovenous hemofiltration

PVVHD Continuous venovenous hemodialysis

PVVGDF Continuous venovenous hemodiafiltration

GFR Glomerular filtration rate

RIFLE Risk, damage, failure, loss, ESRD

ESRD End-stage chronic renal failure

CRF Chronic renal failure

CKD Chronic kidney disease

CVP Central venous pressure

ECMO Extracorporeal membrane oxygenation

Date of development of the protocol: year 2014.

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

Classification

Classification

Causes and classifications of AKI

According to the main development mechanism AKI 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 diuresis value There are 2 forms:

Oliguric (diuresis less than 500 ml/day);

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

Additionally there are:

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 AKI/AKI do not have information about the initial state of renal function, the basal level of creatinine, related to the age and sex of the patient, is calculated at a given level of GFR (75 ml/min) using the MDRD formula using the ADQI proposed by experts (Table 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

Classification of AKI by RIFLE classes (2004) - table 2

Classes	Glomerular filtration criteria	Criteria for diuresis
Risk	Scr* by 1.5 times or ↓ CF** 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 kidney function	Persistent AKI; complete loss of renal function >4 weeks
End-stage renal failure	ESRD>3 months

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

Table 4. Stages of AKI (KDIGO, 2012)

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of basic diagnostic measures

Basic (mandatory) diagnostic examinations performed on an outpatient basis:

After discharge from 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 performed on an outpatient basis:

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

Rheumatoid factor;

Doppler ultrasound of renal vessels;

Ultrasound of the abdominal organs.

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

Due to the need for urgent emergency hospitalization, data on the volume of urine excreted (oliguria, anuria) and/or increased creatinine, according to the diagnostic criteria of paragraph 12.3, is sufficient.

Basic (mandatory) diagnostic examinations carried out at the hospital 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;

Coagulogram (PT-INR, APTT, fibrinogen);

General urine test (if diuresis is present!);

Ultrasound of the kidneys;

Notes:

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

All urgent admissions must be accompanied by 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 RRT and prognosis should be determined, and the patient should be sent to a multidisciplinary hospital with an extracorporeal hemocorrection department.

Additional diagnostic examinations carried out at the hospital level:

Urinalysis according to Zimnitsky;

Rehberg test (daily);

Daily albuminuria/proteinuria or albumin/creatinine ratio, protein/creatinine ratio;

Urine protein electrophoresis + urine M-gradient;

Excretion of potassium, sodium, calcium in urine;

Daily excretion of uric acid;

Urine test for Bence 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 tests: 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 renal vessels;

X-ray of the chest organs;

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 damage is suspected, if paraneoplastic nephropathy is suspected to exclude neoplasms, metastatic lesions; in case of sepsis - to search for the primary source of infection);

Urine osmolality, urine osmolality;

Needle biopsy of the kidney (used for AKI in difficult diagnostic cases, indicated for renal AKI of unknown etiology, AKI with a period of anuria lasting more than 4 weeks, AKI associated with nephrotic syndrome, acute nephritic syndrome, diffuse lung damage such as necrotizing vasculitis);

Biopsy of the skin, muscles, rectal mucosa, gums - to diagnose amyloidosis, as well as to verify 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 (RFMC, ethanol test, antithrombin III, platelet functions);

CT/MRI of the brain;

MRI of the thoracic segment, abdominal segment, pelvic organs (if a systemic disease with multiple organ damage 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 cultures three times for sterility from both hands;

Blood culture for blood culture;

Cultures 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 a 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 a neoplasm if a paraneoplastic process is suspected.

Diagnostic measures carried out at the stage of emergency care:

Collection of complaints and medical history, data regarding contact with a toxic substance;

Data on hydrobalance, diuresis;

Physical examination;

Blood pressure measurement, blood pressure correction, 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 absence 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). If you have recently had gastroenteritis or bloody diarrhea, you 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;

Presence of arterial hypertension, diabetes mellitus or malignant neoplasms (possibility of hypercalcemia);

Increased urge and weakened 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;

Determine what medications the patient took and whether there were any cases of intolerance to these drugs. The following intake deserves special attention: ACE inhibitors, ARB-II, NSAIDs, aminoglycosides, administration of radiocontrast agents. Find out contact with toxic, poisonous substances;

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

Information about kidney disease 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 renal dysfunction: AKI or CKD?

Violation of renal blood flow - arterial or venous.

Are there any disturbances in the outflow of urine due to obstruction?

History of kidney disease, exact diagnosis?

Physical examination

The main directions for a physical examination are as follows:

Assessing the degree of hydration of the body is of paramount importance for determining the management of the patient (thirst, dry skin, mucous membranes or the presence of edema; weight loss or gain; central venous pressure level; shortness of breath).

Skin color, rashes. Thermometry.

Assessment of the central nervous system

Assessing the condition of the lungs (swelling, wheezing, bleeding, etc.).

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

Presence of hepatosplenomegaly, reduction in liver size.

Palpation can reveal enlarged kidneys with polycystic diseases, an enlarged bladder with tumors, and urethral obstruction.

