How to cure glomerulonephritis: its symptoms and timely diagnosis. When you need the help of a surgeon. Video: symptoms and treatment of glomerulonephritis

The kidneys are the most important organ responsible for removing unnecessary and harmful substances from the body. Human health depends on the stable functioning of the kidneys. Chronic glomerulonephritis is a pathology that leads to kidney failure and severe consequences for the whole organism. This disease does not tolerate a frivolous attitude and requires long-term and serious treatment.

What is chronic glomerulonephritis

Chronic glomerulonephritis is a progressive inflammatory lesion renal glomeruli, leading to their sclerosis (scarring) and loss of functionality. Over time, chronic renal failure develops.

The disease has a relatively high prevalence, while it can occur at any age, but most often the first signs of damage to the glomeruli (glomeruli) are diagnosed at 25–40 years of age. Men get sick more often. The difference between a chronic process and an acute one is in the long-term (more than a year) course of inflammatory-destructive changes and extensive (diffuse) bilateral kidney damage.

In the structure of each kidney there is a complex structural system, including nephrons, consisting of glomeruli (capillary entanglements) in capsules and the smallest tubules, tubules, in which a continuous process of blood filtration occurs with the formation of urine containing substances unnecessary for the body. Required Items remain in the bloodstream.

In the renal glomeruli (glomeruli) there is a continuous process of blood filtration

With glomerulonephritis, the following changes occur in the kidneys:

• due to the inflammatory process, the walls of the glomerular vessels become permeable to blood cells;
• in the lumen of the capillaries of the glomeruli, small blood clots are formed that clog their lumen;
• in the affected glomeruli, the blood flow slows down or completely stops;
• blood cells clog the lumen of the Bowman's capsule (the membrane that covers the glomerulus) and the renal tubules;
• in the affected nephron, the entire sequential filtration process is disrupted;
• there is a replacement of the tissue of glomerular capillaries, renal tubules, and then the whole nephron with scar tissue - nephrosclerosis develops;
• the death of nephrons leads to a significant decrease in the volume of filtered blood, as a result of which the syndrome of renal failure develops;
• functional insufficiency of the kidneys leads to the accumulation of harmful substances in the blood and the excretion of elements necessary for the body in the urine.

Chronic inflammation of the renal glomeruli is more often the outcome of an acute immunoinflammatory process in the kidneys, but it can also be primary chronic.

Glomerulonephritis causes inflammation and destruction of the glomeruli

Classification of pathology: types and forms

Chronic glomerulonephritis can be infectious-immune or non-infectious-immune in nature. During the course of the disease, phases of exacerbation and remission are distinguished. According to the rate of development, pathology can progress quickly (from 2 to 5 years) or slowly (longer than 10 years).

Chronic inflammation can occur in different forms Oh. In accordance with the main syndrome, the following types of clinical course are distinguished:

• latent - with a predominance of urinary syndrome. Accompanied by moderate swelling and slight hypertension, protein, erythrocytes and leukocytes are detected in the urine. It occurs most often - in almost half of patients;
• hypertonic, or hypertensive. Diagnosed in 20% of all cases of chronic glomerulonephritis. It is manifested by consistently high blood pressure, polyuria (an increase in the volume of urine excreted during the day), nocturia (nighttime urge to urinate). In the analysis of urine - high protein and altered erythrocytes, the density is slightly below normal;
• hematuric - with a predominance of macrohematuria, that is, blood in the urine. Occurs infrequently (5% of total number patients), is manifested by a high content of altered erythrocytes in the urine;
• nephrotic - with severe nephrotic syndrome. Diagnosed in a quarter of all patients. It is manifested by severe swelling, high blood pressure, a decrease in the amount of daily urine. Urine indicators: high density, proteinuria (high protein), in the blood - a decrease in protein, high cholesterol;
• mixed - with manifestations of nephrotic and hypertensive syndromes.

In different forms of glomerulonephritis, pathological changes are based on a single mechanism

Each type of chronic inflammation of the glomeruli occurs with successive periods of compensation and decompensation of the filtering function of the kidneys.

Based on the morphological changes in the affected kidneys, several main types of the disease are also distinguished:

• glomerulonephritis with minimal changes;
• membranous - with a sharp edema and splitting of the membranes of the glomerular capillaries; separate focal and diffuse damage to membranes;
• proliferative intracapillary - manifested by the proliferation of cells of the inner layer of the capillaries of the glomeruli and tissue located between the vessels (mesangia);
• proliferative extracapillary - characterized by the formation of specific crescents due to the growth of epithelial cells of the glomerular capsules. Formations fill the lumen of the capsules and squeeze the capillaries, disrupting blood circulation in them. Subsequently, the crescents are replaced by connective tissue, which leads to the death of the glomeruli. This type of glomerulonephritis has a malignant course;
• membranous-proliferative type combines signs of proliferative and membranous lesions of the glomeruli, while pathological changes are diffuse;
• sclerosing, or fibroplastic, type. Such chronic glomerulonephritis can be the outcome of any other form of the disease, while distinguishing between focal and diffuse varieties.

In chronic glomerulonephritis, the glomeruli, and then the nephrons themselves, are replaced by fibrous tissue.

Reasons for the development of the disease

Why chronic inflammation of the glomeruli occurs is not always possible to find out. Pathology may be the result of untreated acute inflammation or occur primarily.

The leading role in the occurrence of the inflammatory process is played by nephrogenic strains of streptococci, along with the presence in the body of chronic infectious foci in different bodies. External and internal factors provoke the formation of specific immune complexes circulating in the bloodstream and deposited on the glomerular membranes, which leads to damage to the latter. The resulting reactive inflammation and circulatory disorders in the glomerular apparatus eventually lead to degenerative changes in the kidneys.

Chronic glomerulonephritis may be infectious or non-infectious in nature.

Provoking factors in the development of pathology can be:

• diseases caused by bacterial flora:
  • tonsillitis;
  • pharyngitis;
  • sinusitis;
  • adnexitis;
  • caries;
  • scarlet fever;
  • periodontitis;
  • infective endocarditis;
  • cholecystitis;
  • pneumococcal pneumonia;
• diseases with viral etiology:
  • herpes;
  • flu;
  • Hepatitis B;
  • rubella;
  • mononucleosis;
  • chicken pox;
  • parotitis;
  • cytomegalovirus infection;
• autoimmune diseases:
  • systemic vasculitis;
  • rheumatism;
  • lupus erythematosus;
• hereditary predisposition: birth defects in the immune system;
• malformations - renal dysplasia;
• congenital syndromes:
  • pulmonary-renal;
  • Scheinlein-Henoch disease.

