The clinical picture of acute renal failure includes four periods (stages):

1) period of action of the etiological factor;

2) a period of oliguria - anuria, in which daily diuresis is less than 500 ml (duration up to 3 weeks);

3) the period of restoration of diuresis with the phase of initial diuresis (when the amount of urine exceeds 500 ml per day) and with the phase of polyuria (the amount of urine is 2-3 liters or more per day), duration up to 75 days;

4) the recovery period, starting from the moment of normalization of azotemia.

Approximately 10% of patients experience non-oliguric acute renal failure, i.e. changes in biochemical blood parameters occur against the background of normal or even increased diuresis. The most common cause of non-oliguric acute renal failure is acute interstitial nephritis.

Acute interstitial nephritis (AIN)– multifactorial diffuse kidney disease with predominant damage to tubulointerstitial tissue. Morphologically, AIN is characterized by interstitial edema, more pronounced in the medulla, uneven focal infiltration of mono- and polynuclear cells. Characterized by plasma cell infiltration, dystrophy or atrophy of the tubular epithelium. Moderate segmental mesangial proliferation, an increase in the mesangial matrix, and sclerosis of the glomeruli develop in the glomeruli.

The most common cause of acute AIN is exposure to drugs, primarily antibiotics, as well as a number of chemicals. AIN often develops after the administration of serums and vaccines. It is still not clear why, among a huge number of patients taking various medications, AIN develops in a relatively small number of people. The acute onset of the disease in the first hours or days of taking the drug is considered typical for AIN. Characteristic: fever, eosinophilia, decreased kidney function, short-term allergic rash. With a detailed clinical picture, urinary syndrome is typical: hematuria, leukacyturia, moderate proteinuria, eosinophilia, red blood cell casts are possible.

The clinical picture and course of AIN are characterized by the following signs:

against the background of polyuria, an increase in the level of creatinine in the blood plasma begins from the first day;

combination of creatinemia, polyuria with proteinuria and hematuria;

absence of hyperkalemia;

When oliguria develops in AIN, it can quickly be replaced by polyuria, but the increase in creatinin levels persists.

Clinical picture of acute renal failure

Early clinical signs (harbingers) 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 ARF is masked by extrarenal symptoms (acute gastroenteritis due to poisoning with salts of heavy metals, local and infectious manifestations in multiple trauma, systemic manifestations in drug-induced AIN). In addition, many early symptoms of acute renal failure (weakness, anorexia, nausea, drowsiness) are nonspecific. Therefore, laboratory methods are of greatest value for early diagnosis: determining the level of creatinine, urea and potassium in the blood.

Clinical manifestations appear in the oligoanuric period. During this period, there is a phase of “imaginary” well-being, which can last up to several days, and a phase of intoxication, caused by water-electrolyte disturbances, changes in acid-base balance and nitrogen excretory function of the kidneys. The polymorphism of signs of acute renal failure is due to the clinical manifestations of disorders of 5 main renal functions that ensure homeostasis: isovolumia, isoionia, isosomia, isohydria, azotemia. For acute renal failure, the most characteristic manifestations are:

Anuria(diuresis less than 50 ml).

Oliguria(diuresis less than 500 ml) 400-500 mOsm should be excreted daily in urine. substances (urea, creatinine, uric acid, ammonia, electrolytes) that are products of normal metabolism. With physical exertion and pathological conditions accompanied by increased catabolism, this load increases. The maximum osmolarity of urine in a healthy person reaches 1200 mOsm/kg; to excrete the daily osmotic load, the volume of urine must be at least 400-500 ml. Accordingly, when the daily amount of urine is less than 500 ml, the end products of nitrogen metabolism accumulate in the body.

Azotemia- increased levels of urea and creatinine in the blood.

Hyperkalemia- increase in serum potassium concentration to a level of more than 5.5 mEq/L

Metabolic acidosis - with a decrease in serum bicarbonate levels to 13 mmol/l

Heavy violationfunctions of the immune system - The phagocytic function and chemotaxis of leukocytes are inhibited, the synthesis of antibodies is suppressed, and cellular immunity is impaired (lymphopenia). Therefore, acute infections - bacterial and fungal - develop in 30-70% of patients with acute renal failure and often determine the patient’s prognosis.

CLINICAL SYMPTOMATOLOGY OF MAIN WATER ELECTROLYTE DISORDERS IN ARF.

1. Extracellular dehydration	Hypovolemia, dry, pale skin, reduced turgor, scleral icterus, decreased blood pressure, thready pulse, shortness of breath
2. Cellular dehydration	Thirst, increased body temperature, headaches, psychomotor disorders, convulsions
3.Overhydration	Shortness of breath, edema, increased blood pressure, pulmonary edema
4.Hypokalemia	Severe drowsiness (or coma), adynamia, speech is slow, deep reflexes are absent, paralytic intestinal obstruction, enlarged heart boundaries, tachycardia, arrhythmia, ECG symptoms (decreased voltage, ST segment depression, P wave inversion)
5.Hyperkalemia	Apathy, drowsiness, convulsions, hypotension, bradycardia, shortness of breath, arrhythmia; ECG symptoms (enlarged T wave, decreased ST interval below the isoelectric line, widened QRS complex, flattened T wave, conduction disturbances).
6. Hyponatremia	Apathy, hypotension, tachycardia, muscle pain, orthostatic collapse, pathological respiratory rhythms.
7.Hypocalcemia	Tetany, increased neuromuscular excitability, laryngeal spasm, 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,

on the severity of kidney damage,

the effectiveness of specialized treatment.

On average, the duration of oliguria is 7–12 days. In case of ethylene glycol poisoning, crash syndrome, obstetric-gynecological pathology, the duration of oliguria is up to 4 weeks, and in case of a complicated course - up to 6 weeks. When after 4 weeks of treatment there is no restoration of diuresis, then one must think about the possible development of cortical necrosis and the formation of “primary” chronic renal failure.

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

Brief 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: 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.

Figure 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 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 test;

General urine test;

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). Fundus of the eye.

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, seizures with headache, and confusion is a precursor to 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

Biochemical blood test: 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
	. Bence Jones squirrels	Multiple myeloma
Specific immunological studies	. ANA, anti-double-stranded DNA antibodies	SLE
	. r- 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 specialist consultation:

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
	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 deficiency of bcc is replenished;

Furosemide 200-400 mg IV through a perfusor, 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)

Long-term replacement therapy (CRRT) is 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

Used as an alternative for AKI peritoneal dialysis (PD). The procedure technique 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 according to 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 - Cockroft-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.

Clinic at the republican level (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.