Assessment of diuresis (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.

Period of development of oliguria:

Oliguria, anuria;

Peripheral and cavitary edema;

Rapidly increasing hyponatremia with nausea, convulsions with headache, and confusion is a harbinger of cerebral edema;

Clinical manifestations of azotemia are anorexia, uremic pericarditis, ammonia odor 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 disseminated intravascular coagulation),

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 are typical);

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

Period of diuresis recovery:

Normalization of nitrogen excretion 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:

UAC: 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).

Blood acid base: acidosis, decreased bicarbonate levels.

Differential diagnostic laboratory signs.

Research	Characteristic	Causes of AKI
Urine	Red blood cell casts, dysmorphic red blood cells Proteinuria ≥ 1g/l	Glomerular diseases Vasculitis TMA
	. Leukocytes, leukocyte casts	OTIN
	Proteinuria ≤ 1g/l Low molecular weight proteins Eosinophiluria	OTIN Atheroembolic disease
	. Visible hematuria	Postrenal causes Acute GN 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 paraproteinemias
	. uric acid	Tumor lysis syndrome
	. LDH	GUS
	. Creatine kinase	Injuries and metabolic diseases
Biochemical	. Na+, creatinine to calculate the excreted fraction of Na (FENa)	Prerenal and renal AKI
Biochemical	. Bence Jones squirrels	Multiple myeloma
Specific immunological studies	. ANA, anti-double-stranded DNA antibodies	SLE
	. p- and s-ANCA	Small vessel vasculitis
	. anti-GBM antibodies	Anti-GBM nephritis (Goodpasture syndrome)
	. ASL-O titer	Poststreptococcal GN
	. Cryoglobulinemia, sometimes + rheumatoid factor	Cryoglobulinemia (essential or in various diseases)
	. Antiphospholipid antibodies (anticardiolipin antibodies, lupus anticoagulant)	APS syndrome
	. ↓С 3, ↓С 4, СН50	SLE, infective endocarditis, shunt nephritis
	. ↓ C 3, CH50	Poststreptococcal 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 studies:

. 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 (renal artery stenosis, dissecting aneurysm of the abdominal aorta, ascending thrombosis of the inferior vena cava).

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

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

. Computed and magnetic resonance imaging.

. Kidney biopsy according to indications: used for AKI in complex diagnostic cases, indicated for renal AKI of unknown etiology, AKI with a period of anuria prolonged over 4 weeks, AKI associated with nephrotic syndrome, acute nephritic syndrome, diffuse lung damage such as necrotizing vasculitis.

Indications for consultation with specialists:

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

Consultation with a hematologist - 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 source of infection with subsequent sanitation;

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

Consultation with a urologist - for the diagnosis and treatment of postrenal AKI;

Consultation with a traumatologist - for injuries;

Consultation with a dentist - to identify foci of chronic infection with subsequent sanitation;

Consultation with an obstetrician-gynecologist - for pregnant women; if gynecological pathology is suspected; in order to identify foci of infection and their subsequent sanitation;

Consultation with an ophthalmologist - to assess changes in the fundus;

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

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

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

Consultation with a psychotherapist is a mandatory consultation with conscious patients, 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 conscious refusal of treatment.

Consultation with 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

For disorders 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	AKI	CKD
Diuresis	Oligo-, anuria → polyuria	Polyuria→Anuria
Urine	Normal, 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 on CKD and CKD.

Signs	AKI	AKI on CKD	CKD
History of renal disease	No or short	Long	Long
Creatinine in the blood before AKI	Normal	Promoted	Promoted
Creatinine in the blood against the background of AKI	Promoted	Significantly increased	Promoted
Polyuria	rarely	No	Almost always
History of polyuria before AKI	No	Long-term	Long-term
AG	rarely	Often	Often
SD	rarely	Often	Often
History of nocturia	No	Eat	Eat
Causing factor (shock, trauma..)	Often	Often	Rarely
Acute increase in creatinine >44 µmol/l	Always	Always	Never
Kidney sizes ultrasound	Normal or enlarged	Normal or reduced	Reduced

To confirm the diagnosis of AKI, its postrenal form is first 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, and antegrade pyelography are used to verify obstruction. To diagnose renal artery occlusion, ultrasound and renal X-ray contrast angiography are indicated.

Differential diagnosis of prerenal and renal AKI .

