Kidney damage due to infections in pediatric practice. Tubulointerstitial nephritis in children Tin kidney disease

Kidney diseases can develop in people of all ages and genders, causing serious harm to the body. Often, a late-diagnosed pathology can unsettle a person for a long time and bring a lot of not only physical, but also psychological suffering. Over the past 10 years, doctors have increasingly had to deal with one of the most formidable and unpleasant diseases called tubulointerstitial nephritis. Since it can lead to undesirable consequences and even disability, it is necessary to know the first signs of the development of the disease and immediately seek advice from a urologist.

Definition of tubulointerstitial nephitis and its features

Tubulointerstitial nephritis is a pathology in which renal function is impaired due to damage to the tubules and parenchyma (the main substance) of the organ. The result of this disease is gradual shrinkage and reduction in size of the kidney.

With tubulointerstitial nephritis, the kidney becomes smaller and deformed

It is believed that older people (from 65 to 80 years old) are more likely to develop tubulointerstitial nephritis, since at this age the function of the immune system is impaired and all metabolic processes proceed much more slowly.

At the heart of a healthy kidney is a system of tiny vessels that form the glomeruli. They filter the blood, cleanse it of toxic impurities and bacteria, after which some of it is returned to the mainstream, and the processed liquid is excreted in the urine. Urine is collected first in small cups, from which pelvises are then formed, which pass into the ureters.

Video: doctor's lecture about the disease

How is tubulointerstitial nephritis classified?

Depending on the mechanism of occurrence, the following types of illness are distinguished:

primary (formed in a previously unchanged kidney, most often found in children, adolescents and young girls before pregnancy);
secondary (develops against the background of damage to glomerular formations by inflammatory or tumor processes).

According to the international classification of diseases, the following types of disease are distinguished according to the nature of the course:

Acute tubulointerstitial nephritis is accompanied by a pronounced clinical picture. Manifestations increase during the first 7–21 days, and then slowly decline. The disease responds well to therapy and may result in complete restoration of kidney function.
Chronic tubulointerstitial nephritis. This form is characterized by a slower and more gradual development of the main symptoms; the disease exists in the body for about six months. It is extremely unfavorable, since remission does not occur in all cases.
Unspecified acute or chronic tubulointerstitial nephritis. This diagnosis is made if it is not possible to determine the nature of the course and features of the pathological process. Often used for late detection of the disease.

Why does the disease occur?

It is believed that in 90% of cases, tubulointerstitial nephritis develops in people who have a hereditary predisposition and have certain diseases. But factors external environment can also provoke the development of pathology even in an initially healthy body.

The main reasons contributing to the occurrence of the disease include:

cystic cavities in the kidneys;
inflammatory diseases;
tumor formations of the urogenital tract;
endocrine diseases associated with metabolic disorders (diabetes mellitus type 1 and 2, gout, urolithiasis);
connective tissue constrictions in the kidney area, preventing the normal flow of urine;
traumatic injuries of the lumbar area;
pathologies of the blood system (anemia, leukemia, multiple myeloma);
tendency to thrombosis;
diseases associated with damage to the immune system (scleroderma, lupus erythematosus, rheumatoid arthritis);
developmental anomalies;
taking medications (hormones, antibiotics, anabolic steroids) and narcotic drugs;
intoxication with alcohol, gases, breakdown products of chemicals;
ionizing radiation and radiation;
pollution environment where the patient lives.

It is not always possible to discover the true cause of the disease. In my practice, I had to deal with a hereditary form of tubulointerstitial nephritis, which was diagnosed in 5 out of 7 family members.

Video: medical program about factors that have a negative impact on the kidneys

Clinical manifestations of tubulointerstitial nephritis

The intensity of the increase in symptoms and the speed of their development are determined by the form of the disease. The patient may experience a sharp deterioration in health during a cold, intense physical or mental stress, overeating and stress. The clinical picture of tubulointerstitial nephritis includes the following signs:

General intoxication syndrome. It is accompanied by an increase in body temperature by 1.5–2 degrees above normal, nausea and vomiting without connection with meals. In some cases, fatigue, drowsiness and lethargy may occur.
Pain in the lumbar region and discomfort when urinating. These manifestations are directly related to damage to the kidney tissue. The larger the affected area, the more intensely they are expressed.
An increase in blood pressure occurs due to the accumulation of fluid in the body that is not excreted by the kidneys. It accumulates in the bloodstream and tissues, affecting the walls of blood vessels. Externally, this manifests itself in the form of swelling of the upper and lower half of the body. Headache in the occipital region also indicates an increase in blood pressure.

How to identify the disease

If you suspect tubulointerstitial nephritis in yourself or your loved ones, you should contact the clinic for consultation with a urologist or nephrologist. First, the doctor needs to collect an anamnesis: try to talk about the time of onset of the first symptoms, their characteristics and intensity. If you have previously experienced kidney disease, it is worth mentioning this too. Next, temperature and blood pressure are measured: an increase in these indicators also helps in making a diagnosis. There are additional external signs that allow one to suspect the presence of the disease in a patient:

dry and brittle hair;
burst blood vessels in the whites of the eyes;
peeling nail plates;
seizures in the corners of the mouth;
the appearance of bags under the lower eyelids;
puffiness and pastiness of the face and neck.

Photo gallery: what patients with tubulointerstitial nephritis look like

Edema forms due to fluid accumulation Redness of the whites of the eyes is the result of ruptured blood vessels Bags under the eyes are the first sign of kidney problems

One of the most common laboratory tests is a urine test. However, not all patients are aware of how to properly give urine, which causes a delay in receiving results. For example, one of my patients decided to bring urine immediately after menstruation: it contained a large amount of blood and clots, against which she was diagnosed with hematuria and began a completely different treatment, which did not bring relief. After repeated sampling, it turned out that the patient was suffering from chronic tubulointerstitial nephritis, which was in the acute phase. To avoid late diagnosis, it is recommended to bring urine only in disposable jars after toileting the external genitalia. Women should not donate biological fluids during menstruation and 5–7 days after it ends.

Basic methods for identifying the disease:

general urinalysis: with tubulointerstitial nephritis, urine has yellow, cloudy due to impurities of protein, leukocytes and cylindrical cells, bacteria are found in less than 10% of cases;
Ultrasound examination of the kidneys helps to assess the size of the organ, various deformations of the pyelocaliceal system, and also thanks to it it is possible to compare the pathology with pyelonephritis;
endoscopy with biopsy - access to the kidney is carried out through a small incision, a piece of tissue is taken for microscopic examination and confirmation of damage to the tubular system.

Table: differential diagnosis of tubulointerstitial nephritis and other diseases

Comparative characteristics	Tubulointerstitial nephritis	Urolithiasis disease	Pyelonephritis
What is the essence of the disease?	Damage to tubules and renal tissue (almost always non-infectious)	Formation of pathological conglomerates in various parts of the urogenital tract, obstructing the outflow of urine	Inflammation of the bladder mucosa	Changes in the pyelocaliceal system are predominantly of the inflammatory type
Predominant changes in urine	Slight cloudiness	Presence of blood, clots and sand, small stones	Red urine, increased white blood cell count	Urine colors meat slop, protein predominance
Localization and characteristics of pain syndrome	In the lower back, aching and pressing	Along the ureters (right and left parts of the abdomen), acute, like renal colic	Above the pubis, pulling and cutting	In the lumbar region, aggravated by physical activity

Various ways to treat the disease

If the patient’s condition is relatively stable and he does not experience serious problems with urination, he can be observed in the clinic at his place of residence by a urologist or nephrologist. In cases where the patient feels unwell and needs additional help and support, he is sent to a hospital for treatment. All patients are required to be prescribed a low-salt diet. Drug therapy is aimed at eliminating the symptoms of tubulointerstitial nephritis and normalizing the patient’s general condition. At the recovery stage, physiotherapy is widely used: they not only eliminate the residual effects of pathology, but also help strengthen the immune system.