Short-acting human insulin Calcium gluconate Calcium chloride Methylprednisolone Sodium hydrocarbonate Sodium chloride Norepinephrine Fresh frozen plasma Rituximab Torasemide Phenylephrine Furosemide Cyclophosphamide

Groups of drugs according to ATC used in treatment

Hospitalization

Indications for hospitalization

Special risk groups of patients on the development of acute illness:

Information

Sources and literature

1. 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. Study guide. 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 RSE 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

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Acute renal failure

Yu.S. Milovanov, A.Yu. Nikolaev
Problem Laboratory of Nephrology MMA named after. THEM. Sechenov

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

This division of acute renal failure is of great practical importance, as it allows one to outline specific measures to prevent and combat acute renal failure.
Among the triggers prerenal acute renal failure - decreased cardiac output, acute vascular insufficiency, hypovolemia and a sharp decrease in circulating blood volume. Impaired general hemodynamics and circulation and a sharp depletion of renal circulation induce renal afferent vasoconstriction with redistribution (shunting) of renal blood flow, ischemia of the renal cortex and a decrease in glomerular filtration rate (GFR). As renal ischemia worsens, prerenal acute renal failure can develop into renal acute renal failure due to ischemic necrosis of the epithelium of the renal convoluted tubules.
Renal acute renal failure in 75% of cases it is caused by acute tubular necrosis (ATN). Most often this ischemic OKN , complicating shock (cardiogenic, hypovolemic, anaphylactic, septic), coma, dehydration. Among other factors that damage the epithelium of convoluted renal tubules, drugs and chemical compounds that cause nephrotoxic ACI occupy an important place.
In 25% of cases, renal acute renal failure is caused by other reasons: inflammation in the renal parenchyma and interstitium (acute and rapidly progressive glomerulonephritis - AGN and RPGN), interstitial nephritis, damage to the renal vessels (thrombosis of the renal arteries, veins, dissecting aortic aneurysm, vasculitis, scleroderma kidney, hemolytic -uremic syndrome, malignant hypertension), etc.
Nephrotoxic OKN is diagnosed in every 10th patient with acute renal failure admitted to an acute hemodialysis (HD) center. Among more than 100 known nephrotoxins, one of the first places is occupied by drugs, mainly aminoglycoside antibiotics, the use of which in 10-15% of cases leads to moderate, and in 1-2% to severe acute renal failure. Of the industrial nephrotoxins, the most dangerous are salts of heavy metals (mercury, copper, gold, lead, barium, arsenic) and organic solvents (glycols, dichloroethane, carbon tetrachloride).
One of the common causes of renal acute renal failure is myorenal syndrome , pigmentary myoglobinuric nephrosis caused by massive rhabdomyolysis. Along with traumatic rhabdomyolysis (crash syndrome, convulsions, excessive physical exertion), non-traumatic rhabdomyolysis often develops due to the action of various toxic and physical factors (CO poisoning, zinc, copper, mercury compounds, heroin, electrical trauma, frostbite), viral myositis, muscle ischemia and electrolyte disorders (chronic alcoholism, coma, severe hypokalemia, hypophosphatemia), as well as prolonged fever, eclampsia, prolonged status asthmaticus and paroxysmal myoglobinuria.
Among inflammatory diseases of the renal parenchyma, in the last decade the proportion of drug-induced (allergic) acute interstitial nephritis within the framework of hemorrhagic fever with renal syndrome (HFRS), as well as interstitial nephritis in leptospirosis, has increased significantly. The increase in the incidence of acute interstitial nephritis (AIN) is explained by the growing allergy of the population and polypharmacy.
Postrenal acute renal failure caused by acute obstruction (occlusion) of the urinary tract: bilateral ureteral obstruction, bladder neck obstruction, adenoma, prostate cancer, tumor, schistosomiasis of the bladder, urethral stricture. Other causes include necrotizing papillitis, retroperitoneal fibrosis and retroperitoneal tumors, diseases and injuries of the spinal cord. It should be emphasized that for the development of postrenal acute renal failure in a patient with chronic kidney disease, unilateral ureteral obstruction is often sufficient. The mechanism of development of postrenal acute renal failure is associated with afferent renal vasoconstriction, developing in response to a sharp increase in intratubular pressure with the release of angiotensin II and thromboxane A2.
Special emphasis is placed on ARF developing as part of multiple organ failure , due to the extreme severity of the condition and the complexity of treatment. Multiple organ failure syndrome is manifested by a combination of acute renal failure with respiratory, cardiac, hepatic, endocrine (adrenal) failure. It is found in the practice of resuscitators, surgeons, in the clinic of internal diseases, and complicates terminal conditions in cardiological, pulmonary, gastroenterological, gerontological patients, in acute sepsis, and in multiple trauma.

Pathogenesis of acute renal failure

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

Clinical picture of acute renal failure

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

Diagnosis of acute renal failure

At the first stage of diagnosing acute renal failure, it is important to distinguish anuria from acute urinary retention. You should ensure that there is no urine in the bladder (by percussion, ultrasound or catheterization) and urgently determine the level of urea, creatinine and potassium in the blood serum. The next stage of diagnosis is to establish the form of acute renal failure (prerenal, renal, postrenal). First of all, obstruction of the urinary tract is excluded using ultrasound, radionuclide, radiological and endoscopic methods. Urine testing is also important. In prerenal acute renal failure, the content of sodium and chlorine in the urine is reduced, and the urine creatinine/plasma creatinine ratio is increased, indicating a relatively preserved concentrating ability of the kidneys. The opposite relationship is observed in renal acute renal failure. The excreted sodium fraction in prerenal acute renal failure is less than 1 and in renal acute renal failure is 2.
After excluding prerenal AKI, it is necessary to establish the form of renal AKI. The presence of erythrocyte and protein casts in the sediment indicates damage to the glomeruli (for example, with AGN and RPGN), abundant cellular debris and tubular casts indicate ACN, the presence of polymorphonuclear leukocytes and eosinophils is characteristic of acute tubulointerstitial nephritis (ATIN), detection of pathological casts ( myoglobin, hemoglobin, myeloma), as well as crystalluria typical for intratubular blockade.
It should, however, be taken into account that the study of urine composition in some cases does not have a decisive diagnostic value. For example, when diuretics are prescribed, the sodium content in urine in prerenal acute renal failure may be increased, and in chronic nephropathies, the prerenal component (decreased natriuresis) may not be detected, since even in the initial stage of chronic renal failure (CRF), the ability of the kidneys to conserve sodium is largely lost and water. At the onset of acute nephritis, the electrolyte composition of urine may be similar to that of prerenal acute renal failure, and later similar to that of renal acute renal failure. Acute obstruction of the urinary tract leads to changes in the composition of urine characteristic of prerenal acute renal failure, and chronic obstruction causes changes characteristic of renal acute renal failure. A low excreted sodium fraction is found in patients with hemoglobin- and myoglobinuric acute renal failure. In the final stages, a kidney biopsy is used. It is indicated for prolonged anuric periods of acute renal failure, for acute renal failure of unknown etiology, for suspected drug-induced acute respiratory syndrome, and for acute renal failure associated with glomerulonephritis or systemic vasculitis.