Streptococcus is the main cause of infectious glomerulonephritis

Non-infectious factors include:

• allergic reactions to the transfusion of blood components or the introduction of sera and vaccines;
• poisoning with mercury, lead, organic solvents;
• drug intoxication;
• alcohol poisoning.

Chronic inflammation of the renal glomeruli may occur during radiation therapy. Provoking factors are also the constant effect of low temperatures and a decrease in the overall resistance of the body to harmful influences.

Manifestations of pathology

Symptoms of chronic glomerulonephritis depend on the form in which the pathology proceeds. There are two main stages of the disease: compensation and decompensation. At the first stage, external signs are practically absent. There may be slight intermittent swelling and a slight increase in blood pressure.

In chronic glomerulonephritis, inflammatory and destructive changes slowly occur in the kidneys, which leads to the progression of symptoms.

In the stage of decompensation, a progressive impairment of renal functions occurs - their insufficiency develops. Due to the accumulation of nitrogenous wastes in the blood, the patient experiences:

• constant nausea;
• headache;
• weakness;
• bouts of vomiting.

Violations of the electrolyte balance and hormonal balance lead to chronic edema and a persistent increase in blood pressure (BP). The inability of the kidneys to concentrate urine is manifested by polyuria - an increase in the daily amount of urine excreted.

This symptom is accompanied by:

• constant thirst;
• a feeling of general weakness;
• headaches;
• dry skin, hair and nails.

The result of the decompensation phase is a secondary wrinkled kidney. Azotemic uremia develops when the kidneys completely lose their ability to maintain normal blood composition. Severe intoxication can lead to uremic coma.

In chronic glomerulonephritis, edema is a characteristic symptom

Table: symptoms of chronic glomerulonephritis depending on the clinical form

Signs of exacerbation

Any form of chronic inflammation of the glomeruli can occur with periodic exacerbations. Most often, such episodes are observed in spring or autumn and usually occur 2-3 days after an infection (viral or streptococcal).

One of the characteristic signs of glomerulonephritis, especially during exacerbation, is urine the color of meat slops.

Manifestations in the acute stage:

• pain in the lumbar region;
• temperature increase;
• feeling of thirst;
• poor appetite;
• weakness;
• headache;
• swelling on the eyelids, face, legs;
• violation of urine output;
• urine the color of meat slops.

Video: what happens with glomerulonephritis

How is the diagnosis made?

Diagnosis of the disease is carried out by nephrologists. The main criterion in the detection of chronic glomerulonephritis is the data of clinical and laboratory studies. First, the doctor collects an anamnesis, takes into account the fact of existing chronic infections, systemic pathologies, and an acute attack of glomerulonephritis.

Laboratory examination of the patient includes the following tests:

1. Clinical analysis of urine. Many altered erythrocytes, cylinders (hyaline, granular), leukocytes, a large number of protein, while the density of urine is reduced or increased - it depends on the stage of the disease.
2. Zimnitsky test. The daily volume of urine and its density are reduced or increased. An increase in the amount of urine and a decrease in density indicate the stage of decompensation of the disease.
3. Blood chemistry. There is a decrease in protein fractions (hypoproteinemia and dysproteinemia), the presence of C-reactive protein, sialic acids, high levels of cholesterol and nitrogenous compounds (in the stage of decompensation).
4. Immunogram of blood. The analysis determines an increase in the titer of antibodies to streptococcus (antistreptolysin, antihyaluronidase, antistreptokinase, antideoxyribonuclease), an increase in the level of immunoglobulins, a decrease in complement factors (proteins involved in the formation of the body's immune response during the interaction of antibodies and antigens).
5. Microscopic analysis of a sample of kidney tissue taken during a biopsy. The method allows to evaluate structural changes in the renal glomeruli, which is important for the appointment of adequate therapy. Detect signs of growth (proliferation) of glomerular structures, their infiltration by immune cells - monocytes and neutrophils, the presence of deposits in the glomeruli of IC (immune complexes).

Urine analysis for glomerulonephritis shows deviations from the norm and allows you to determine the stage of the disease

Instrumental examination of the patient includes the following procedures:

1. Sonography (ultrasound) of the kidneys. A decrease in the size of the kidneys is found due to sclerosis of the parenchyma.
2. Excretory (intravenous) urography. The method, which consists in introducing a special radiopaque substance into the patient's blood, followed by a series of images that demonstrate the ability of the kidneys to accumulate and remove this substance. Thus, the degree of violation of the filtering and concentration functions of the kidneys is assessed.
3. Doppler ultrasound renal vessels. It is used to assess violations of the renal blood flow.
4. Dynamic nephroscintigraphy - radionuclide kidney scan. Allows you to evaluate structural and functional disorders in these organs.
5. A kidney biopsy is necessary to assess destructive changes in the affected organ at the cellular level.

To assess changes in the structure of the kidneys, an ultrasound examination is performed.

To detect changes in other organs, ultrasound of the heart and pleural cavities, ECG, examination of the fundus.

Chronic glomerulonephritis should be differentiated from pathologies such as:

• chronic pyelonephritis;
• polycystic kidney disease;
• nephrotic syndrome;
• amyloidosis of the kidneys;
• nephrolithiasis;
• cardiac pathologies with arterial hypertension;
• kidney tuberculosis.

Video: diagnosis of chronic glomerulonephritis

Principles of treatment

Care and features of treatment depend on the clinical form of the pathology, the rate of its progression and the presence of complications. In any case, doctors recommend observing a sparing regimen, eliminating hypothermia, overwork, and harmfulness associated with professional activities.

During the period of exacerbation, a full inpatient course of treatment, adherence to strict bed rest and diet are required. Bed rest is necessary in order to reduce the load on the kidneys. A decrease in physical activity slows down metabolic processes, which is necessary to inhibit the formation of toxic nitrogenous compounds - products of protein metabolism.

During remission, supportive outpatient therapy is carried out, sanitation of foci of infection that provokes the appearance of an inflammatory process in the renal glomeruli (treatment of diseased teeth, removal of adenoids, tonsils, relief of inflammation in paranasal sinuses nose). Sanatorium treatment at climatic resorts is recommended.

During the period of remission, a patient with chronic glomerulonephritis should periodically visit the ENT and dentist in order to stop inflammation in the foci of infection in time

The use of medicines

The basis of drug therapy is immunosuppressants, that is, drugs that suppress the body's immune reactivity. By reducing the activity of immunity, such drugs inhibit the development of destructive processes in glomeruli. In addition to immunosuppressive therapy, symptomatic agents are also used.

The main treatment is immune suppression. For this purpose, use:

• steroid drugs: Prednisolone or Triamcinolone in an individual dosage, during an exacerbation - pulse therapy, that is, short-term administration of ultra-high doses of Prednisolone or Methylprednisolone;
• cytostatics:
  • Cyclosporine;
  • Imuran;
  • Cyclophosphamide;
• immunosuppressants:
  • Delagil;
  • Plaquenil.