Drug therapy for tubulointerstitial nephritis

To get rid of the symptoms of the disease, doctors prescribe regular use of pharmaceuticals. They are available in the form of capsules, tablets and powders, as well as ampoules for intravenous or intramuscular administration. Dosages of drugs are calculated based on the patient’s weight, age and the presence of other acute or chronic diseases.

Do not try to find treatment on your own. Many drugs have a number of serious contraindications and side effects, which should be read in advance.

What groups of medications are used to treat pathology:

Hormonal anti-inflammatory drugs. They reduce the severity of soft tissue swelling and also help normalize metabolic processes in the body. For this purpose they prescribe: Dexazone, Cortef, Laticort, Kenalog, Prednisolone.
Antihypertensive medications normalize blood pressure and protect against the development of a hypertensive crisis. Most often used: Enap, Perindopril, Capoten, Valsartan, Bisoprolol, Larista, Methyldopa.
Nonsteroidal anti-inflammatory drugs are used to lower body temperature and reduce pain. These include: Piroxicam, Celebrex, Naprosyn, Paracetamol, Aspirin, Analgin, Viox, Erazon, Nimesid, Ibuklin.
Diuretics stimulate the removal of fluid from the body and indirectly lower blood pressure. For this purpose they prescribe: Mannitol, Furosemide, Torasemide, Hypothiazide, Lasix.

Photo gallery: medications to eliminate pathology

Cortef eliminates inflammatory swelling
Celebrex reduces pain
Furosemide removes fluid from the body

Natural recipes to combat symptoms of the disease

Certain manifestations of tubulointerstitial nephritis can be eliminated through the competent use of folk remedies. Many plants, herbs and fruits have healing properties, which makes them useful in the fight against disease. But remember that it is impossible to replace traditional medicine with them, since they are not so highly effective.

Some herbal components in a sensitive person with a tendency to urticaria, dermatitis and bronchial asthma can cause undesirable symptoms. Most often, an allergic reaction develops in the form of a spontaneous attack of breathing problems and also requires emergency assistance. It is recommended to always have an antihistamine (Tavegil, Zodak) with you to cope with such manifestations.

Most Popular folk recipes to fight the disease:

Mix 20 g of lingonberries, 130 g of blackberries and 100 g of honeysuckle (you can use both fresh and frozen berries). Pour 2 liters of boiling water over them and cook for half an hour over low heat. After cooling, you can add cane sugar or honey for taste. Drink 1 glass of the product every 3-4 hours (it is recommended to spend this day at home). This combination of berries stimulates increased urination, due to which the body is cleansed of toxins and waste. The procedure needs to be carried out once a month.
Pour 50 g of pine nuts with a liter of vodka or medical alcohol and place in a dry, dark place for 30–45 days. After the specified period has expired, every evening before going to bed, add 10-15 drops of the product to a glass of water and drink. This tincture based on pine nuts has an anti-inflammatory and antiseptic effect. It is recommended to undergo a course of treatment consisting of 20 procedures with an interval of 1 day.
Brew two teaspoons of chopped plantain in a thermos with 0.5 liters of boiling water and leave overnight. In the morning before breakfast, drink 1 glass of the product. Plantain stimulates the regeneration of soft tissues and accelerates the healing process. It is recommended to use it daily for 3 months to achieve noticeable results.

Photo gallery: folk remedies for treating illness

Lingonberry has diuretic properties Pine nuts have an antiseptic effect Plantain accelerates tissue healing

How to properly organize nutrition for patients with tubulointerstitial nephritis

Don't forget that most toxic substances enter the body through food and water. For this reason, it is extremely important to normalize your diet and reduce the load on your kidneys. Doctors advise organizing meals at certain hours: this way the gastrointestinal tract absorbs foods better. It is necessary to maintain a balance of proteins, fats and carbohydrates in a ratio of 1:1:4. And you also don’t need to limit yourself in fluid intake in order to normalize the water-salt balance.

With tubulointerstitial nephritis, the amount of salt consumed should be reduced to 5–6 g per day, as it contributes to the occurrence of edema in the soft tissues.

What needs to be included in the diet:

Vegetables and fruits in the form of stews, slices, salads, purees and jellies. They contain the necessary amount of vitamins and minerals, and are also a source of fiber, which has a cleansing function and removes toxins from the body.
Dairy products: kefir, cottage cheese, sour cream, fermented baked milk, yogurt without additives. This diet will help meet your calcium and protein needs.
Lean meat and offal. Particularly useful: chicken, pork, beef, liver, stomachs and hearts. You should not give up meat, since animal protein is actively involved in the construction of new cells and tissues.
Porridge and cereals are an excellent option not only for breakfast, but also for a side dish. They contain more than half of the healthy carbohydrates that are responsible for saturating the body.

Vegetables and fruits give you a boost of energy throughout the day Dairy products are a source of calcium and protein Cereals are a source of slow carbohydrates

Table: the role of physiotherapy in the fight against pathology

Name of the technique	How is the procedure performed?	Main effects of the appointment	Approximate number of sessions required
Mud wrap	Using a brush, a healing composition based on algae and medicinal clay is applied to the patient’s body, and then a film is applied on top, the patient is covered with a blanket and left for 30 minutes.	Reducing inflammatory swelling of soft tissues	7–10
Acupuncture (acupuncture)	Thin needles are inserted into certain reflexogenic zones of the body to the depth of the skin and fatty tissue.	Improving blood supply and lymphatic drainage in the selected area, thereby accelerating the healing and regeneration of soft tissues	5–15
The area where the kidneys are located is targeted by the laser	Death of pathogenic microorganisms, prevention of proliferation connective tissue and the formation of adhesions in the area of the collecting system	20–25
Ultrasound therapy	The sound wave passes through the affected areas of the organ	Normalization of metabolic processes, protection against increased blood clotting, pain relief	10–15

Photo gallery: physiotherapy to eliminate symptoms of the disease

Acupuncture is the art of stimulating the reflex zones of the body Laser protects against the growth of adhesions Mud wraps also have a beneficial effect on the skin

Features of treatment of tubulointerstitial nephritis in children

The body of a baby has significant differences from the body of an adult. Tubulointerstitial nephritis in children in 95% of cases develops acutely and is a consequence of some kind of intoxication. For this reason, hemodialysis is one of the main treatment methods. It is a procedure for artificially purifying blood from harmful impurities (including chemicals, microbes) using a filtration membrane. After hemodialysis is completed, the little patient’s condition improves and he is transferred to the general ward.

Hemodialysis helps cleanse the blood

Another important aspect is nutrition. In children under one year of age, most of the diet consists of breast milk or artificial formulas, so it is recommended to pay attention to the baby’s health during feeding. For a more mature child, nutrition is organized according to the same principles as for adults. Of the medications, detoxification agents are most often used to remove harmful substances: Acesol, Trisol, Regidron, Reamberin.