Treatment of acute renal failure

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

Treatment of renal acute renal failure

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

Dialysis treatment

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

Prognosis and outcomes

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

Classmates

– potentially reversible, sudden onset of severe impairment or cessation of renal function. Characterized by a violation of all renal functions (secretory, excretory and filtration), pronounced changes in water and electrolyte balance, rapidly increasing azotemia. The development of acute renal failure is divided into 4 successive phases: initial, oligoanuric, diuretic and the recovery period. Diagnosis is carried out according to clinical and biochemical tests of blood and urine, as well as instrumental studies of the urinary system. Treatment depends on the stage of acute renal failure. It includes symptomatic therapy, methods of extracorporeal hemocorrection, maintaining optimal blood pressure and diuresis.

Acute renal failure is a potentially reversible, sudden onset of severe impairment or cessation of renal function. Characterized by a violation of all renal functions (secretory, excretory and filtration), pronounced changes in water and electrolyte balance, rapidly increasing azotemia.

The following forms of OPN are distinguished:

• Hemodynamic(prerenal). Occurs due to acute hemodynamic disturbance.
• Parenchymatous(renal). The cause is toxic or ischemic damage to the renal parenchyma, or less commonly, an acute inflammatory process in the kidneys.
• Obstructive(postrenal). Develops as a result of acute obstruction of the urinary tract.

Etiology of prerenal acute renal failure

Prerenal acute renal failure can develop in conditions that are accompanied by a decrease in cardiac output (pulmonary embolism, heart failure, arrhythmia, cardiac tamponade, cardiogenic shock). Often the cause is a decrease in the amount of extracellular fluid (with diarrhea, dehydration, acute blood loss, burns, ascites caused by cirrhosis of the liver). May occur due to severe vasodilation that occurs during bacteriotoxic or anaphylactic shock.

Etiology of renal acute renal failure

Occurs due to toxic effects on the renal parenchyma of fertilizers, poisonous mushrooms, copper salts, cadmium, uranium and mercury. Develops with uncontrolled use of nephrotoxic medications (antitumor drugs, a number of antibiotics and sulfonamides). X-ray contrast agents and the listed drugs, prescribed in the usual dosage, can cause renal acute renal failure in patients with impaired renal function.

In addition, this form of acute renal failure occurs when a large amount of myoglobin and hemoglobin circulates in the blood (with severe macrohemaglobinuria, transfusion of incompatible blood, prolonged compression of tissue during injury, drug and alcohol coma). Less commonly, the development of renal acute renal failure is caused by inflammatory kidney disease.

Etiology of postrenal acute renal failure

It develops when there is a mechanical disturbance in the passage of urine due to bilateral obstruction of the urinary tract by stones. Less commonly occurs with tumors of the prostate gland, bladder and ureters, tuberculous lesions, urethritis and periurethritis, dystrophic lesions of the retroperitoneal tissue.

In severe combined injuries and extensive surgical interventions, acute renal failure is caused by several factors (shock, sepsis, blood transfusion, treatment with nephrotoxic drugs).

Symptoms of acute renal failure

There are four phases of acute renal failure:

The patient's condition is determined by the underlying disease causing acute renal failure. Clinically, the initial phase is usually not detected due to the absence of characteristic symptoms. The circulatory collapse that occurs in this phase has a very short duration and therefore goes unnoticed. Nonspecific symptoms of acute renal failure (drowsiness, nausea, lack of appetite, weakness) are masked by manifestations of the underlying disease, injury or poisoning.

Anuria occurs rarely. The amount of urine excreted is less than 500 ml per day. Characterized by severe proteinuria, azotemia, hyperphosphatemia, hyperkalemia, hypernatemia, metabolic acidosis. There is diarrhea, nausea, and vomiting. With pulmonary edema due to overhydration, shortness of breath and moist rales appear. The patient is lethargic, drowsy, and may fall into a coma. Pericarditis and uremic gastroenterocolitis, complicated by bleeding, often develop. The patient is susceptible to infection due to decreased immunity. Possible pancreatitis, stomatitis, mumps, pneumonia, sepsis.

The oligoanuric phase of acute renal failure develops during the first three days after exposure. Late development of the oligoanuric phase is considered a prognostically unfavorable sign. The average duration of this stage is 10-14 days. The period of oliguria can be shortened to several hours or extended to 6-8 weeks. Prolonged oliguria more often occurs in elderly patients with concomitant vascular pathology. In the oliguric stage of acute renal failure, which lasts more than a month, it is necessary to carry out additional differential diagnosis to exclude progressive glomerulonephritis, renal vasculitis, occlusion of the renal artery, diffuse necrosis of the renal cortex.

The duration of the diuretic phase is about two weeks. Daily diuresis gradually increases and reaches 2-5 liters. There is a gradual restoration of water and electrolyte balance. Hypokalemia is possible due to significant losses of potassium in the urine.

There is further restoration of renal function, which takes from 6 months to 1 year.

Complications of acute renal failure

The severity of disorders characteristic of renal failure (fluid retention, azotemia, water-electrolyte imbalance) depends on the state of catabolism and the presence of oliguria. With severe oliguria, there is a decrease in the level of glomerular filtration, the release of electrolytes, water and nitrogen metabolism products is significantly reduced, which leads to more pronounced changes in blood composition.

With oliguria, the risk of developing water and salt overload increases. Hyperkalemia in acute renal failure is caused by insufficient excretion of potassium while the level of its release from tissues remains unchanged. In patients who do not suffer from oliguria, the potassium level is 0.3-0.5 mmol/day. More pronounced hyperkalemia in such patients may indicate an exogenous (blood transfusion, medications, presence of potassium-rich foods in the diet) or endogenous (hemolysis, tissue destruction) potassium load.

The first symptoms of hyperkalemia appear when potassium levels exceed 6.0-6.5 mmol/l. Patients complain of muscle weakness. In some cases, flaccid tetraparesis develops. ECG changes are noted. The amplitude of the P waves decreases, the P-R interval increases, and bradycardia develops. A significant increase in potassium concentration can cause cardiac arrest.

In the first two stages of acute renal failure, hypocalcemia, hyperphosphatemia, and mild hypermagnesemia are observed.

The consequence of severe azotemia is inhibition of erythropoiesis. The lifespan of red blood cells is reduced. Normocytic normochromic anemia develops.

Immune suppression contributes to the occurrence of infectious diseases in 30-70% of patients with acute renal failure. The addition of infection aggravates the course of the disease and often causes the death of the patient. Inflammation develops in the area of ​​postoperative wounds, the oral cavity, respiratory system, and urinary tract suffer. A common complication of acute renal failure is sepsis, which can be caused by both gram-positive and gram-negative flora.

There is drowsiness, confusion, disorientation, lethargy, alternating with periods of excitement. Peripheral neuropathy occurs more often in older patients.

• Complications from the cardiovascular system

With acute renal failure, congestive heart failure, arrhythmia, pericarditis, and arterial hypertension may develop.

Patients are concerned about a feeling of discomfort in the abdominal cavity, nausea, vomiting, and loss of appetite. In severe cases, uremic gastroenterocolitis develops, often complicated by bleeding.