Symptomatic treatment:

• drugs to lower blood pressure:
  • Kapoten;
  • Enalapril;
  • Reserpine;
  • Christepin;
  • Raunatin;
  • Corinfar;
    • for very severe hypertension:
      • Ismelin;
      • Isobarin;
        • for the treatment of eclampsia (convulsive syndrome) during an exacerbation - 25% magnesium sulfate solution;
• diuretics (diuretics) to remove excess fluid:
  • Hypothiazide;
  • Veroshpiron;
  • Lasix (Furosemide);
  • Aldactone;
  • Uregit;
• anticoagulants and antiplatelet agents to improve blood flow and prevent the formation of blood clots in the glomerular vasculature:
  • Phenindione;
  • Dipyridamole;
  • Ticlid;
• non-steroidal anti-inflammatory drugs for pain relief and suppression of inflammatory mediators due to the immune response:
  • Indomethacin (Metindol);
  • Ibuprofen.

Antibiotics are used to sanitize the infectious focus. Antibacterial therapy is selected individually, taking into account the tolerability of the drug by the patient and the sensitivity of the bacterial pathogen.

Photo gallery: drugs for the treatment of the disease

Eufillin is used to improve renal blood flow
Prednisolone is the mainstay of suppressive therapy for chronic glomerulonephritis
Furosemide - a strong diuretic, used for severe edema
Nifedipine - a drug for lowering blood pressure
Chlorambucil refers to cytostatics, it is used to suppress autoimmune reactions.
Heparin thins the blood, which prevents microthrombosis of the glomerular vessels
Indomethacin suppresses the inflammatory process

Nutrition for chronic glomerulonephritis

In case of a disease, diet No. 7 and its subspecies (7A, 7B and 7D) are prescribed, depending on the activity of the pathological process.

The dietary table is aimed at such aspects:

• maximum relief of the work of the kidneys;
• increased excretion of toxic metabolites from the body;
• improvement of diuresis and elimination of edema, which is especially important for nephrotic and mixed forms;
• normalization of blood pressure and stimulation of microcirculation in the kidneys.

Food should be taken in small portions 5-6 times a day. With glomerulonephritis, it is very important to reduce salt and fluid intake as much as possible. Restriction of proteins is necessary only in the case of the development of hyperazotemia, that is, excessive accumulation of nitrogenous compounds in the blood. Excluded from food:

• spicy, hard to digest, too fatty foods;
• food rich in oxalic acid and essential oils;
• sauces, spices;
• smoked products, sausages;
• pickles, marinades;
• pastry, chocolate;
• fast food.

Foods that are harmful to the kidneys should be excluded from the diet.

Food should have a normal calorie content (2700-2900 kcal per day), be fortified, rich in trace elements, especially potassium and calcium.

A chronic process without complications requires the constant use of diet No. 7 with a normal content of proteins (1 g per 1 kg of body weight), carbohydrates and fats, salt restriction to 3–5 g and liquid to 0.8–1.0 liters per day. In the acute stage, diet No. 7 B is used with a restriction of protein foods, strict fluid accounting (200 ml more urine excreted the day before) and salt restriction to 2 g (in products), that is, food is not salted. In chronic glomerulonephritis in the stage of decompensation, diet No. 7 A is needed with a decrease in the calorie content of food by a third of the norm, a minimum protein content, complete restriction of sodium and fluid, as with a diet of 7 B.

The basis of nutrition should be vegetable, dairy, cereal dishes. Food should be prepared by baking, boiling, stewing.

The basis of nutrition in chronic glomerulonephritis should be cereals, vegetable dishes, soups, salads

Sample menu for chronic glomerulonephritis - table

Physiotherapy

Physiotherapeutic procedures are prescribed during the period of remission and are aimed at improving metabolic processes, blood circulation and stopping inflammation.

The following methods are applied:

• electrophoresis on the kidney area with Eufillin, calcium gluconate, antiseptic and antihistamines;
• UHF to eliminate the inflammatory process;
• SMW-therapy - exposure to an electromagnetic field with a certain frequency and wavelength to improve microcirculation and eliminate the inflammatory response;
• inductothermy - the use of a high-frequency magnetic field to normalize blood circulation in the glomeruli;
• lumbar irradiation infrared rays(sollux lamp) to improve blood flow in the tubules of the kidneys.

Physiotherapy for chronic glomerulonephritis is aimed at eliminating inflammation and normalizing blood circulation in the kidneys

Surgical methods

Glomerulonephritis itself does not require surgical intervention. The help of surgeons may be needed in case of severe complications - nephrosclerosis (wrinkling of the kidney), leading to chronic uremia. In this case, regular hemodialysis is performed, and if it is not effective enough, a kidney transplant is performed. However, glomerulonephritis can recur even in a transplanted organ.

Folk methods of treatment

Use only traditional medicine methods instead traditional treatment it is forbidden. Glomerulonephritis is a severe pathology leading to serious consequences, up to death. This must be remembered and not neglected prescribed medications. The use of herbs should also be discussed with the attending physician, since some plants traditionally used by populists in the treatment of kidney ailments cannot be used for inflammation of the glomeruli. These herbs include bear ears (bearberry) and horsetail, which are strong diuretic but may increase hematuria.

In chronic inflammation, the following remedies will alleviate the patient's condition:

1. Anti-inflammatory, diuretic collection:
   1. In equal parts, take birch leaves, rose hips, chopped parsley, harrow and lovage roots, anise seeds.
   2. Take 1 large spoon of the mixture and pour a glass of cold water for 40 minutes.
   3. To put on water bath and boil for 15 minutes.
   4. Cool and strain.
   5. Drink the decoction in small portions throughout the day.
2. Kidney tea for edema:
   1. Pour a tablespoon of the herb orthosiphon staminate with water (200 ml).
   2. Brew in a water bath for 10 minutes.
   3. Leave until cool and strain.
   4. Drink the remedy 100 ml twice a day half an hour before meals.
3. Diuretic fee:
   1. In equal proportions, you need to take the grass of the nettle, leaves blackcurrant, stinging nettle, cornflower flowers and parsley root.
   2. Grind all components, mix, select a tablespoon of the mixture and pour water (250 ml).
   3. Boil in a water bath for 15 minutes.
   4. Pour into a thermos and leave for 1.5 hours.
   5. Strain and top up with boiled water to the original volume.
   6. Drink 50 ml 4 times a day before meals.
4. Collection to improve metabolic processes and relieve inflammation:
   1. The fruits of juniper and hops, birch and currant leaves take 1 spoon each.
   2. To them add 2 tablespoons of lingonberry and plantain leaves, 4 tablespoons of strawberries and rose hips.
   3. Shred everything.
   4. Select 2 tablespoons of the collection, pour water (600 ml) and keep in a water bath for 20 minutes.
   5. Strain and take 100 ml three times a day in a warm form.