Indicators	AKI
Indicators	prerenal	Renal
Relative density of urine	> 1020	< 1010
Urine osmolarity (mosm/kg)	> 500	< 350
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
Ratio of urine urea to plasma urea	> 8	< 3
Ratio of urine creatinine to plasma creatinine	> 40	< 20
Renal Failure Index 2	< 1	> 1

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

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

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

High extrarenal losses

Reducing fluid intake in the body

Urine passing through unnatural pathways

Hot climate

Fever

Diarrhea

Gastrostomy

mechanical ventilation

Psychogenic oligodipsia

Water shortage

Esophageal tumors

Rumination

Esophageal achalasia

Esophageal strictures

Nausea

iatrogenic

Cloaca (vesico-rectal junction)

Urinary tract injuries

Urine leakage with nephrostomy

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Treatment

Treatment goals:

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

Restoration of diuresis;

Elimination of azotemia, diselectrolythemia;

Correction of acid-base status;

Relieving swelling, cramps;

Normalization of blood pressure;

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 treatment of AKI

OPP form	Treatment	Treatment methods
Prerenal	Conservative	Infusion and antishock therapy
Acute urate nephropathy	Conservative	Alkalinization infusion therapy, allopurinol,
RPGN, allergic ATIN	Conservative	Immunosuppressive therapy, plasmapheresis
Postrenal	Surgical (urological)	Relief of acute urinary tract obstruction
UPS	Surgical	Angioplasty of the renal arteries
OKN, myorenal syndrome, MODS	Active (dialysis)	Acute HD, hemodiafiltration (HDF), acute PD

Application of dialysis techniques in different stages of AKI(approximate diagram)

Manifestations and stages of renal AKI	Methods of treatment and prevention
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
AKI	Intermittent HD, acute PD, PGF
OPPN	Plasmasorption, hemofiltration, hemodiafiltration, Albumin dialysis

Non-drug treatment

Mode bed the first day, then ward, general.

Diet: restriction of table salt (mainly sodium) and fluid (the volume of fluid received is calculated taking into account diuresis for the previous day + 300 ml) with sufficient caloric intake and vitamin content. In the presence of edema, especially during the period of its increase, 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 body weight, mainly due to account of animal proteins, origin.

Drug treatment

Drug treatment provided on an outpatient basis

(having a 100% probability of application:

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

(less than 100% chance of application)

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

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

Drug treatment provided at the inpatient level

List of essential medicines(having a 100% probability of application):

Potassium antagonist - calcium gluconate or chloride 10% 20 ml IV for 2-3 minutes No. 1 (if there are no changes on the ECG, repeated administration in the same dose, if there is no effect - hemodialysis);

20% glucose 500 ml + 50 IU of soluble human short-acting insulin intravenously 15-30 units every 3 hours for 1-3 days, until the level of potassium in the blood normalizes;

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

Sodium bicarbonate 8.4% w/drops. Dose calculation using the formula: X = BE * 0.3 * weight (kg);

Sodium chloride 0.9% intravenously 500 ml or 10% 20 ml intravenously 1-2 times a day - until the deficit of bcc is replenished;

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

Dopamine 3 mcg/kg/min intravenously for 6-24 hours, under blood pressure control, heart rate - 2-3 days;

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

List of additional medicines(less than 100% chance of application):

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

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

Cyclophosphamide, powder for solution for intravenous administration 200 mg;

Torasemide, tablets 5, 10, 20 mg;

Rituximab, vial for intravenous infusion 100 mg, 500 mg;

Human immunoglobulin normal, 10% solution for infusion 100 ml.

Drug treatment provided at the emergency stage:

Relief of pulmonary edema, hypertensive crisis, convulsive syndrome.

Other treatments

Dialysis therapy

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

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

When is the best time to start SRT treatment?

What type of RRT should I use?

Which access is best?

What level of clearance of soluble substances should be maintained?

Start of PRT

Absolute indications for conducting RRT sessions 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 pronounced changes on the ECG (bradyarrhythmia, rhythm dissociation, severe slowing of electrical conduction).

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

To relative indications for conducting RRT 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 developing clinical manifestations of uremic intoxication.

Indications for “renal support” RRT methods are: providing adequate nutrition, removing fluid in congestive heart failure, and maintaining adequate fluid balance in a patient with multiple organ failure.

By duration of therapy There are the following types of PTA:

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 inpatient hemodialysis)

Extended RRT (CRRT) methods are designed to replace kidney function over a long period of time (24 hours or more). CRRT is conventionally divided into:

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

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

Constant for more than a day (see MES constant hemo(dia)filtration)

CRRT selection criteria:

1) Renal:

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

AKI/MOF due to high hypercatabolism (sepsis, pancreatitis, mesenteric thrombosis, etc.)

2) Extrarenal indications for CRRT

Volume overload, provision of infusion therapy

Septic shock

ARDS or risk of ARDS

Severe pancreatitis

Massive rhabdomyolysis, burn disease

Hyperosmolar coma, preeclampsia in pregnancy

RRT methods:

Hemodialysis intermittent and extended

Slow low effective dialysis (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).

Extended venovenous hemofiltration (PGF),

Extended venovenous hemodiafiltration (PVVHDF).

According to the recommendations of KDIGO (2012), for CRRT 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 at high risk of bleeding (DIC, coagulopathy) when systemic anticoagulation is absolutely contraindicated.

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

Continuous venovenous hemodiafiltration (CVVHDF) is an extracorporeal circuit with a blood pump, a high-flow or high-porous dialyzer, as well as replacement and dialysate fluids.

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

Table 8.

Stable

Unstable

IGD

CRRT

Severe hyperphosphatemia

Stable/unstable

CRRT

Brain swelling

Unstable

CRRT

Short-acting human insulin