Diagnostics of acute renal failure

The main marker of acute renal failure is an increase in potassium and nitrogenous compounds in the blood against the background of a significant decrease in the amount of urine excreted by the body, up to a state of anuria. The amount of daily urine and the concentrating ability of the kidneys are assessed based on the results of the Zimnitsky test. Monitoring blood biochemistry parameters such as urea, creatinine and electrolytes is important. It is these indicators that make it possible to judge the severity of acute renal failure and the effectiveness of the treatment measures taken.

The main task in diagnosing acute renal failure is to determine its form. To do this, an ultrasound of the kidneys and bladder is performed, which allows to identify or exclude urinary tract obstruction. In some cases, bilateral catheterization of the pelvis is performed. If both catheters pass freely into the pelvis, but no urine is released through them, we can confidently exclude the postrenal form of acute renal failure.

If necessary, assess renal blood flow by performing an ultrasound scan of the renal vessels. Suspicion of tubular necrosis, acute glomerulonephritis, or systemic disease is an indication for renal biopsy.

Treatment of acute renal failure

Treatment in the initial phase

Therapy is aimed primarily at eliminating the cause that caused renal dysfunction. In case of shock, it is necessary to replenish the volume of circulating blood and normalize blood pressure. In case of nephrotoxin poisoning, the patient's stomach and intestines are washed. The use of such modern treatment methods in urology as extracorporeal hemocorrection allows you to quickly cleanse the body of toxins that have caused the development of acute renal failure. For this purpose, hemosorption and plasmapheresis are performed. If obstruction is present, normal urine passage is restored. This includes removal of stones from the kidneys and ureters, surgical removal of ureteral strictures and removal of tumors.

Treatment in the oliguria phase

To stimulate diuresis, the patient is prescribed furosemide and osmotic diuretics. To reduce vasoconstriction of the renal vessels, dopamine is administered. When determining the volume of fluid administered, in addition to losses during urination, vomiting and bowel movements, it is necessary to take into account losses during sweating and breathing. The patient is transferred to a protein-free diet and the intake of potassium from food is limited. The wounds are drained and areas of necrosis are removed. When choosing the dose of antibiotics, the severity of kidney damage should be taken into account.

Indications for hemodialysis

Hemodialysis is carried out when the level of urea increases to 24 mmol/l, potassium - to 7 mmol/l. Indications for hemodialysis are symptoms of uremia, acidosis and overhydration. Currently, to prevent complications arising from metabolic disorders, nephrologists are increasingly performing early and preventive hemodialysis.

Mortality primarily depends on the severity of the pathological condition that caused the development of acute renal failure. The outcome of the disease is influenced by the patient’s age, the degree of renal dysfunction, and the presence of complications. In surviving patients, renal function is restored completely in 35-40% of cases, partially in 10-15% of cases. 1-3% of patients require continuous hemodialysis.

Acute renal failure (AKI) develops as a complication of many diseases and pathological processes. Acute renal failure is a syndrome that develops as a result of disturbances in renal processes (renal blood flow, glomerular filtration, tubular secretion, tubular reabsorption, renal concentrating ability) and is characterized by azotemia, disturbances in water-electrolyte balance and acid-base status.

Acute renal failure can be caused by prerenal, renal and postrenal disorders. Prerenal acute renal failure develops due to a violation of renal blood flow, renal acute renal failure - with damage to the renal parenchyma, postrenal acute renal failure is associated with a violation of the outflow of urine.

The morphological substrate of OPN is acute tubulonecrosis, manifested by a decrease in the height of the brush border, a decrease in folding of the basolateral membranes, and necrosis of the epithelium.

Prerenal acute renal failure is characterized by a decrease in renal blood flow as a result of vasoconstriction of afferent arterioles in conditions of impaired systemic hemodynamics and a decrease in circulating blood volume, while renal function is preserved.

long-term or short-term (less often) decrease in blood pressure below 80 mm Hg. (shock due to various reasons: post-hemorrhagic, traumatic, cardiogenic, septic, anaphylactic, etc., extensive surgical interventions);

decrease in circulating blood volume (blood loss, plasma loss, uncontrollable vomiting, diarrhea);

an increase in intravascular capacity, accompanied by a decrease in peripheral resistance (septicemia, endotoxemia, anaphylaxis);

decreased cardiac output (myocardial infarction, heart failure, pulmonary embolism).

The key element in the pathogenesis of prerenal acute renal failure is a sharp decrease in the level of glomerular filtration due to spasm of afferent arterioles, shunting of blood in the juxtaglomerular layer and ischemia of the cortical layer under the influence of a damaging factor. Due to a decrease in the volume of blood perfused through the kidneys, the clearance of metabolites decreases and develops azotemia. Therefore, some authors call this type of surge arrester prerenal azotemia. With a long-term decrease in renal blood flow (more than 3 days) prerenal acute renal failure transforms into renal acute renal failure.

The degree of renal ischemia correlates with structural changes in the epithelium of the proximal tubules (reduction in the height of the brush border and the area of ​​the basolateral membranes). Initial ischemia increases the permeability of the membranes of tubular epithelial cells for ions, which enter the cytoplasm and are actively transported by a special carrier to the inner surface of mitochondrial membranes or to the sarcoplasmic reticulum. The energy deficit developing in cells due to ischemia and energy consumption during the movement of ions leads to cell necrosis, and the resulting cellular detritus obstructs the tubules, thereby aggravating anuria. The volume of tubular fluid under conditions of ischemia is reduced.

Damage to nephrocytes is accompanied by impaired sodium reabsorption in the proximal tubules and excess sodium intake into the distal tubules. Sodium stimulates macula densa production of renin; in patients with acute renal failure, its content is usually increased. Renin activates the renin-angiotensin-aldosterone system. Sympathetic nerve tone and catecholamine production are increased. Under the influence of components of the renin-apgiotensin-aldosterone system and catecholamines, afferent vasoconstriction and renal ischemia are maintained. In the glomerular capillaries, the pressure drops and, accordingly, the effective filtration pressure decreases.

With a sharp restriction of perfusion of the cortical layer, blood enters the capillaries of the juxtaglomerular zone (“Oxford shunt”), in which stasis occurs. An increase in tubular pressure is accompanied by a decrease in glomerular filtration. Hypoxia of the distal tubules that are most sensitive to it is manifested by necrosis of the tubular epithelium and basement membrane up to tubular necrosis. Obstruction of the tubules occurs with fragments of necrotic epithelial cells, cylinders, etc.

Under conditions of hypoxia in the medulla, changes in the activity of enzymes of the arachidonic cascade are accompanied by a decrease in the formation of prostaglandins, which have a vasodilator effect, and the release of biologically active substances (histamine, serotonin, bradykinin), which directly affect the renal vessels and disrupt renal hemodynamics. This, in turn, contributes to secondary damage to the renal tubules.

After restoration of renal blood flow, the formation of reactive oxygen species, free radicals and activation of phospholipase occurs, which maintains membrane permeability disorders for ions and prolongs the oliguric phase of acute renal failure. In recent years, calcium channel blockers (nifedipine, verapamil) have been used to eliminate unwanted calcium transport into cells in the early stages of acute renal failure, even against the background of ischemia or immediately after its elimination. A synergistic effect is observed when calcium channel inhibitors are used in combination with substances that can scavenge free radicals, such as glutathione. Ions, adenine nucleotides protect mitochondria from damage.