As a diuretic and anti-inflammatory agent, you can use an infusion of elderberry color (1 spoon per cup of boiling water). To remove excess fluid, corn stigmas are recommended, and with a high level of nitrogen in the blood, pharmacy alcohol tincture of lespedeza beans (Lespenefril). Tincture is taken 1 teaspoon 2 times a day.

Photo gallery: plants for the treatment of the disease

Staminal orthosiphon is recommended for nephrotic form of glomerulonephritis for effective removal of edema
Strawberries purify the blood, relieve inflammation, normalize metabolism
Corn silk- proven diuretic
Rose hips have a tonic and anti-inflammatory effect
Lespedeza - a plant that can reduce the level of nitrogen in the blood
Lingonberry leaf - a strong diuretic and anti-inflammatory agent
Birch leaves have a mild diuretic and anti-inflammatory effect.
Juniper fruits effectively relieve inflammation and normalize diuresis
Parsley root has diuretic and anti-inflammatory properties

Prognosis and complications of the disease

Active treatment of pathology allows minimizing the manifestations of the disease (edema, hypertension), significantly delaying the development of chronic renal failure and prolonging the life of the patient. All patients with chronic inflammation of the glomeruli are registered in the dispensary for life.

The prognosis of treatment depends on the form of the disease: latent has the most favorable prognosis, hematuric and hypertensive - more serious, and the most unfavorable - mixed and nephrotic forms.

Complications that aggravate the prognosis:

• thromboembolism;
• pleuropneumonia;
• pyelonephritis;
• renal eclampsia.

Chronic glomerulonephritis leads to shrinkage of the organ and the development of chronic kidney failure, which is fraught with uremia, in which the patient must regularly undergo hemodialysis. In pathology, the patient is given a disability, the group of which depends on the degree of impaired renal function.

Prevention

Factors provoking the development of irreversible changes in the kidneys are most often streptococcal and viral infections, as well as wet hypothermia. Therefore, their impact should be minimized. To prevent the development of the disease, it is necessary:

• lead a healthy lifestyle;
• temper;
• timely treat infectious diseases and pathologies of the genitourinary system;
• eat rationally.

Glomerulonephritis leaves a serious imprint on the quality of human life. Chronic inflammation of the renal glomeruli cannot be completely cured, but stable remission can be achieved and the consequences of the disease can be significantly delayed. To do this, it is necessary to complete courses of therapy, follow a diet and not refuse anti-relapse treatment, including physiotherapy sessions and visits to sanatoriums and resorts.

Glomerulonephritis is a whole group of diseases that affect the very basis of the functioning of the kidneys - the glomeruli, with a different morphological picture (determined by biopsy using a microscope), but with approximately the same symptoms and signs. Successful treatment glomerulonephritis largely depends on this very morphological picture, on the mutual understanding of the doctor and the patient, as well as on how timely the patient goes to the doctor and begins treatment.

Modern classification of glomerulonephritis

There are acute and chronic glomerulonephritis. Acute glomerulonephritis is provoked by streptococcus (the same that causes tonsillitis and skin lesions - streptoderma). Not all people who have had a sore throat develop kidney damage, but only those whose immune system fails and cannot recognize the difference between streptococcus and its own cells (especially the kidneys and myocardium) and attacks both.

Chronic glomerulonephritis develops in people whose immune system has a more significant failure, due to which it constantly attacks its cells, regardless of the factor that provoked aggression. Quite often the glomerulonephritis develops at passing heavy diseases.

Factors that cause kidney damage

1. Bacteria and viruses: streptococcus, staphylococcus, cytomegalovirus and pathogens of tuberculosis, syphilis, brucellosis, hepatitis B and C, measles.
2. Toxic substances: alcohol, drugs, organic solvents, mercury, lead, insect poisons. Some drugs can also be dangerous from this point of view (gold preparations, D-penicillamine, iodine-containing contrast agents, foreign proteins from vaccines or sera).
3. External factors: single and significant hypothermia, excessive insolation, trauma, stress.

There are also primary glomerulonephritis (when the disease occurs on its own, provoked by the above reasons) and secondary, when kidney damage in a patient occurs with an already existing serious disease. This may be, for example, diabetes, oncology or systemic diseases. connective tissue. Thus, lupus glomerulonephritis largely determines the severity of systemic lupus erythematosus and the prognosis for this disease.

Clinical manifestations of glomerulonephritis

Acute glomerulonephritis begins 2-3 weeks after the infection (tonsillitis). An increase in blood pressure, swelling of the face, and in the evening of the ankles, red urine - these are its characteristic signs, which doctors call the "diagnostic triad". In addition, patients are worried about lower back pain, and protein, red blood cells, and a high specific gravity are determined in the urine. In severe cases, swelling can be very significant (throughout the body), and the amount of urine discharge is reduced until it is completely absent.

In the chronic form, the signs and symptoms of glomerulonephritis vary greatly. Common to all clinical options nephrites are as follows:

• Increase in blood pressure
• The presence of edema
• Changes in the urine: the presence of protein, erythrocytes, leukocytes to a lesser extent, a decrease in the amount of urine separated
• General symptoms: weakness, malaise, discomfort in the lower back, decreased performance, headaches.

The severity of symptoms can be different: from a latent variant (there is no clinic, nephritis can be detected only by urinalysis) to nephrotic syndrome with severe edema, sharp decline blood protein and persistent hypertension. Separately, a rapidly progressive variant of the course of glomerulonephritis is distinguished - the most unfavorable with the rapid formation of renal failure.

Some more details about the symptoms and development of this kidney disease are described in the video:

How is glomerulonephritis treated?

Glomerulonephritis is a rather serious disease. Is there a cure for glomerulonephritis? Of course, it is treated. At the same time, the treatment of acute and chronic forms of glomerulonephritis differs significantly.

At acute glomerulonephritis necessary:

1. Observe bed rest until normalization of urination, reduction of edema.
2. Adhere to the restriction of fluid, salt and protein intake during the acute period. Exclude the use of any salty foods, meat and fish broths, fatty meat, poultry; sausages, smoked meats, canned food, salted cheeses, legumes, onions, garlic, sorrel, mushrooms; pickled and pickled vegetables, chocolate, strong coffee, cocoa, any alcohol, sodium-rich mineral water.