During the period of treatment, it is better to exempt the baby from attending kindergarten, school and additional clubs in order to reduce the likelihood of infection and other complications.

Forecasts for recovery and undesirable consequences of the disease

Tubulointerstitial nephritis is a serious kidney disorder. In the acute form of the disease, it can be cured within 1.5–6 months, while the chronic type of the disease can only be transferred to the remission phase. Against the background of additional complications ( renal failure) life expectancy is reduced by approximately 2–4 years. The following factors increase the risk of developing undesirable consequences:

elderly age;
immunodeficiency conditions (AIDS);
diseases of the nervous, cardiovascular and endocrine systems.

In children, with a favorable course of the disease and timely treatment, complications practically do not arise. Kidney function can be fully restored in 3–8 months, which is associated with the high intensity of regeneration processes.

During the period of fighting pathology, it is extremely important to adhere to a diet and limit yourself in consuming fatty, fried and salty foods, as well as alcoholic beverages. One of my patients, suffering from chronic tubulointerstitial nephritis, was discharged from the department with an improvement in his general condition. However, within a week the man violated his diet several times. During the last episode he drank a large amount of alcohol, which was not compatible with the prescribed pills. Against this background, the patient developed serious intoxication, an ambulance was called and gastric lavage was performed. If the man had not violated his diet and did not drink alcohol, such an illness could have been avoided.

What complications can develop against the background of tubulointerstitial nephritis:

acute and chronic kidney failure: pathological condition, in which organs cease to perform their function and gradually shrink;
a decrease in the number of red blood cells and a decrease in hemoglobin levels (anemia, which is accompanied by hair loss, brittle nails, general weakness and lethargy);
residual pain syndrome in the lumbar region (may respond to changes in weather conditions and atmospheric pressure);
inflammatory diseases of neighboring organs (cystitis, urethritis, myometritis);
attachment of pyogenic microflora and formation of a renal carbuncle;
miscarriage, premature birth and miscarriages early stages(among women);

How to prevent the development of tubulointerstitial nephritis

Such an illness can lead to disability, significantly worsening the quality of life, and in especially severe cases, death can occur. For this reason, many doctors believe that it is best to prevent the occurrence of tubulointerstitial nephritis in advance. Those who have previously had other kidney diseases should monitor their health especially carefully.

One of the most important roles in preventing the development of tubulointerstitial nephritis and its complications is played by preventive medical examination, which employees of almost all enterprises and organizations undergo 1 or 2 times a year. One of my friends, who was a chef in a restaurant, took tests every year to receive a health certificate. Thanks to the urine test, it was possible to detect kidney problems in a timely manner and prescribe additional methods to confirm the results. As a result, the woman was diagnosed with tubulointerstitial nephritis and specific treatment was started. According to doctors, if the patient had applied a little later, the situation could have ended extremely unfavorably for the life and health of the patient. That is why it is necessary to regularly take urine and blood tests, as well as visit a therapist, even in the absence of complaints.

Rules for individual prevention of tubulointerstitial nephritis:

try to minimize the amount of alcohol consumed and drink only natural products in small quantities (this will avoid poisoning from scorched ethyl alcohol);
stop smoking (including hookahs, electronic cigarettes and vapes);
Visit the gym or swimming pool 2-3 times a week, spend more time outdoors;
if you suffer from drug addiction, you should consult a psychiatrist to treat this problem;
most of the food should be natural (it is better to get rid of dyes and additives);
watch your weight: obesity can also cause kidney problems due to blood supply pathology;
do not limit yourself in drinking water: in the absence of other diseases, drink about 2–2.5 liters of liquid daily;
all medications and their dosages must be agreed with the doctor (self-administration of medications often causes toxic damage to the glomeruli);
regularly see a therapist and surgeon, take blood and urine tests, and undergo other necessary tests;
Minimize stress and allocate more time for hobbies and favorite activities.

Tubulointpersitial (or interstitial) nephritis called inflammation and damage to the tubules and interstitial tissue of the kidneys with relative safety of the glomeruli and blood vessels. There are not only primary forms of acute and chronic interstitial nephritis, but also its secondary forms with primary damage to the glomeruli and in systemic diseases.

Main distinctive features acute tubulointerstitial nephritis are lymphocytic infiltration of interstitial tissue, edema and tubular damage. Eosinophils may be present in the infiltrates, especially in drug-induced tubulointerstitial nephritis, and sometimes granulomas. The pathogenesis is not fully understood. The involvement of T-cell immune mechanisms has been postulated. Causing agents include medications, especially antimicrobials, anticonvulsants, and anticonvulsants, as well as infections, primary glomerular diseases, and systemic diseases (eg, SLE).

Clinical manifestations of acute tubulointerstitial nephritis. Classic signs of tubulointerstitial disease are fever, rash, and arthralgia associated with elevated serum creatinine levels. However, this typical triad of manifestations does not occur in all patients. The rash is often transient and varies in appearance, from maculopapular to urticaria. Nonspecific symptoms are common: nausea, vomiting, weakness, weight loss. Enlargement of the kidneys, leading to stretching of the renal capsule, usually causes pain in the lumbar region.

At acute tubulointerstitial nephritis- complications of other diseases (for example, SLE) - specific signs of the underlying disease are usually observed. In contrast to glomerular lesions, which are characterized by acute renal failure with oliguria, oliguria is absent in 30-40% of patients with acute tubulointerstitial nephritis. In drug-induced nephritis, peripheral eosinophilia is observed. In all cases, microhematuria of varying degrees occurs, but macrohematuria or proteinuria, as a rule, is absent. The exception is patients with nephritis caused by NSAIDs, in whom nephrotic syndrome is possible.
In the urine there are leukocytes and granular cylinders, but red blood cell casts, characteristic of glomerular diseases, are rarely observed. The presence of eosinophils in the urine is not a specific sign.

Diagnosis of acute tubulointerstitial nephritis. The diagnosis is made based on the clinical picture and laboratory data. It is extremely important to find out the time dependence of the onset of the disease on the use of certain medications. Since immune mechanisms are involved in the pathogenesis of tubulointerstitial nephritis, its signs and symptoms usually appear after 1-2 weeks. After exposure to drugs. In children, the cause of the disease is often antimicrobial drugs, as well as NSAIDs.

Urinalysis should be performed periodically and levels monitored. creatinine and electrolytes in blood serum. Ultrasound of the kidneys does not have diagnostic value, but it can detect their enlargement and increased echogenicity. Improvement in renal function after elimination of all possible reasons These factors provide convincing evidence of the correctness of the diagnosis; further research is usually not required.

In more complex cases, when cause remains unclear or the patient's renal function is rapidly deteriorating, a kidney biopsy is indicated. Treatment and prognosis. Symptomatic treatment is aimed at eliminating complications of acute renal failure, such as hyperkalemia and volume overload. Some data indicate the effectiveness of corticosteroids in severe renal impairment. In case of rapid spontaneous improvement, the prognosis is very favorable. However, in patients with long-term renal failure, the prognosis is unclear. Severe acute tubulointerstitial nephritis of any origin often becomes chronic.

Tubulointerstitial nephritis is an inflammatory and metabolic lesion of interstitial renal tissue, which is characterized by disruption of the renal tubules with relatively intact glomerular function.

The main causes of tubulointerstitial nephritis are infectious agents, exogenous toxins, metabolic and immune disorders, and the use of certain medications.