The degree of kidney ischemia correlates with structural changes in the tubular epithelium; the development of vacuolar degeneration or necrosis of individual nephrocytes is possible. Vacuolar dystrophy is eliminated within 15 days after the cessation of the damaging factor.

Renal acute renal failure develops as a result of renal ischemia, that is, it occurs secondary to primary impaired renal perfusion or under the influence of the following reasons:

inflammatory process in the kidneys (glomerulonephritis, interstitial nephritis, vasculitis);

endo- and exotoxins (medicines, radiopaque substances, heavy metal salts - compounds of mercury, lead, arsenic, cadmium, etc., organic solvents, ethylene glycol, carbon tetrachloride, poisons of animal and plant origin;

renovascular diseases (thrombosis and embolism of the renal artery, dissecting aortic aneurysm, bilateral renal vein thrombosis);

pigmentemia - hemoglobinemia (intravascular hemolysis) and myoglobinemia (traumatic and non-traumatic rhabdomyolysis);

This type of acute renal failure is characterized by acute tubular necrosis caused by ischemia or nephrotoxins that bind to renal tubular cells. First of all, the proximal tubules are damaged, dystrophy and necrosis of the epithelium occurs, followed by moderate changes in the interstitium of the kidneys. Glomerular damage is usually minor.

To date, more than 100 nephrotoxins have been described that have a direct damaging effect on renal tubular cells (acute tubular necrosis, nephrosis of the lower nephron, vasomotor vasopathy). Acute renal failure caused by nephrotoxins accounts for about 10% of all patient admissions to acute hemodialysis centers.

Nephrotoxins cause damage to tubuloepithelial structures of varying severity - from dystrophies (hydropic, vacuolar, balloon, fatty, hyaline droplet) to partial or massive coagulative necrosis of nephrocytes. These changes occur as a result of reabsorption and deposition of macro- and microparticles in the cytoplasm, as well as fixation of nephrotoxins on the cell membrane and in the cytoplasm, filtered through the glomerular filter. The occurrence of a particular dystrophy is determined by the operating factor.

Nephrotoxicity of poisons " thiol group"(compounds of mercury, chromium, copper, gold, cobalt, zinc, lead, bismuth, lithium, uranium, cadmium and arsenic) is manifested by blockade of sulfhydryl (thiol) groups of enzymatic and structural proteins and a plasmacoagulating effect, which causes massive coagulative necrosis of the tubules. Sublimate causes selective kidney damage - “ mercuric nephrosis." Other substances in this group are not selective in action and damage kidney tissue, liver and red blood cells. For example, a feature of poisoning with copper sulfate, dichromates, and arsenous hydrogen is the combination of coagulation necrosis of the epithelium of the proximal tubules with acute hemoglobinuric nephrosis. In case of poisoning with dichromates and arsenic hydrogen, centrilobular necrosis of the liver with cholemia and chelation is observed.

Poisoning ethylene glycol and its derivatives is characterized by irreversible destruction of intracellular structures, called balloon dystrophy. Ethylene glycol and its breakdown products are reabsorbed by the epithelial cells of the renal tubules, a large vacuole is formed in them, which displaces the cellular organelles along with the nucleus to the basal sections. Such dystrophy, as a rule, ends with liquefaction necrosis and complete loss of function of the affected tubules. Sequestration of the damaged part of the cell along with the vacuole is also possible, and the preserved basal sections with the displaced nucleus can be a source of regeneration.

Poisoning dichloroethane, less often chloroform, accompanied by fatty degeneration nephrocytes (acute lipid nephrosis) proximal, distal tubules and loop of Henle. These poisons have a direct toxic effect on the cytoplasm, changing the ratio of protein-lipid complexes in it, which is accompanied by inhibition of reabsorption in the tubules.

Reabsorption of protein pigment aggregates (hemoglobin, myoglobin) epithelial cells of the proximal and distal tubules causes hyaline-droplet dystrophy. Pigment proteins filtered through the glomerular filter move along the tubule and are gradually deposited on the brush border in the proximal tubules and are partially reabsorbed by nephrocytes. The accumulation of pigment granules in epithelial cells is accompanied by partial destruction of the apical sections of the cytoplasm and their sequestration into the lumen of the tubules along with the brush border, where granular and lumpy pigment cylinders are formed. The process unfolds over 3-7 days. During this period, unreabsorbed pigment masses in the lumen of the tubules become denser and move into the loop of Henle and distal tubules. In the apical sections of epithelial cells overloaded with pigment granules, partial necrosis occurs. Individual pigment granules are converted into ferritin and remain in the cytoplasm for a long time.

Nephrotoxicity aminoglycosides(kanamycin, gentamicin, monomycin, neomycin, tobarmycin, etc.) is associated with the presence of free amino groups in the side chains in their molecules. Aminoglycosides are not metabolized in the body, and 99% of them are excreted unchanged in the urine. The filtered aminoglycosides are fixed on the apical membrane of the cells of the proximal tubules and the loop of Henle, bind to vesicles, are absorbed by pinocytosis and are sequestered in the lysosomes of the tubular epithelium. In this case, the concentration of the drug in the cortex becomes higher than in the plasma. Kidney damage caused by aminoglycosides is characterized by an increase in membrane anionic phospholipids, in particular phosphatidylinositol, damage to mitochondrial membranes, accompanied by loss of intracellular potassium and magnesium, impaired oxidative phosphorylation and energy deficiency. The combination of these changes leads to necrosis of the tubular epithelium.

Characteristically, the ions prevent the fixation of aminoglycosides on the brush border and thus reduce their nephrotoxicity. It has been noted that the tubular epithelium, which regenerates after damage by aminoglycosides, becomes resistant to the toxic effects of these drugs.

Therapy osmotic diuretins(solutions of glucose, urea, dextrans, mannitol, etc.) may be complicated by hydropic and vacuolar degeneration of nephrocytes. At the same time, in the proximal tubules, the osmotic gradient of liquids on both sides of the tubular cell changes - blood washing the tubules and provisional urine. Therefore, it is possible for water to move into the tubular epithelial cells from peritubular capillaries or from provisional urine. Hydropy of epithelial cells when using osmotic diuretins persists for a long time and, as a rule, is associated with partial reabsorption of osmotically active substances and their retention in the cytoplasm. Water retention in a cell sharply reduces its energy potential and functionality. Thus, osmotic nephrosis is not the cause of acute renal failure, but an undesirable effect of its treatment or a consequence of replenishment of energy substrates in the body by parenteral administration of hypertonic solutions.

The composition of urine in renal acute renal failure is similar in composition to the glomerular filtrate: low specific gravity, low osmolarity. The content in urine is increased due to a violation of its reabsorption.