Used in drug therapy:

• Antibiotics (since streptococcus plays a role in the origin of this disease) mainly of the penicillin series for 10-14 days.
• Diuretics to increase urine output (eg, furosemide, torasemide).
• Antihypertensives, mainly ACE inhibitors(they reduce pressure and protect the kidneys, increasing their functional reserve).
• Disaggregants (Tiklid, Trental, Curantil). Curantil with glomerulonephritis reduces blood clotting and prevents the formation of blood clots and blockage of the vessels of the renal glomeruli.

Acute post-streptococcal glomerulonephritis mostly affects adolescents, individuals young age, the most susceptible colds type of angina. Can glomerulonephritis be cured in these patients? Fortunately, the answer to this question in most cases is positive, with the elimination of streptococcal infection, glomerulonephritis is also cured, and only in 10-15% of cases does it become chronic. The basic principles for the treatment of glomerulonephritis are the same regardless of the age of the patient.

Treatment of chronic glomerulonephritis

As already mentioned, chronic nephritis- This is a group of kidney diseases with different microscopic levels of damage. In this case, kidney biopsy data are of decisive importance in the problem of how to treat glomerulonephritis in this particular patient. The volume and duration of therapy are determined by microscopic changes, according to which nephrologists distinguish several types of nephritis.

Here are the main groups of drugs:

• Glucocorticoids, most often Prednisolone. They reduce the activity of autoimmune damage to the renal glomeruli, reduce proteinuria (protein loss in the urine).
• Cytostatics - inhibit the activity of cells that implement autoimmune reactions. The most commonly used are Cyclophosphamide and Chlorbutin.
• Hypotensive - ACE inhibitors (Enalapril, Ramipril, Fosinopril, Lisinopril).
• Diuretics (Furosemide, Hypothiazide, Torasemide).
• Anticoagulants (Heparin, Curantil, Trental).

Combinations of these agents differ depending on what symptoms each individual patient has and the treatment is selected strictly individually. Glucocorticoids and cytostatics have a lot of side effects varying degrees severity: weight gain, stretch marks on the skin, erosion in the stomach, hair loss, impaired liver function, etc. However, they do not occur in all patients and not all symptoms at once. In any case, the treatment of chronic forms of nephritis takes a lot of time, so the pills will have to be taken for a long time and regularly.

Additional drugs and methods

When an infection (pyelonephritis, cystitis) is attached, antibacterial drugs are used a wide range actions: Tsiprolet, Lomfloks, Aviloks, etc. Additionally, as an aid, in order to increase diuresis, prevent infection urinary tract and the formation of stones, Canephron can be used - a drug from herbal ingredients in the form of dragees and solutions.

How to cure glomerulonephritis, if it is chronic, completely? Unfortunately, world medicine has not found a way to radically cure this disease. The goal of treatment of chronic glomerulonephritis is to achieve stable remission and prevent severe renal failure. In some morphological forms, renal failure still develops. In this case, the solution is a kidney transplant. The selection of a compatible donor is often time-consuming, the shortage of donor organs also plays a role here, and the loss of time can be fatal for a patient with kidney disease.

In the process of waiting for transplantation, to prevent complications of kidney failure, patients are prescribed kidney dialysis. This may be hemodialysis, when the patient's blood is cleared of nitrogenous wastes and other end products of metabolism, passing through an apparatus with a special membrane - an "artificial kidney". Or peritoneal dialysis, when the patient's abdominal cavity is washed several times with special solutions. These procedures take many hours and must be carried out regularly 2-3 times a week to maintain normal life.

Glomerulonephritis: the choice of spa treatment

Patients with glomerulonephritis can receive spa treatment. They are recommended resorts in their climate zone.

Who can be treated in nephrological sanatoriums:

• Convalescents (recovered) after acute glomerulonephritis
• Patients with chronic glomerulonephritis in a stable condition, without high arterial hypertension and edema, with normal blood protein levels
• Stable patients with moderate nephrotic syndrome
• Kidney transplant patients in recovery.

The choice of a sanatorium with the proper conditions and procedures, the selection of a suitable climatic zone is a responsible matter and should be carried out by a nephrologist. Sanatorium treatment helps to recover much faster after therapy, however, if you want to get to a particular resort, be sure to consult your doctor.

Vaccination for glomerulonephritis: yes or no?

Unfortunately, children also suffer from this disease; pediatricians and pediatricians are involved in their treatment. More often it is an acute form of post-streptococcal glomerulonephritis, which in 80% of cases ends in recovery. Concerned parents naturally have a question, is it possible to vaccinate with glomerulonephritis?

The question is not easy. According to the Guidelines MU 3.3.1.1095-02 of January 9, 2002, glomerulonephritis is not a contraindication for vaccinations according to the calendar. After recovery from acute nephritis after 6 months, vaccination can be carried out, with nephrotic syndrome - after the end of treatment with corticosteroids. On the contrary, the Ministry recommends that patients also be vaccinated against influenza, since all SARS worsen the prognosis for renal pathology (this is a fact!).

On the other hand, if the function is impaired immune system and her “autoimmune attitude”, the introduction of foreign proteins contained in vaccines and sera can provoke the development of glomerulonephritis. Here no one will give guarantees of 100% safety, and even if the child is 7 years old, there is still a risk of complications during vaccination. With a progressive course of glomerulonephritis, children are not subject to vaccination.

Viral hepatitis and glomerulonephritis

Quite often there is a combination of viral hepatitis C and glomerulonephritis in one person. How to be? The combination of these diseases is not favorable. Is it possible to treat the hepatitis C virus with glomerulonephritis? There may be two situations here.

If hepatitis C was in a person before glomerulonephritis was detected, then the virus can cause secondary damage to the kidneys, as it persists and “harms” not only the liver, but also any organs, including the kidneys. In this case, it is necessary to treat viral hepatitis, after the destruction of the virus, glomerulonephritis itself is treated with appropriate drugs.

Treatment abroad

If you are not constrained by means, then it becomes possible for you to be treated at university hospitals in Germany, which are the highest standards of medical care for patients. Based on the bases of universities, they have the most modern equipment and technologies, qualified specialists. The university clinic in Freiburg is widely known, there are excellent and multidisciplinary centers in Baden-Baden, Tübingen, Munich, Frankfurt, Düsseldorf, Hannover.

Quite often, patients also seek treatment in Israel, a well-known high quality rendering medical services. Both in Israel and in Germany, in addition to therapeutic treatment, for more late stages dialysis and, if necessary, a kidney transplant. When treated abroad, patients with glomerulonephritis sometimes achieve stable remission.

However, in order to go abroad for treatment, the patient first needs to choose a clinic and a doctor, then find out the cost of staying in a hospital (bed-day), examinations (our tests will not work), the actual treatment, and pay for it. After that, the clinic will send official invitation for treatment, with which you can apply for a visa to enter the country (today, a visa to Israel is not needed).