This disease can occur in acute and chronic forms, manifested by moderate proteinuria, microhematuria, abacterial leukocyturia, hyponatremia, hypovolemia, polyuria and a decrease in the relative density of urine.

The goal of treatment of tubulointerstitial nephritis is to eliminate the pathogenetic factor and restore kidney function.

Causes of tubulointerstitial nephritis

Acute tubulointerstitial nephritis can be caused by various infections (diphtheria, brucellosis, mycoplasmosis, toxoplasmosis, syphilis, cytomegalovirus infection, leptospirosis and others), poisoning. Also, this disease can be the result of taking certain medications, hemolysis, burns, injuries, circulatory disorders, or can act as a complication after vaccination.

Chronic tubulointerstitial nephritis can also be caused by the patient's hereditary predisposition, renal dysembryogenesis, chronic infections and intoxications, metabolic disorders, diseases of the immune system, adverse environmental influences (intake of radionuclides, heavy metal salts into the body).

If left untreated, acute tubulointerstitial nephritis can become chronic.

Post-infectious tubulointerstitial nephritis develops as a result of exposure to the basement membrane of the tubules and capillary endothelium of the interstitium to toxins produced by various microorganisms, as well as their antigens, which leads to cell damage, increased capillary permeability and the inclusion of nonspecific inflammatory factors. In addition, damage to the endothelium and tubules of an immunological nature occurs.

Direct damaging effects on the tubular epithelium are also exerted by various chemical substances and medications. The range of drugs that cause this disease is quite wide. These include antibiotics, diuretics, non-steroidal anti-inflammatory drugs, and antihistamines. Allopurinol, azathioprine, diazepam, aspirin, captopril can also provoke the development of tubulointerstitial nephritis.

Tubulointerstitial nephritis in children can develop against the background of dysmetabolic nephropathies. But most often this is facilitated by the frequent use of sulfonamide drugs and beta-lactam antibiotics.

Symptoms of tubulointerstitial nephritis

Acute tubulointerstitial nephritis is characterized by a rapid onset and occurs 1-30 days after exposure to the etiological factor. The first symptoms are: thirst, large amounts of urine (polyuria), fever, rash, and in some cases, lower back pain. Also, in rare cases, swelling and a decrease in the volume of urine produced may occur. Increased protein content in the urine and edema are more typical of tubulointerstitial nephritis, which is caused by taking NSAIDs.

Chronic tubulointerstitial nephritis is characterized by a low protein content in the urine, the absence of hematuria and edema. In the early period of the disease, the patient's blood pressure is normal or slightly increased. If a large amount of blood and protein is found in the urine, this indicates damage to the glomeruli. With abnormal functioning of the renal tubules, the symptoms of chronic tubulointerstitial nephritis are similar to those in the acute form of the disease.

In certain forms of chronic tubulointerstitial nephritis, stones can form in the kidneys.

Diagnosis of tubulointerstitial nephritis

When making a diagnosis, the doctor uses medical history data and the results of laboratory tests of the patient’s biological material.

For this purpose the following are assigned:

Clinical blood test. With this disease, eosinophilia and anemia are detected, and an increase in ESR and leukocytosis are possible;
General urine analysis. Proteinuria, decreased urine density, hematuria, cylindruria are detected;
Blood chemistry. There are increased levels of creatinine and urea, blood transaminases, metabolic acidosis, and changes in the electrolyte composition of the blood.

In addition, the patient may be prescribed a kidney ultrasound and nephrobiopsy.

Treatment of tubulointerstitial nephritis

Treatment of tubulointerstitial nephritis should begin with eliminating the cause that caused it (withdrawal of the drug that caused the disease - antibiotics, analgesics, cessation of contact with toxins).

After this, correction of disorders caused by impaired kidney function is performed. For this purpose the following are assigned:

Soda solution intravenously (correction of acidosis);
Iron supplements, erythropoietin (correction of anemia);
Oral antihypertensive drugs (blood pressure correction);

Measures are also taken to normalize the water-electrolyte balance, and renal failure is treated (diuretics, drugs that improve renal blood flow, antihistamines).

If the effect of the treatment does not occur after 7 days or the increase in renal failure continues, then the use of glucocorticosteroids is considered.

In the treatment of tubulointerstitial nephritis in children and adults, bed rest, adequate fluid intake, and rational, gentle diet therapy with salt limitation are recommended, aimed at reducing the metabolic load on the renal tissue.

Also, for this disease, antibacterial therapy is indicated after urine culture for sensitivity to antibiotics, antifungal and uroseptic drugs, and immunostimulants.

If the patient receives adequate treatment, does not take drugs that provoke the disease, and his body responds well to therapy, then kidney function is completely restored.

In the acute form of the disease, the patient must be hospitalized. After discharge from the hospital, he is subject to clinical observation for 5 years; he must be examined by a nephrologist twice a year and undergo regular urine and blood tests.

Thus, this disease, provided that the influence of the provoking factor is timely eliminated, has a favorable prognosis for the patient. But the longer the contact, the lower the likelihood of reversibility of changes. Therefore, you should not uncontrollably take non-steroidal anti-inflammatory drugs and diuretics. Infectious diseases must be treated promptly and healthy image life.

Acute tubulointerstitial nephritis (TIN) is nonspecific. If measures are not taken in time, the passages (tubules) of the kidneys gradually atrophy, and the kidneys themselves cease to function normally. Due to disruption of the blood filtration process, all body systems suffer. The nature of tubulointerstitial nephritis may be hidden in metabolic or immune changes, external influences of infection and chemicals. Inflammation of all structures of the renal tissue and canals of the kidneys occurs.

In the CIS countries, the disease is not widespread; according to statistics, 1.7% of the population have TIN. Every year such patients must undergo hemodialysis (extrarenal blood purification).

There are several criteria by which TIN is divided:

by the nature of the flow;
due to occurrence;
by pathogenesis;
by the nature of the tubular disorder.

The nature of the tubular disorder can be of three types:

Endocrine dysfunctions.
Partial violations.
Disorders of the tubules.

The form of the disease can be acute or chronic.

The disease can be hereditary, in which case it is called Alport syndrome. A child is born with glomerulopathy or hematuria, which reduces kidney function and leads to. Tubulointerstitial nephritis in children is accompanied by visual and hearing impairment.

The sudden onset of renal failure is the main symptom of the acute form. This occurs as a result of damage to the kidney tubules and tissues.

Chronic tubulointerstitial nephritis appears after damage to these same structures on a larger scale. The most common reason is prolonged or uncontrolled use of medications, the influence of another kidney disease.

Tubulointerstitial nephritis can be primary or secondary. The primary one is caused by a harmful agent, for example, chemicals, infections, toxins, or metabolic failure. Secondary tubulointerstitial nephritis appears if the body already has chronic kidney disease, namely radiation nephritis, amyloidosis, nephroangiosclerosis, etc.

The following classification according to the nature of the damaging factor:

infectious;
drug;
immune;
metabolic disorders.

Causes of the disease

Unspecified acute tubulointerstitial nephritis occurs when the body is exposed to external harmful factors. The main harmful agents are infections, medications and allergens.

Which substances most affect the tissues and tubules of the kidneys:

non-narcotic analgesics;

antibiotics;
sulfonamides;
immunosuppressants;
substances for chemotherapy;
iodine, lithium;
biological toxins, pesticides;
heavy metals;
medicinal herbs, herbicides;
alcohol.