Postrenal acute renal failure occurs due to a violation of the outflow of urine through the urinary tract as a result of the following disorders:

occlusion of the urinary tract by stones or blood clots;

obstruction of the ureters or ureter by a tumor located outside the urinary tract;

Violation of the outflow of urine is accompanied by overstretching of the urinary tract (ureters, pelvis, calyces, collecting ducts, tubules) and the inclusion of the reflux system. Urine flows back from the urinary tract into the interstitial space of the renal parenchyma (pyelorenal reflux). But pronounced edema is not observed due to the outflow of fluid through the system of venous and lymphatic vessels (pyelovenous reflux). Therefore, the intensity of hydrostatic pressure on the tubules and glomerulus is very moderate, and filtration is slightly reduced. There are no significant disturbances in peritubular blood flow and, despite anuria, renal function is preserved. After removing the obstruction to the outflow of urine, diuresis is restored. If the duration of occlusion does not exceed three days, the phenomena of acute renal failure after restoration of patency of the urinary tract quickly disappear.

With prolonged occlusion and high hydrostatic pressure, filtration and peritubular blood flow are disrupted. These changes, combined with persistent reflux, contribute to the development of interstitial edema and tubular necrosis.

Clinical course of acute renal failure has a certain pattern and stages, regardless of the reason that caused it.

1st stage– short in duration and ends after the factor ceases to act;

2nd stage – period of oligoanuria (the volume of urine excreted does not exceed 500 ml/day), azotemia; in case of prolonged oliguria (up to 4 weeks) the likelihood of developing cortical necrosis sharply increases;

3rd stage– period of polyuria – restoration of diuresis with a phase of polyuria (the volume of urine excreted exceeds 1800 ml/day);

4th stage– restoration of kidney function. Clinically, stage 2 is the most severe.

Extracellular and intracellular hyperhydration and non-gas excretory renal acidosis develop (depending on the location of tubular damage, acidosis of types 1, 2, 3 is possible). The first sign of overhydration is shortness of breath due to interstitial or cardiogenic pulmonary edema. Somewhat later, fluid begins to accumulate in the cavities, hydrothorax, ascites, and swelling of the lower extremities and lumbar region occur. This is accompanied by pronounced changes in biochemical blood parameters: azotemia (the content of creatinine, urea, uric acid is increased), hyperkalemia, hyponatremia, hypochloremia, hypermagnesemia, hyperphosphatemia.

The blood creatinine level increases regardless of the patient’s diet and the intensity of protein breakdown. Therefore, the degree of creatinemia gives an idea of ​​the severity and prognosis of acute renal failure. The degree of catabolism and necrosis of muscle tissue reflects hyperuricemia.

Hyperkalemia occurs as a result of decreased potassium excretion, increased release of potassium from cells, and developing renal acidosis. Hyperkalemia 7.6 mmol/l is clinically manifested by cardiac arrhythmias up to complete cardiac arrest; hyporeflexia occurs, muscle excitability decreases with the subsequent development of muscle paralysis.

Electrocardiographic indicators for hyperkalemia: T wave – high, narrow, the ST line merges with the T wave; disappearance of the P wave; widening of the QRS complex.

Hyperphosphatemia is caused by impaired phosphate excretion. The genesis of hypocalcemia remains unclear. As a rule, shifts in phosphorus-calcium homeostasis are asymptomatic. But with rapid correction of acidosis in patients with hypocalcemia, tetany and seizures may occur. Hyponatremia is associated with water retention or excess water intake. There is no absolute sodium deficiency in the body. Hypersulfatemia and hypermagnesemia are usually asymptomatic.

Anemia develops within a few days, the genesis of which is explained by overhydration, hemolysis of red blood cells, bleeding, and inhibition of erythropoietin production by toxins circulating in the blood. Anemia is usually combined with thrombocytopenia.

The second stage is characterized by the appearance of signs of uremia, with predominant symptoms from the gastrointestinal tract (lack of appetite, nausea, vomiting, flatulence, diarrhea).

When antibiotics are prescribed at the beginning, the symptoms of diarrhea increase. Subsequently, diarrhea gives way to constipation due to severe intestinal hypokinesia. In 10% of cases, gastrointestinal bleeding (erosions, ulcers of the gastrointestinal tract, bleeding disorders) is observed.

Timely prescribed therapy prevents the development of coma and uremic pericarditis.

During the oliguric stage (9-11 days), urine is dark in color, proteinuria and cylindruria are pronounced, natriuria does not exceed 50 mmol/l, urine osmolarity corresponds to plasma osmolarity. In 10% of patients with acute drug-induced interstitial nephritis, diuresis is preserved.

3rd stage characterized by restoration of diuresis by 12-15 days from the onset of the disease and polyuria (more than 2 l/day) that persists for 3-4 weeks. The genesis of polyuria is explained by the restoration of the filtration function of the kidneys and insufficient concentration function of the tubules. During the polyuric stage, the body is unloaded from the fluid accumulated during the period of oliguria. Secondary dehydration, hypokalemia and hyponatremia are possible. The severity of proteinuria decreases.

Differential diagnosis of prerenal and renal acute renal failure

Acute renal failure (ARF) is a sudden loss of function of both kidneys caused by a decrease in renal blood flow and a slowdown in glomerular filtration and tubular reabsorption. As a result, there is a delay or complete cessation of the removal of toxic substances from the body and a disorder of acid-base, electrolyte and water balance.

With proper and timely treatment, these pathological changes are reversible. According to medical statistics, cases of acute renal failure are registered annually in approximately 200 people per 1 million.

Forms and causes of acute renal failure

Depending on what processes led to the occurrence of acute renal failure, prerenal, renal and postrenal forms are distinguished.

Prerenal form of acute renal failure

The prerenal form of acute renal failure is characterized by a significant reduction in renal blood flow and a decrease in glomerular filtration rate. Such disturbances in kidney function are associated with a general decrease in the volume of circulating blood in the body. If normal blood supply to the organ is not restored as soon as possible, ischemia or necrosis of the renal tissue is possible. The main reasons for the development of prerenal acute renal failure are:

• decreased cardiac output;
• pulmonary embolism;
• operations and injuries accompanied by significant blood loss;
• extensive burns;
• dehydration caused by diarrhea, vomiting;
• taking diuretics;
• sudden decrease in vascular tone.

Renal form of acute renal failure

In the renal form of acute renal failure, damage to the renal parenchyma is observed. It can be caused by inflammatory processes, toxic effects or pathologies of the kidney vessels, which lead to insufficient blood supply to the organ. Renal acute renal failure is a consequence of necrosis of renal tubular epithelial cells. As a result, the integrity of the tubules is disrupted and their contents leak into the surrounding kidney tissue. The following factors can lead to the development of the renal form of acute renal failure:

• intoxication with various poisons, medications, radiopaque compounds, heavy metals, snake or insect bites, etc.;
• kidney diseases: interstitial nephritis, acute pyelonephritis and glomerulonephritis;
• damage to the renal vessels (thrombosis, aneurysm, atherosclerosis, vasculitis, etc.);
• kidney injuries.

Important: Long-term use of medications that have a nephrotoxic effect, without prior consultation with a doctor, can cause acute renal failure.