Traditional medicine and glomerulonephritis

Traditional methods of treatment primarily include medicinal herbs. It is recommended to use for the treatment of glumerulonephritis at home, for example, such charges:

• Collection No. 68: calamus root 1, oak bark 2, St. swamp cudweed 6 parts
• Collection No. 70: Marshmallow root 2, speedwell grass 5, sweet clover grass 3, St.

The use of fees can improve kidney function, general well-being, reduce protein loss in the urine. But remember the cure folk remedies does not replace the main therapy for the treatment of glomerulonfrit, but only expands its capabilities.

Glomerulonephritis: alternative methods?

Ukrainian healer Bolotov B.V. and his follower, colleague Naumov D.V., created their own healing methods. Let's make a reservation right away that these methods contradict the canons of modern medicine and the principles of the treatment of glomerulonephritis both in Russia and abroad, and are not recognized by official science.

The method of Bolotov and Naumov invites patients to "dissolve slags" with the help of table salt 1 gr. after meals up to 10 times (!) a day and generally actively salt food, even fruits. Doctors, on the contrary, in every possible way warn patients with glomerulonephritis from consuming more than 4 g of salt per day (this includes salt naturally found in food).

As we can see, this "treatment" in many respects contradicts the medical recommendations for the nutrition of patients with glomerulonephritis, however, a number of patients still tend to use unconventional methods. However, it is important to remember that kidney disease is a very serious disease, and you should not risk your health.

Homeopathic remedies and other non-traditional remedies

The most important thing to remember when using the following means: they are not drugs as such and cannot be used as monotherapy (alone on their own)! Homeopathic treatment can only be used as an auxiliary, against the background of the main therapy, and only after consultation with a nephrologist! The most popular drugs:

1. Biologische Heilmittel Hel GmbH produces complex homeopathic preparations mild action, non-toxic, normalizing body functions, improving drug tolerance. Here is a complete list of Hel's drugs for the treatment of glomerulonephritis: Albumoheel S (correction of albuminuria), Apis-Homaccord (for edema), Lymphomyosot (antitoxic action, prevents the formation of edema), Reneel (for infection), Engystol N and Ren suis-Injeel (in recovery period after suffering glomerulonephritis), Rauwolfia compositum (with increased pressure).
2. Argo preparations are made from natural ingredients: extracts medicinal plants, natural minerals, vitamins, trace elements. They belong to dietary supplements, are produced in Russia and approved for use by the Institute of Nutrition of the Academy of Sciences, the Ministry of Health. Patient reviews of these drugs are mostly positive.

You may also be recommended other drugs for treatment, for example, Chinese medicine: Tienshi, amino acid concentrates from the departments sports nutrition. For example, can I take power system L-carnitine? Of course, you should not try to treat glomerulonephritis with them and make up for protein deficiency in proteinuria, for this there are special balanced drugs specifically for patients with kidney diseases, including those diagnosed with glomerulonephritis.

Genetically determined immune-mediated inflammation with a predominant initial lesion of the glomeruli and involvement of all renal structures in the pathological process, clinically manifested by renal and (or) extralocular symptoms.

Classification. The ICD-10 provides clear guidelines for the presentation and diagnosis of glomerular lesions.
1. Acute nephritic syndrome (N00): sudden onset of hematuria, proteinuria, hypertension, decreased GFR, sodium and water retention. Typical histopathological examples of diseases: all forms of diffuse GN, dense deposit disease, focal forms of nephritis.
Secondary GN: in Henoch-Schonlein disease, lupus nephritis, Alport disease, UP, Wegener's granulomatosis.
2. Rapidly progressive nephritic syndrome (N01): sudden onset of hematuria, proteinuria, anemia and rapidly progressive renal failure. Typical histopathologic examples are: Populunal GN, Goodpasture's syndrome, acute GN, mesangiocapillary GN and crescentic GN, hemolytic uremic syndrome, essential cryoglobulinemia, Henoch-Schonlein disease, UP, Wegener's granulomatosis.
3. HC (N04): massive proteinuria, edema, hypoalbuminemia, hypercholesterolemia. Associated with a variety of glomerular lesions. Typical histopathological examples of diseases: all named in point 2. In addition, diabetic glomerulosclerosis, amyloidosis, hereditary nephritis, lipoid nephritis, focal glomerulosclerosis, transplant rejection.
4. Recurrent or persistent hematuria (N02): Acute gross or microhematuria with little or no proteinuria. There are no other signs of nephritic syndrome. Typical histopathological examples of diseases: all named in point 2. There may be no other signs of nephritic syndrome.
5. Chronic nephritic syndrome (N03): slowly developing renal failure, accompanied by proteinuria, hematuria, hypertension.

Clinical manifestations.
Urinary, nephrotic and hypertensive syndromes are considered. urinary syndrome is determined by the quantitatively varying presence of erythrocytes, leukocytes, protein, cylinders in the urine.
There is a concept of the most typical urinary sediment for different forms of GN. So for MzPGN (IgA-nephropathy), the predominance of micro- or macrohematuria is characteristic. NS, which includes massive (more than 3.5 r/day) proteinuria, hypercholesterolemia, hypoalbuminemia, and edema, is more common in mesangiocapillary GN.

Hypertensive syndrome at the onset of GN occurs in no more than 23% of patients. In the terminal stages of GN, hypertension develops in 95% of patients.

A few words about the features of the main forms.

Post-streptococcal glomerulonephritis

Poststreptococcal glomerulonephritis (AGN) is manifested by gross hematuria, edema, hypertension, and oliguria. The frequency of these symptoms, respectively: 50%, 83%, 60%, 35%.
Gastrointestinal and pulmonary disorders are possible.
Diagnostics.
The diagnosis of AGN can be made on the basis of a combination of the following clinical signs: acute onset with proteinuria more than 2 g/day and micro- or macrohematuria; transient hypertension in the background possible reduction kidney function; the presence of edema and acute heart failure with epileptiform seizures; absence of systemic diseases, renal pathologies, hypertension and proteinuria in the past. AGN is a disease predominantly of young people, although occasionally this form is detected in middle-aged and elderly patients.

Thus, AGN can be established on the basis of three symptoms: edema, hypertensin, and changes in the urine. This should take into account the acute onset and the possibility of the absence of one or two of these symptoms. The final diagnosis can be made after nephrobiopsni. Laboratory data: azotemia in 72%, a drop in creatinine clearance Glomerular kidney disease 389 below 76 ml / min in 85%, hypocomplementemia in 84%, hematuria in 100%, proteinuria in 87% (including nephrotic syndrome in 13%), leukocyturia at 78%.