TIN develops as a result of metabolic disorders, namely:

clogging of blood vessels with cholesterol;
increased levels of uric acid in the blood.

The kidneys suffer due to the following systemic diseases:

hepatitis;
oncological diseases;
diseases of the lymphatic system;
anemia;
myeloma;
diseases of the genitourinary system;
vasculitis;
sarcoidosis;
Sjögren's syndrome.

Manifestations of vasculitis on the neck and chest

Infections that cause negative impact on the kidneys:

The above factors negatively affect human kidneys only with increased sensitivity to certain components. If the patient is at risk, then it is almost impossible to protect yourself from the problem.

Chronic tubulointerstitial nephritis appears in a person when a person does not consult a doctor in a timely manner or when treatment tactics are chosen incorrectly. The more common cause is severe intoxication, exposure to radiation, immune or metabolic disorders, nephropathy. The most susceptible to the disease are patients suffering from liver cirrhosis, diabetes, abusing caffeine, analgesics and antibiotics, and having heart pathologies.

Diabetes mellitus is one of the possible causes of tubulointerstitial nephritis

Symptoms

The disease develops at least 30 days after exposure to a harmful factor. At the beginning of the development of the acute phase, the patient’s pressure increases, blood through the tubules begins to move more slowly, and the quality of filtration decreases. Due to decreased water reabsorption, the amount of urine increases. Symptoms can be confused with inflammatory kidney disease. Therefore, the patient must undergo laboratory testing. As the disease progresses, the amount of fluid in the body increases, kidney stones appear, and protein appears in the urine.

Depending on the form, the disease has different symptoms. The acute form is characterized by the following symptoms:

increased body temperature;
backache;
enlarged kidneys, which can be detected during palpation or ultrasound;
painful urination;
discharge of pus in the urine;
rashes on the body.

Some patients experience no or mild symptoms. Kidney failure is detected during a routine examination using a blood test.

In chronic forms of tubulointerstitial nephritis, symptoms initially also appear to a mild degree, gradually increasing the impact. The patient has:

general weakness of the body;
decreased appetite;
increased fatigue.

Despite water retention in the body, the limbs do not swell. The more the kidneys suffer, the more severe the symptoms of acute nephritis. These include dry mouth and frequent urination.

Symptoms often appear several weeks after exposure to a toxic substance. Some patients begin to feel the disease only after repeated exposure. If the cause of TIN is the use of non-steroidal anti-inflammatory drugs, then the disease begins to actively develop after a year and a half.

Edema appears after the development of renal failure. Along with this, polyuria appears. If renal function is impaired, then the symptoms of renal failure become pronounced.

Diagnostic methods

Determining the presence of tubulointerstitial nephritis is not easy, and there is no single test that will definitely show the problem. The patient needs to undergo a comprehensive examination. If the TIN is available, the following inconsistencies will be identified:

increased amounts of protein, white and red blood cells in the urine;
alkaline urine reaction;
decreased density of urine;
hemoglobin level less than 100 units;
increased levels of eosinophils and sodium in the blood.

A general analysis of urine and blood is examined in comparison before and after certain loads.

Before starting treatment, the doctor must exclude the presence of prostatitis, urolithiasis, nephroptosis, and tumors. The above problems give symptoms similar to TIN.

An ultrasound of the kidneys is required. In the presence of TIN in the acute phase, the organs will be swollen and enlarged in size; in the chronic form, the size of the kidneys is normal. The kidney tubules are enlarged and cysts are detected. Computed tomography provides more reliable information about the condition of the kidneys. MRI, CT, and radiography provide information about the size of organs, the shape of the edge, and the degree of calcification.

Additional information will be provided by urine culture and kidney biopsy.

Treatment

Goals of drug therapy:

relief of symptoms;
restoration of the filtration process;
stabilization of the body's condition;
exclude the development of renal failure.

Treatment of tubulointerstitial nephritis begins after eliminating the harmful factor. To do this, the patient's medical history is studied. If the reason is long-term use of medications, then it is replaced with another one.

A patient with tubulointerstitial nephritis is prescribed a diet, especially in the acute phase of the disease. Avoid salt, seasonings, spicy and smoked dishes, drinking plenty of fluids is recommended. The amount of protein in the diet is reduced, coffee and tea are replaced with herbal infusions. Useful are lingonberry leaves, bearberry, and flax seeds.

If possible, the patient should avoid stressful situations, physical and intellectual stress, and hypothermia.

Viral TIN is treated with antiviral drugs, bacterial TIN with antibiotics. If medications lead to a blood clotting disorder, anticoagulants are prescribed; the danger is the increased thickness of the blood, which causes blood clots. Antifungal drugs, uroseptics, and immunostimulants may be prescribed.

Drug therapy includes taking the following drugs:

Isoniazid.
Omeprazole.
Fluoroquinolone.
Sulfanilamide.
Ranitiline.

Depending on the results of the analysis, the following may be prescribed:

Pyridoxine.
Cholestyramine.
Calcium lactate.

Forecast

The genetic, toxic and metabolic type of the disease cannot be corrected, and end-stage renal failure occurs. Advanced disease can cause pulmonary edema.

In case of chronic tubulointerstitial nephritis stage of the disease, as well as continued exposure to the body of a harmful agent, there is a risk in prescribing lifelong hemodialysis.

After treatment, kidney fibrosis remains, the functions themselves are restored, and the prognosis is favorable.

Catad_tema Kidney pathology - articles

Acute tubulointerstitial nephritis

ICD 10: N10, N14.0, N14.1, N14.2, N16.4

Year of approval (revision frequency):

ID: KR468

Professional associations:

Approved

Agreed

CT – computed tomography

MRI – magnetic resonance imaging

NSAIDs – non-steroidal anti-inflammatory drugs

AKI – acute kidney injury

ATIN – acute tubulointerstitial nephritis

TMA – thrombotic microangiopathy

CKD – chronic kidney disease

Terms and Definitions

NSAIDs – non-steroidal anti-inflammatory drugs (including drugs with a predominant anti-inflammatory and predominant analgesic effect).

AKI is the rapid development of kidney dysfunction as a result of direct exposure to renal or extrarenal damaging factors.

1. Brief information

1.1 Definition

Acute tubulointerstitial nephritis (ATIN) is an acute kidney disease that develops in response to exposure to exo- and endogenous factors and manifested by inflammatory changes in the tubulointerstitial tissue of the kidneys with the frequent development of acute kidney injury (AKI).

1.2 Etiology and pathogenesis

The causes leading to the development of ATIN may be infectious processes caused by bacteria, viruses, metabolic disorders, heavy metals, diseases of immune origin, neoplastic diseases, radiation, hereditary diseases kidney

The problem of drug-induced kidney damage is one of the current problems modern nephrology. Approximately 6–60% of all cases of AKI are due to interstitial nephritis, as determined by nephrobiopsy. In half of the cases, the etiology of acute interstitial nephritis is drugs.

Interstitial nephritis most often develops in response to antibiotics and nonsteroidal anti-inflammatory drugs (NSAIDs). NSAIDs are the cause of 44–75% of cases of ATI, antibiotics - 33–45% of cases. The relative risk of developing ATIN when taking NSAIDs is 1.6–2.2%, and increases to 13.3% at the age of over 66 years. However, no significant difference was found in the risk of developing ATIN between different NSAIDs, including selective and non-selective. Also, ATIN can develop in response to the use of other drugs; the most common culprits of ATIN are presented in Table. 1.