Postrenal acute renal failure

Postrenal acute renal failure develops as a result of acute disturbance of urinary passage. In this form of acute renal failure, kidney function is preserved, but the process of urine excretion is difficult. Ischemia of the kidney tissue may occur, as the pelvis, overfilled with urine, begins to compress the surrounding kidney tissue. The causes of postrenal acute renal failure include:

• bladder sphincter spasm;
• blockage of the ureters due to urolithiasis;
• tumors of the bladder, prostate, urinary canals, pelvic organs;
• injuries and hematomas;
• inflammatory diseases of the ureters or bladder.

Stages and symptoms of acute renal failure

The characteristic symptoms of acute renal failure develop very quickly. There is a sharp deterioration in the patient's general condition and impaired renal function. In the clinical picture of acute renal failure, stages are distinguished, each of which is characterized by certain signs:

• initial stage;
• stage of oligoanuria;
• stage of polyuria;
• recovery stage.

In the first stage of acute renal failure, symptoms are determined by the cause of the disease. These may be signs of intoxication, shock, or manifestations of some disease. So, with infectious kidney damage, fever, headache, and muscle weakness are noted. In case of intestinal infection, vomiting and diarrhea are present. Toxic kidney damage is characterized by jaundice, anemia, and possible convulsions. If the cause of acute renal failure is acute glomerulonephritis, then urine mixed with blood and pain in the lumbar region are noted. The first stage of acute renal failure is characterized by a decrease in blood pressure, pallor, rapid pulse, and a slight decrease in diuresis (up to 10%).
The stage of oligoanuria in acute renal failure is the most severe and poses the greatest danger to the patient’s life. It is characterized by the following symptoms:

• a sharp decrease or cessation of urine output;
• intoxication with nitrogen metabolism products, manifested in the form of nausea, vomiting, itching of the skin, increased breathing, loss of appetite, tachycardia;
• increased blood pressure;
• confusion and loss of consciousness, coma;
• swelling of the subcutaneous tissue, internal organs and cavities;
• increased body weight due to the presence of excess fluid in the body;
• general serious condition.

The further course of acute renal failure is determined by the success of the therapy performed at the second stage. With a favorable outcome, the stage of polyuria and subsequent recovery begins. First, there is a gradual increase in diuresis, and then polyuria develops. Excess fluid is removed from the body, swelling is reduced, and the blood is cleansed of toxic products. The polyuria stage can be dangerous due to dehydration and electrolyte imbalance (for example, hypokalemia). After about a month, diuresis returns to normal and a recovery period begins, which can last up to 1 year.

If the treatment was chosen incorrectly or carried out too late and turned out to be ineffective, then the terminal stage of acute renal failure develops with a high probability of death. It is characterized by:

• shortness of breath, cough caused by the accumulation of fluid in the lungs;
• sputum mixed with blood;
• subcutaneous hemorrhages and internal bleeding;
• loss of consciousness, coma;
• muscle spasms and cramps;
• severe heart rhythm disturbances.

Advice: If even a slight decrease in diuresis is detected, especially if kidney disease or other pathologies are present, you should immediately contact a nephrologist. Such disorders may be the beginning of the development of acute renal failure.

Diagnostics of acute renal failure

In acute renal failure, diagnosis of the disease is carried out using both laboratory and instrumental methods. Laboratory tests show the following deviations from the norm:

• a general blood test is characterized by a decrease in hemoglobin levels, an increase in the concentration of leukocytes, and an increase in ESR;
• a general urine test reveals protein, casts, decreased density, increased levels of red and white blood cells, and decreased platelet levels;
• daily urine analysis is characterized by a significant decrease in diuresis;
• a biochemical blood test reveals increased levels of creatinine and urea, as well as increased potassium concentrations and decreased sodium and calcium concentrations.

Among the instrumental diagnostic methods used:

• ECG is used to monitor heart function, which may be impaired due to hyperkalemia;
• Ultrasound allows you to assess the size of the kidneys, the level of blood supply and the presence of obstruction;
• kidney biopsy;
• radiography of the lungs and heart.

Treatment and emergency care for acute renal failure

In case of acute renal failure, emergency care consists of quickly transporting a person to a hospital hospital. In this case, the patient needs to be provided with a state of rest, warmth and a horizontal body position. It is best to call an ambulance, since in this case qualified doctors will be able to take all necessary measures right on the spot.

In acute renal failure, treatment is carried out taking into account the stage of the disease and the cause that caused it. After eliminating the etiological factor, it is necessary to restore homeostasis and excretory function of the kidneys. Depending on the cause of the surge arrest, you may need to:

• taking antibiotics for infectious diseases;
• replenishment of fluid volume (with a decrease in circulating blood volume);
• using diuretics and fluid restriction to reduce swelling and increase urine production;
• taking heart medications for heart problems;
• taking medications to lower blood pressure if it increases;
• surgery to restore kidney tissue damaged as a result of injury or to remove obstacles that interfere with the outflow of urine;
• taking medications to improve blood supply and blood flow in the nephrons;
• detoxification of the body in case of poisoning (gastric lavage, administration of antidotes, etc.).

To remove toxic products from the blood, hemodialysis, plasmapheresis, peritoneal dialysis, and hemosorption are used. Acid-base and water-electrolyte balance is restored by administering saline solutions of potassium, sodium, calcium, etc. These procedures are used temporarily until renal function is restored. With timely treatment, acute renal failure has a favorable prognosis.

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But perhaps it would be more correct to treat not the effect, but the cause?

Failure of the functioning of two kidneys, provoked by a weakening of the blood supply, a delay in glomerular filtration is called acute renal failure (ARF).

The result is an absolute stop in the removal of toxins, a failure of acid-base, electrolyte, and 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, stoppage of kidney function, provoking an increase in nitrogen metabolism metabolites, metabolic failure. Pathologies of the nephron are caused by a reduction in blood supply and a reduction in oxygen.

The pathology of acute renal failure requires from a couple of hours to a week to occur and lasts more than a day. An earlier visit to the doctor ensures the absolute restoration of the affected organ. ARF becomes an exacerbation of painful pathologies and is divided into forms:

1. Hemodynamic (pereneral), caused by a sudden disruption of hemodynamics. It is characterized by a decrease in blood supply and a decrease in the rate of glomerular filtration. Failures of this type are caused by a reduction in the amount of pulsating blood. If blood supply is not restored, then kidney tissue is likely to die.
2. Parenchymal (renal) - occurs due to a toxic or ischemic effect on the renal parenchyma or acute inflammation. As a result, the integrity of the tubules is damaged and their insides are released into the tissue.
3. Obstructive (postrenal) – formed after obstruction of the urinary canals has formed. This type involves preservation of functions; urination will be difficult.

Based on the level of preservation of diuresis, they are divided into non-oliguric and oliguric forms.

Causes of acute renal failure

The etiology of the disease is distinguished by its form. Factors in the formation of prerenal acute renal failure include:

• reduction in cardiac output;
• pulmonary artery blockage;
• surgical interventions, trauma with blood loss;
• tissue damage due to high temperatures;
• loss of large amounts of water and salts due to loose stools and vomiting;
• taking diuretics;
• drop in vascular tone.