MEsangioproliferative glomerulonephritis

Mesangioproliferative glomerulonephritis (MzPGN).
The main place among the variants of MzPHN is occupied by nephritis with deposition of IgA in the glomeruli - IgA nephropathy with hematuria as the leading clinical symptom. With long-term observation, it was found that in 20-50% of adult patients, kidney function worsens over time.
IgA nephropathy is regarded as a persistent or slowly progressive disease. Genetic factors play a decisive role. Strong associations have been described between IgA nephropathy and HLA BW35 as well as HLA-DR4.
Family cases are possible.
Genetic disorders may interact with environmental factors. There are indications of a connection between the progression of IgA nephropathy and ACE gene polymorphism - the proportion of patients with the DD genotype was higher among those with elevated creatinine levels than among patients with normal levels (33 and 4%, respectively).
The disease develops at a young age, more often in men (1.5:1).
In 50% of patients, recurrent gross hematuria is observed, which occurs with febrile respiratory diseases in the first days or even hours of the disease (“synpharyngitis macrohematuria”), less often after other diseases, vaccination or heavy physical exertion.
Often macrohematuria is accompanied by mild dull pains in the lower back, transient hypertension, sometimes fever.
Episodes of gross hematuria can sometimes be with transient oliguric acute renal failure, presumably caused by blockage of tubules by erythrocyte casts.
In most cases, these episodes pass without a trace, however, patients have been described in whom renal function did not fully recover after acute renal failure.
Perhaps a latent course, with microhematuria, with a slight proteinuria. In 15-50% of patients (often older and / or with microhematuria) in the later stages, NS may join, in 30-35% - AH. Among patients with microhematuria, systemic signs were often noted - arthralgia, myalgia, Raynaud's syndrome, polyneuropathy, hyperuricemia.

Diagnostics.
Clinically characterized by proteinuria, hematuria, in some cases - nephrotic syndrome, hypertension. Laboratory data. Urinary syndrome: in 80% of patients in single portions of urine less than 10 leukocytes are detected in the field of view, in 60-70% of patients in single portions the number of erythrocytes is less than 10 in the field of view, in 25-30% it is in the range of 10-100 in the field vision and only 3-7% exceed this value. In a daily portion of urine, the number of erythrocytes in 70-80% of patients is less than 5 million, in 10-20% it is within 5-10 million, and only in 4-10% it exceeds this figure. Cylinders are detected in the urine in 50-70% of patients, and hyaline 2 times more often than granular ones.
Daily cylindruria in 10-20% exceeds 100 thousand km.
Changes in biochemical parameters are not very typical.
total protein serum, as a rule, is within the normal range, although in 40% of patients the albumin-globulin coefficient decreases, which is mainly due to a slight increase in globulin fractions. At immunological study different data are found depending on the stage of the process (exacerbation or remission).

In the blood serum of 35-60% of patients, the content of IgA is increased, its polymeric forms predominate.
The degree of IgA increase does not reflect the clinical course of the disease and does not affect the prognosis. In serum, high titers of IgA immune complexes are also detected, which in some cases contain AT against bacterial, viral and food antigens. Serum complement is usually normal.

The course of IgA nephropathy is relatively favorable, especially in patients with gross hematuria. PN develops in 10-15 years in 15-30% of patients, progresses slowly. Renal survival at 5, 10, and 15 years after the onset of symptoms is 93, 85, and 76%, and after biopsy, 89, 80, and 69%.
Kidney failure usually progresses slowly.
The prognosis is significantly influenced by the amount of proteinuria and the presence of hypertension, but not by the content of IgA in serum.
FgA nephropathy often recurs in the graft, in 50% of recipients within 2 years.
Predicting the recurrence of IgA nephropathy in the graft presumably allows the study of IgA affinity for type IV collagen.
However, graft survival is better than for other kidney diseases.

MEZANGIOCAPILLARY (MEMBRANOPROLIFERATIVE) GLOMERULONEPHRITIS

Mesangiocapillary (membranoproliferative) glomerulonephritis (MzKGN). Along with the idiopathic form, MzKGN is detected in SLE, mixed cryoglobulinemia, Sjögren's syndrome, nonspecific ulcerative colitis, sarcoidosis, lymphomas, neoplasms, etc.
Genetic factors may play a role in the development of MgCHN. Family cases of the disease have been described in siblings, as well as in several generations.
Men of young age, as well as children, get sick somewhat more often. It is rare in the elderly.

The clinical picture is the same for all morphological variants of MzKGN: hematuria is characteristic (10-20% of patients have transient macrohematuria), severe proteinuria and NS (often with elements of acute nephritic), decreased renal function.
MCGGN is responsible for 10% of NS cases in adults and 5% in children. AH is observed in a third of patients (during the period of sufficient kidney function). The combination of NS with hematuria and possible hypertension should be alert to the possibility of mesangiocapillary nephritis. Anemia (which is associated with the presence of activated complement on the surface of red blood cells) is possible.
In type II, a peculiar retinopathy is described (diffuse bilateral symmetrical formations yellow color).
The disease often begins with acute nephritic syndrome, with the sudden development of hematuria, severe proteinuria, edema and hypertension, in which case the diagnosis of acute nephritis is erroneously diagnosed. In almost 1/3 of patients, the disease can manifest itself as rapidly progressive PI with the presence of "crescents" in the renal biopsy.

Diagnostics. The peculiarity of MzKGN is hypocomplementemia with a decrease in the level of C3 and / or C4 components, which is especially often detected in type II. It should be borne in mind that the complement level is also reduced in acute GN and lupus nephritis, but remains normal in other types of GN, MzKGN (more often type II) is sometimes combined with partial lipodystrophy (a disease that also occurs with hypocomplementemia).

The course of the process is steadily progressing, spontaneous remissions are rare.
MzKGN - one of the most unfavorable forms, in the absence of treatment, terminal PI develops after 10 years in almost 50%, after 20 years - in 90% of patients.
As a special feature of the course of MCGN, a “stepwise” progression and a relatively sudden deterioration in kidney function in individual patients are noted.
Clinically poor prognostic signs are the presence of NS, diastolic hypertension, decreased renal function, and detection of serological signs of HCV and HBV infection.

Rapidly progressive glomerulonephritis (RPGN).
Typically acute onset, oliguria, gross hematuria, massive proteinuria, often NS - up to 30% of cases.
Hypertension also occurs quite early, but in some patients it precedes the onset of nephritis (a reason to think about the generality hereditary predisposition).
The above must be supplemented with a variety of extrarenal manifestations. Possible weight loss, fever, asthenia, arthralgia, rash.
Most of similar symptoms associated with rapidly emerging and also rapidly progressive renal failure.