Table 1. Drugs that can cause interstitial nephritis

Drug class	Examples
Antibiotics	Aminoglycosides, cephalosporins, fluoroquinolones (ciprofloxacin), ethambutol, isoniazid, macrolides, penicillin, rifampicin, sulfonamides, tetracycline, vancomycin
Antiviral drugs	Acyclovir, interferon
NSAIDs, analgesics	Almost all representatives of NSAIDs, phenacetin, metamizole sodium
Diuretics	Furosemide, thiazide, indapamide, triamterene
Antisecretory drugs	Hydrogen pump blockers (omeprazole, lansoprazole), H2-histamine blockers (ranitidine, cimetidine, famotidine)
Antihypertensive drugs	Amlodipine, captopril, diltiazem
Miscellaneous	Allopurinol, azathioprine, carbamazepine, clofibrate, phenytoin, angiographic contrast agents, polyvilylperolidone-based drugs, calcineurin inhibitors (cyclosporine A)

Nephropathy due to Chinese herbs is known as Chinese herb nephropathy" It is characterized by rapid progression of chronic renal failure (CRF) and manifests morphologically as extensive interstitial fibrosis without glomerular damage. It occurs mainly in women taking herbal medicines containing Chinese herbs. Nephrotoxicity is determined by the presence of aristolochic acid in herbs. It has been shown that the cumulative dose of the extract Aristolochia fangchi from the place Stephania tetrandra leads to the development of chronic renal failure in 30.8% of cases.

In the pathogenesis of ATIN, several links are distinguished: intrarenal vasoconstriction; blockade of microcirculation due to interstitial edema, development of thrombotic microangiopathy (TMA); direct tubulotoxicity; acute inflammation of the interstitium.

Exposure to the causative factor leads to lymphohistiocytic infiltration and swelling of tubulointerstitial tissue, degeneration and necrosis of the tubular epithelium. In the process of resolution of ATIN, an increase in reparative phenomena in the form of tubulointerstitial fibrosis is observed, which can lead to the formation of chronic renal failure.

1.3 Epidemiology

The issue of the prevalence of ATIN is one of the most difficult. Significant differences in the prevalence of nephritis of microbial and drug origin in Russia and abroad are determined by the imperfection of technologies for identifying and recording this pathology, inconsistency of diagnostic criteria, and sometimes the nonspecificity of the clinical manifestations of some forms of interstitial nephritis. According to a number of centers, during puncture nephrobiopsy, ATIN is registered in 2.3–9% of cases. Of course, a biopsy is performed when the clinical picture does not allow a full diagnosis of ATIN and the majority of patients with ATIN do not undergo a biopsy.

1.4 Coding according to ICD 10

Tubulointerstitial kidney disease(N10–N16):

N10 – Acute tubulointerstitial nephritis;

N14.0 – Nephropathy caused by analgesics;

N14.1 – Nephropathy caused by other drugs, medications or biologically active substances;

N14.2 – Nephropathy caused by unspecified medicine, medicine or biological active substance;

N16.4 – Tubulointerstitial kidney damage in systemic connective tissue diseases.

Systemic connective tissue lesions(M30 – M36)

M32.1 – Systemic lupus erythematosus with damage to other organs or systems.

1.5 Classification

Infectious origin:

Bacterial, viral, fungal, mixed, including acute pyelonephritis.

Non-infectious origin: toxic (exogenous or endogenous intoxication), medicinal (a special case of toxic nephritis) - antibiotics, NSAIDs, antitumor drugs, etc., immune-mediated (including autoimmune), dysmetabolic (eg, hyperuricemic).

2. Diagnostics

2.1 Complaints and anamnesis

Complaints are usually few or not pathognomonic. More often associated with manifestations of AKI, in particular, a decrease in urine volume, an increase in blood pressure, and there may be a dull aching pain in the lumbar region.

Obligatory manifestations of ATIN are urinary syndrome and AKI syndrome. Urinary syndrome is manifested by proteinuria less than 1 g/day (91–95%), erythrocyturia (21–40%), abacterial leukocyturia (41–47%), including eosinophiluria (21–34%). AKI occurs in all patients. More often, according to the registers of intensive care centers, stage 3 AKI occurs in half of the cases, while stage 1 and 2 AKI divide the remaining half approximately in half. However, general statistics indicate underdiagnosis of ATI with AKI stages 1–2. Quantitative changes in urine are often recorded. Both polyuria and oliguria or anuria may be observed. The last two symptoms indicate more severe kidney damage. In 30–45% of patients, acute hypertension syndrome or worsening of pre-existing arterial hypertension (AH) is observed. Of the extrarenal manifestations of ATIN, the most common are arthralgia (20–45%), leukocytosis (20–39%), eosinophilia (14–18%), low back pain (21%), rash (13–17%), fever ( 14–17%), and with drug-induced ATIN these symptoms are more common.

One of the possible manifestations of kidney damage, more often observed with analgesic ATIN, is papillary necrosis. Papillary necrosis is caused by capillary necrosis of the papillary zone of the kidneys. The clinical picture includes renal colic (mutilation of the papilla causes blockage of urination in the area of the pelvis, ureteropelvic segment or ureter), micro- and macrohematuria.

Risk factors for the development of ATIN that increase the likelihood of kidney damage when exposed to exogenous factors are age over 60 years, diabetes mellitus, CKD, vascular diseases, hypoalbuminemia, multiple myeloma, heart and liver failure, dehydration, sepsis, heart surgery, organ transplantation.

2.2 Physical examination

Increased blood pressure may be observed, and palpation of the kidneys may cause pain or discomfort upon palpation. Fever is observed with infectious genesis of ATIN. Polyuria, normuria, oliguria or anuria may be observed.

2.3 Diagnostics

Recommended in the presence of urinary syndrome and AKI are integral clinical manifestations of ATIN. Establishing the etiological factor contributes to making the correct diagnosis.

It is recommended that when carrying out differential diagnosis, in most cases the leading syndrome should be considered AKI.

Comments: Important For the diagnosis of ATIN, identification of the causative factor is necessary, which, along with the development of urinary syndrome and AKI, allows for a correct diagnosis. Below is the diagnostic algorithm for OTIN..

In addition to studies that make it possible to exclude prerenal and postrenal forms of AKI, clarify the etiology of the process, and also verify urinary syndrome, a number of diagnostic studies are carried out aimed at identifying disorders of water-electrolyte and acid-base balance(ABC-gram, levels of K + , Na + , Cl – , Ca 2+ in the blood, assessment of water balance with calculation of the volume of circulating plasma, diuresis, impedance measurement), damage to other organs (liver, gastric and duodenal mucosa, nervous system, hearts, etc.).

It is recommended that in the case of the use of NSAIDs or analgesics, the cause of ATIN should be taken as the cause only on the basis of anamnestic data, and a large dose of the drug, the combined use of several NSAIDs and/or analgesics, as well as the presence of risk factors for the development of ATIN make the judgment about the etiology of ATIN more reasonable, since There are no specific signs of ATI due to NSAIDs or analgesic effects.

Level of evidence reliability – NGD.

Comments: Morphological diagnosis for ATN is not as relevant as for differentiating glomerulonephritis. However, in a number of cases its implementation is indicated. In particular, puncture nephrobiopsy is performed when diagnosing ATI of unknown origin, when AKI progresses despite the abolition of the causative factor and ongoing therapy, and when ATI develops due to diffuse connective tissue diseases of immune origin.