Prerequisites for the renal form of acute renal failure:

• toxic effect on kidney tissue of poisonous plants, copper, mercury salts;
• uncontrolled use of drugs (anti-blastoma drugs, antimicrobials and sulfonamides);
• Contrast agents and medications can cause pathology in humans;
• increased level of myoglobin with prolonged compression of tissue during injury, drug, alcohol coma;
• inflammatory kidney diseases.

There are many reasons for the development of the disease

Factors in the development of postrenal acute renal failure are:

• pathologies of the cardiac apparatus;
• irregular heartbeat;
• cardiac tamponade, dehydration;
• damage to body tissues by high temperatures;
• ascites, low blood pressure;
• blockage of blood vessels carrying blood to the kidneys;
• poisonous influence of toxic substances;
• the presence of inflammatory pathologies.

In case of injury and extensive surgery, the formation of acute renal failure is caused by: shock, infection or blood transfusion, therapy with nephrotoxic drugs.

Symptoms of acute renal failure

Distinctive features are characterized by development. There is a deterioration in the patient’s well-being and a malfunction of organs. Symptoms of acute renal failure are divided into types according to stages.

The initial stage is accompanied by peripheral swelling and weight gain. The primary phase is not detected due to the lack of signs. The circulatory crisis that appears at this stage is long-lasting and goes unnoticed. Nonspecific signs of renal failure (muscle weakness, nausea, headache) are masked by the symptoms of an underlying illness - shock, injury or poisoning.

The initial stage is accompanied by weight gain

If acute glomerulonephritis is a prerequisite for acute renal failure, blood clots in the urine and back pain are observed. The initial phase of acute renal failure is accompanied by low blood pressure, pale skin color, accelerated heart rate, and decreased diuresis.

Oligoanuria is considered a severe stage. It poses a threat to the patient’s life and is accompanied by the following symptoms:

• reduction or stopping of urine flow;
• 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 connective tissue and internal organs;
• weight gain from excess fluid in the body.

The subsequent course of acute renal failure 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 observed, and polyuria is formed. Fluid is eliminated from the body, swelling is reduced, and the blood will be cleansed of toxins.

The polyuria phase carries the danger of dehydration and electrolyte imbalance. A month later, diuresis normalizes, a recovery stage appears, which lasts up to 12 months.

If therapy is ineffective, a terminal phase of acute renal failure develops with a risk of mortality. Manifests itself in the form of signs:

• difficulty breathing, cough in the lungs;
• discharge of sputum with blood droplets;
• fainting, coma;
• spasms, convulsions;
• critical irregularities in heartbeat.

The disease affects the body, provokes the development of cardiac muscle atrophy, pericarditis, encephalopathy, and weakened immunity.

Diagnosis of kidney failure

The diagnostic process includes the doctor’s actions:

• studying the pathology history, patient complaints;
• study of life history (whether the organs were injured, whether the patient had poisoning, blood loss, the presence of chronic kidney diseases, diabetes), the conjugation of working or living conditions with regular intoxication (paints and varnishes, solvents);
• a complete assessment of the patient’s general condition is carried out (degree of consciousness, color of the skin surface, blood pressure indicators), study of the urinary system by 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 (reduction in the degree of hemoglobin and the number of red blood cells, due to the production of a hormone by the kidneys that ensures the production of red blood cells), an increase in 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 by the kidneys);
• study of electrolytes, urinary components for probable renal pathologies;
• ultrasound examination of the kidneys;
• examination of the bladder and urethra with optical equipment;
• radionuclide methods - allow you to visualize the functional, anatomical structure of organs, determine the type of tissue damage or urinary apparatus, inflammatory features, the presence of stones or tumors;
• according to indications (in case of protracted acute renal failure or its unknown etiology, a kidney biopsy is performed).

A doctor diagnoses the disease

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

In case of acute renal failure syndrome, emergency care involves calling an ambulance or quickly transporting the patient to a hospital hospital, then the patient must be provided with:

• bed rest;
• warming the body;
• removal from hypovolemia and shock (tachycardia, hypotension, difficulty breathing, cyanosis of the skin, mucous tissues, anuria, dehydration);
• jet injection of warm saline solution “Trisol”;
• active therapy for sepsis;
• intravenous drip injections of Dopamine improve blood circulation. Heparin is administered intravenously and is administered by drip.

Treatment is best done in a hospital

Resumption of kidney function occurs during compensation of intravascular fluid volume, therapy for blood poisoning, and stopping the use of nephrotoxic drugs.

Treatment of acute renal failure

At the first stage of the disease, therapy involves eliminating the factor that provoked acute renal failure. In the presence of shock, it is necessary to compensate for the volume of circulating blood and adjust blood pressure levels.

The use of innovative methods by urologists, such as extracorporeal hemocorrection, ensures cleansing of the body from poisons that cause the formation of acute renal failure. Hemosorption and plasmapheresis help. If obstructive signs are present, normal urine passage is restored. To do this, stones are removed from the kidneys and ureters.

Hemosorption procedure

The oliguric phase is accompanied by the administration of furosemide, osmotic diuretics that stimulate diuresis. When setting the amount of fluid administered, excluding losses during urination, vomiting, and bowel movements, you need to take into account sweating and breathing.

The patient is prescribed a protein diet, and the intake of potassium from food is limited. The wounds are dried and areas affected by necrosis are eliminated. Antibiotic dosage is based on the severity of kidney damage.

Possible complications of the disease

The initiating and maintaining stages of acute renal failure are accompanied by disruptions in the removal of nitrogen metabolism products, water, electrolytes and acids. The manifestation of changes in the chemical structure of the blood is due to oliguria, the process of catabolism in the patient.

The degree of glomerular filtration is noted compared to patients without oliguria. In the former, more nitrogen metabolism, water, and electrolytes are released with urine.

Failures in acute renal failure without oliguria in patients are less pronounced than in patients affected by pathology.

The normal increase in potassium concentration in the blood serum in patients without oliguria and catabolism is 0.3 - 0.5 mmol/day. Large volumes indicate potassium load of an 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 may include uremia, as an independent intoxication of the body with products of protein metabolism. There is a malfunction in the functioning of organs and systems:

• hyperkalemia, provoking changes in the ECG, will result in cardiac arrest. Pathology affects the development of muscle weakness and tetraparesis;
• blood changes - suppression of hematopoietic function, red blood cell production. The lifespan of red blood cells decreases, and anemia begins to develop;
• suppression of the immune system, which causes 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, followed by stages of excitement;
• pathologies of the cardiovascular system - arrhythmia, pericarditis, arterial hypertension;
• malfunctions of the gastrointestinal tract - discomfort in the peritoneum, 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 plunges into an unconscious state, and severe disruptions in the functioning of the respiratory and cardiovascular apparatus occur.

Properly administered therapy ensures complete reversibility of the disease, except in the most severe cases. The outcome of the disease depends on the patient’s age, the level of renal dysfunction, and the presence of complications.

In a certain proportion of patients, kidney function is restored completely; 1-3% require hemodialysis.