An infrequent manifestation of analgesic ATIN is papillary necrosis. Diagnosis of papillary necrosis consists of recording renal colic, the appearance or intensification of hematuria, often with the development of gross hematuria, and visualization of the process. According to ultrasound, an isoechoic formation is detected in the abdominal system, a defect or smoothing of the internal contour of the renal parenchyma in the area of the renal papilla is noted. CT or MRI allows you to more accurately verify the process. The absence of a history of indications of urolithiasis and renal colic, information about the administration of an analgesic, and the appearance of gross hematuria allow one to lean toward the diagnostic hypothesis of papillary necrosis at the pre-imaging stage.

A number of ATIs have specific clinical manifestations of the disease that caused them. In particular, with hyperuricemic (gouty) nephropathy, urinary syndrome appears at the height of the clinical manifestations of gout and hyperuricemia, and is also provoked by a number of medicinal effects (the use of diuretics, cytostatics in large doses, for example, in the treatment of blood diseases), possibly against the background of hypovolemia, increased cell death syndrome (tumor diseases with tissue destruction). A severe manifestation of hyperuricemic nephropathy is acute uric acid blockade (hyperuricemic ATI) due to tubular obstruction by uric acid crystals and tubular necrosis, edema and inflammatory infiltration of interstitial tissue.

Another example is myoglobinuric nephropathy, which develops as a result of intensive breakdown muscle fibers. It is observed in long-term crush syndrome, positional compression syndrome, a number of intoxications and diseases (dermatomyositis), manifested by intense rhabdomyolysis. Assessing the medical history and objective status, along with determining an increased level of myoglobinemia/myoglobinuria, helps to understand the cause of AKI.

Typically, there are no diagnostic difficulties in identifying ATIN that has developed as a result of the use of radiocontrast agents, the so-called contrast-induced nephropathy. The risk of its development increases due to a number of reasons. One of the main ones is the use of high-osmolar, less often low-osmolar contrasts, and the use of a large dose of contrast. An important reason is the presence of chronic heart failure, hyperviscose syndrome, diabetes mellitus and gout, undergoing heart surgery with artificial circulation, as well as the presence of pre-existing kidney disease complicated by chronic renal failure. Often, contrast-induced nephropathy is asymptomatic and the only manifestations after an X-ray contrast study (coronary angiography, urography, renal angiography, etc.) may be an increase in blood creatinine levels and the appearance of urinary sediment. In more severe cases, anuria develops and the need for RRT arises.

In a number of diseases, kidney damage is manifested not only by acute inflammatory disease, but also by glomerulitis, pyelitis, and vasculitis. In particular, with sepsis, systemic lupus erythematosus (SLE), polyarteritis nodosa (microangiopathic form), antiphospholipid syndrome (APS), etc. In such situations, in the absence of a morphological picture of the renal biopsy, they often resort to using a term that does not contain a localization component , for example, lupus nephritis, septic nephropathy, etc. The relevant recommendations devoted to these nosologies discuss in detail the issues of their diagnosis and treatment.

2.4 Differential diagnosis

Differential diagnosis is usually carried out with the identification of the leading syndrome - AKI. It is necessary to exclude obstructive uropathy (most often urolithiasis, congenital anomalies of the upper urinary tract), pyelonephritis against the background of reflux nephropathy, occurring with symptoms of obstruction, diagnosed in the form of dilation of the pyelocaliceal system using ultrasound, less often - CT or MRI. It must be remembered that obstruction can also be observed with ATIN of analgesic origin (papillary necrosis with rejection of the papilla). It is necessary to exclude prerenal causes of AKI in the form of shock of various etiologies. Renal forms of AKI suggest differential diagnosis with acute glomerulonephritis, rapidly progressive glomerulonephritis or exacerbation of chronic glomerulonephritis, as well as ATIN of infectious origin (acute pyelonephritis, ATIN of viral origin), TMA with kidney damage (hemolytic-uremic syndrome, atypical hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, APS, secondary TMA with systemic vasculitis, etc.), ATIN of medicinal, toxic and other origin.

3. Treatment

It is recommended to immediately stop exposure to the causative factor, if possible (cancel the drug, dietary supplement, herbal medicine that caused ATIN, stop the action of toxic factors) or weaken its effect on the body.

The level of evidence reliability is 1C.

It is recommended to maintain water and electrolyte homeostasis, acid-base balance of the blood, and blood pressure (BP). In this regard, it is possible to use crystalloid isosmolar solutions containing sodium chloride or dextrose** (glucose**), sodium bicarbonate solution**, loop diuretics*, and antihypertensive drugs.

It is recommended to limit the use of RAAS blockers during the development of AKI.

Level of evidence reliability – 2C

Comments: Metabolic acidosis does not require special therapy if the blood pH is not lower than 7.2 and the concentration of standard bicarbonate is >15 mmol/l. For correction purposes, a 4% sodium bicarbonate solution is used**.

For emergency correction of hyperkalemia, it is necessary to administer a solution of calcium chloride (3-5 ml of 10% for 2 minutes) or calcium gluconate (10 ml of 10% for 2 minutes). A longer-lasting antihyperkalemic effect is achieved by infusion of a solution of dextrose** (glucose**) with insulin, which should begin after the administration of calcium gluconate. Typically, for this purpose, a 40% dextrose** (glucose**) solution is used in an amount of up to 300 ml, adding 8-12 IU of insulin for every 100 ml of a 40% dextrose** (glucose**) solution. The effect of calcium gluconate begins 1–2 minutes after administration and continues for 30–60 minutes. The administration of dextrose** (glucose88) with insulin ensures the transition of potassium from the blood plasma into the cell; its antihyperkalemic effect begins 5–10 minutes after the start of the infusion and lasts up to 4–6 hours.

Moderate and/or asymptomatic hyponatremia does not require special correction. Severe acute, i.e. Hyponatremia lasting less than 48 hours, especially when neurological symptoms appear, is an indication for immediate correction by administering a 0.9% solution** or 3% sodium chloride solution.

It is recommended to prescribe pathogenetic therapy aimed at stopping or weakening the effects of endogenous factors, taking into account the known etiology of the disease.

The level of evidence is 2C.

Comments: This recommendation applies to clinical situations when the endogenous effect is verified and methods of influence exist for it. For example, in case of hyperuricemic ATIN, the use of a short course of colchicine and glucocorticoids, alkalizing hydration therapy, the abolition of uricosurics, if any were prescribed, and subsequently the prescription of uricostatic agents (allopurinol**). It should be remembered that colchicine is contraindicated when creatinine clearance is less than 30 ml/min, and NSAIDs are contraindicated when creatinine clearance is less than 60 ml/min, therefore their traditional use in a short course to relieve an exacerbation of gout in this case should be considered unacceptable. An example would also be antibacterial therapy for sepsis, the introduction of antidotes for toxic effects, immunosuppressive therapy for ATI of immune origin, for example, for SLE or vasculitis, plasma therapy for TMA.

The use of glucocorticoids is recommended in case of development of ATIN due to diffuse connective tissue diseases of autoimmune origin.

The level of evidence is 2C.

The use of glucocorticoids is recommended in the event of the development of ATIN and the absence of improvement in renal function after cessation of exposure to the causative factors.

Level of evidence reliability – NGD.

Comments: In most studies, the use of glucocorticoids did not lead to a significant decrease in blood creatinine with long-term use. In a number of cases there was such an effect, but the quality of the studies themselves did not allow for dissemination this effect as a recommendation for appointment.

It is recommended that RRT should be taken in a timely manner, taking into account absolute and extrarenal indications, common for AKI of various etiologies.

The level of evidence is 2B.

Comments: In 58% of cases, there is a need for RRT. RRT is performed for general indications for AKI

Methods of RRT for AKI include extracorporeal (intermittent, continuous, extended) and intracorporeal - manual and machine peritoneal dialysis. Intermittent methods are carried out daily for 2–4 hours. These include hemodialysis, hemofiltration, hemodiafiltration. Long-term methods, carried out almost around the clock for several days or even weeks, are represented by long-term veno-venous (arteriovenous) hemofiltration, long-term veno-venous (arteriovenous) hemodialysis, long-term veno-venous (arteriovenous) hemodiafiltration, slow long-term veno-venous (arteriovenous) ultrafiltration. Continuous methods, while inferior to intermittent ones in speed, provide slow but constant maintenance of homeostasis without significant fluctuations in hydration and toxemia. The most commonly used is continuous venovenous hemofiltration or hemodiafiltration. Indications for starting RRT for AKI [Kidney Disease: Improving Global Outcomes (KDIGO), 2012] are presented in Table. 2.

Table 2. Indications for starting renal replacement therapy

RRT should be started immediately as soon as life-threatening fluid, electrolyte, and acid-base imbalances (ABD) are detected.
The decision to initiate RRT should be made not only on the basis of blood plasma urea and creatinine levels, but to a greater extent on an assessment of the dynamics of laboratory data and on the basis of a comprehensive analysis of the clinical situation as a whole (NCD).
Absolute indications for starting RRT
	Characteristic
Azotemia	Plasma urea level?36 mmol/l
Uremic complications	Encephalopathy, pericarditis
Hyperkalemia	6.5 mmol/l and/or ECG changes
Hypermagnesemia	4 mmol/l and/or anuria/absence of deep tendon reflexes

Oligoanuria	Diuresis<200 мл/12 час или анурия
Volume overload	Resistant edema (especially pulmonary and cerebral edema) in patients with AKI
Exogenous poisoning	Elimination of dialyzed venom
Severe and/or rapidly progressive AKI
“Extrarenal” indications for starting RRT
Nosologies	Efficiency
Severe sepsis, severe acute pancreatitis, severe burns, acute respiratory distress syndrome, cardiac surgery, severe combined trauma, hepatorenal syndrome, multiple organ failure syndrome	Correction of water-electrolyte balance and acid-base balance
	Correction of systemic inflammation, hypercatabolism, severe thermoregulation disorders
Rhabdomyolysis	Elimination of myoglobin, phosphates, purines

4. Rehabilitation

Rehabilitation involves a system of measures to reduce the risk of re-exposure to the causative factor and a set of measures aimed at reducing the progression of chronic renal failure in the event of transformation of AKI into CKD.

5. Prevention and clinical observation

Prevention of ATIN is possible when the patient’s management takes into account the risk of developing, for example, drug-induced ATIN and in a high-risk group they approach the prescription of nephrotoxic drugs with caution, trying to replace them with safer ones. Effective treatment of urinary tract infections may also be a factor in reducing the risk of acute urinary tract infection of infectious origin. Identifying and eliminating toxic occupational and other factors also reduces the risk of ATI. Dispensary observation by a nephrologist is carried out on an outpatient basis for one year with a frequency of 1/3 months in the event of elimination of the consequences of ATI in the form of AKI, normalization of urinary sediment. If the phenomena of AKI persist or the transformation of AKI into chronic renal failure, as well as if pathological urinary sediment persists, more frequent monitoring once a month or repeated hospitalizations in the nephrology department can be implemented.

6. Additional information affecting the course and outcome of the disease

Hospital mortality in the group of patients with AKI ranges from 10.8 to 32.3%, and AKI is an independent risk factor for death in patients in intensive care units, increasing the risk by 4.43 times. With long-term follow-up over 20 years, progression of CKD is observed in 40–45% of patients who have undergone ATI; stage 5 CKD develops in 4% of patients.

Most often, chronic renal failure is observed as a result of acute renal failure due to exposure to NSAIDs (53%), other dosage forms of acute renal failure are accompanied by the development of chronic renal failure in 36% of cases.

Criteria for assessing the quality of medical care

	Quality criteria	Level of evidence
	Nephrologist was consulted
	A general urine test was performed
	A biochemical blood test was performed (creatinine, urea, uric acid, total protein, albumin, glucose, potassium, sodium, chlorine)
	An ultrasound examination of the kidneys was performed
	Treatment with dialysis methods was performed (if indicated)

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Appendix A1. Composition of the working group

Batyushin M.M. Professor of the Department of Internal Diseases with the Basics of General Physiotherapy No. 2, Rostov State Medical University of the Ministry of Health of Russia, Chief Nephrologist of the North Caucasus Federal District, Doctor of Medical Sciences, Professor
Shilov E.M. head Department of Nephrology and Hemodialysis IPO GBOU VPO First Moscow Medical University named after. THEM. Sechenov of the Ministry of Health of Russia, Vice-President of the National Scientific Research Society, Chief Nephrologist of the Ministry of Health of the Russian Federation, Doctor of Medical Sciences, Professor

No conflict of interest

Nephrologist;
General practitioner;
General practitioner (family doctor).

Assessing the strength of recommendations and the quality of their evidence
For recommendations, strength is indicated as level 1, 2 or “no grade” (Table II1), quality of evidence is indicated as A, B, C, D (Table II2).
Table II1. Assessing the strength of recommendations

Level	Consequences
Level	From the patients' side	From the doctor's side	Further direction of use
	The vast majority of patients in this situation would prefer to follow the recommended path and only a small proportion of them would reject this path	The doctor will recommend that the vast majority of his patients follow this path.
Level 2? “experts believe”	Most patients in this situation would be in favor of following the recommended path, but a significant proportion would reject this path	For different patients, different recommendations should be selected that are suitable for them. Each patient needs assistance in choosing and making decisions that will be consistent with the values and preferences of that patient
“No gradation” (NG)	This level is applied in cases where the recommendation is based on the common sense of the expert researcher or when the topic under discussion does not allow adequate application of the evidence system used in clinical practice

Table II2. Assessing the quality of the evidence base
(compiled in accordance with KDIGO clinical guidelines)

Appendix B. Patient management algorithms

Algorithm 1. ATIN without AKI

Note: UAM - general urine test, Cr - blood creatinine, N - normal, GFR - glomerular filtration rate, CBC - general blood test

Algorithm 2. ATIN with AKI

Note: UAM – general urine analysis, Cr – blood creatinine, N – normal, ? - increase in level, RRT - renal replacement therapy, ACEI - angiotensin-converting enzyme inhibitors, ARA II - angiotensin II receptor antagonists, GFR - glomerular filtration rate, CBC - complete blood count

Appendix B: Patient Information

The patient is required to adhere to the diagnosis and treatment carried out by the doctor. At the outpatient stage, one should adhere to recommendations aimed at limiting or eliminating re-exposure to the causative factor, for example, refusing to use metamizole sodium for pain that previously caused the development of ATIN. It is also recommended that the patient monitor TAM, UAC, and blood creatinine at a frequency of 1 r/3 months and seek advice from a nephrologist for one year after the onset of ATI.