Diagnostics. Typical occurrence of RPGN in white male smokers (ratio M:W = 6:1). The disease usually manifests with pulmonary symptoms - bilateral hemorrhagic pneumonia with hypoxemia and respiratory failure. The development of iron deficiency anemia is natural.

Laboratory manifestations are bright. Most patients have severe proteinuria. Approximately 1/3 have a deployed NS. Regular micro-, (macro) hematuria. An early violation of kidney function is noted - the rapid development of azotemia, while finding anemia and increased ESR. In the acute phase of the disease, the kidneys are macroscopically enlarged due to interstitial edema and inflammation. On the capsular surface and in the cortex, petechiae are often visible due to hemorrhages in the kidney tissue.

Treatment of glomerular diseases

Diet. With sufficient kidney function - some restriction of proteins (0.75-1 g / kg of body weight), in the case of the development of hypertension and NS - restriction of salt to 3 g / day.
At pronounced edema dietary intake of sodium should be sharply limited to the level of its maximum excretion. The same applies to the amount of fluid you drink.
All other restrictions are not scientifically substantiated.
The regimen of patients must be regulated only during the period of exacerbation of the inflammatory process.

etiological treatment. Reversal of renal disease can be achieved primarily through an etiological approach to the treatment of GN, but this approach is possible in only a few patients. Etiological treatment is the use of antibiotics for post-streptococcal nephritis and nephritis associated with subacute infective endocarditis; specific treatment syphilitic, malarial and paratuberculous nephritis with release from IR and complete recovery; tumor removal in paraneoplastic nephrotic syndrome; discontinuation of the corresponding drug that caused drug nephritis; abstinence in alcoholic nephritis, exclusion of allergenic factors in atopic nephritis.

The possibility of reverse development with the timely elimination of the etiological factor is quite real.
Pathogenetic treatment is aimed at immune processes, inflammation, intravascular coagulation. To a certain extent, antihypertensive therapy also belongs to pathogenetic therapy, and in individual cases- and diuretic. Most of the pathogenetic therapy of nephritis (glucocorticosteroids, cytostatics, heparin, plasmapheresis) has a wide range of action, grossly disrupts homeostatic processes, and often causes severe complications.
The pronounced activity and danger of these methods of treatment allow us to call them methods of "active" or "aggressive" treatment of nephritis, as opposed to more mildly acting "sparing" methods using antiplatelet agents and antihypertensive drugs.

The appointment of "active" therapy is indicated at those stages of the development of nephritis, when the predominant role of immunoinflammatory processes or intravascular coagulation processes in the progression of the disease is obvious, i.e., in situations where there is a high activity of the renal process, which largely determines the rate of its progression. Therefore, clinical and morphological assessment of GN activity is important.

The most correct approach - orientation to the morphological picture (assessment of the form of nephritis, its activity and severity of sclerosis) - is not always possible. In this regard, in some situations it is necessary to focus on clinical picture, clinical signs of process activity.

General provisions that should be followed in such a situation: with high activity of GN, especially GN with NS without AH and signs of PN, immunosuppressive therapy is always indicated.

Only in the presence of contraindications to active therapy or the impossibility of its implementation for any reason, one can confine oneself to symptomatic treatment - the appointment of ACE inhibitors;
- for the first time NS, especially without hematuria and hypertension, treatment with glucocorticosteroids (GCS) is always indicated.

For subsequent relapses, start with corticosteroids (if the initial episode of corticosteroid treatment was effective), then prescribe cytostatics or cyclosporine;
- with progressive forms of nephritis (with a rapid increase in the level of creatinine), it is possible to prescribe immunosuppressants - large doses of corticosteroids and cytostatics orally and / or in the form of pulses;
- with latent nephritis with proteinuria> 1 g / day, ACE inhibitors are indicated;
- in relation to hematuric forms, there is no single tactic.

Currently, the following groups of pharmacological drugs are used to treat nephritis: GCS, cytostatics, ACE inhibitors, anticoagulants, antiplatelet agents, lipid-lowering drugs; in some situations, the method of "mechanical" removal of pressure - plasmapheresis - is of great importance.

Glucocorticosteroids. General indications for the appointment of GCS in nephritis: pronounced activity of the renal process, the presence of NS without severe hypertension and hematuria (morphologically - minimal changes in the glomeruli, mesangioproliferative and membranous nephritis).

Treatment is less promising for FSGS, mesangiocapillary, and diffuse fibroplastic GN.

Methods (schemes) of corticosteroid therapy for nephritis.
Possible various ways(modes) of the use of GCS in GN.
To achieve effective concentrations of corticosteroids in areas of immune inflammation and edema in the renal tissue, where blood flow is significantly reduced, 2 methods of administering corticosteroids are effective.

In the first method, long-term daily intake of high and moderately high doses of corticosteroids (prednisolone) is used, while in the second, intravenous administration of ultra-high doses (so-called pulses) of corticosteroids (methylprednisolone or prednisolone) is used.
Depending on the severity of GN, high-dose prednisolone (1-2 mg/kg per day for 1-2 months) can be given by mouth or in separate doses 2-3 times a day, or once in the morning.
In the first case, with a fractional intake of prednisolone, better control of renal inflammation is achieved, but the immediate side effects develop more often and are more pronounced.
Therefore, some authors recommend at the first opportunity (clinical signs of improvement) to transfer the patient from fractional to a single dose. Then, when a positive effect is achieved, the daily dose is slowly reduced to the lowest possible maintenance dose.

When taking GCS every other day, the function of the hypothalamic-pituitary-adrenal system is suppressed much less than with daily intake.
In this case, the dose of prednisolone, which the patient takes every other day once in the morning, is equivalent to a double daily dose of daily intake. This method is used most often in pediatric practice, less often in adults.

Efficiency is close to the generally accepted scheme, but side effects are less common, children do not have growth retardation.
This alternating regimen is especially indicated for maintenance therapy.

Pulse therapy with methylprednisolone has previously been used to treat renal allograft rejection crises. This approach is currently being used to treat rapidly progressive GN with crescents (as idiopathic form and in patients with systemic diseases) and other severe forms of GN that occur without the formation of crescents (for example, diffuse proliferative GN in patients with systemic lupus erythematosus).
The procedure consists in intravenous drip for 20-40 minutes 0.5-1.5 g of methylprednisolone (or prednisolone, somewhat less effective in this situation), which is repeated 2 more times in subsequent days to reach a total dose of 3-4 g of the drug.
The method is contraindicated in patients with severe hypertension, as well as with concomitant myocarditis or severe cardiomyopathy.

supportive therapy. After a course of treatment with high doses (most often within 2 months), the dose is reduced (usually over the same period or more slowly in systemic diseases) to maintenance (10-20 mg).
The timing of maintenance therapy is determined empirically, usually 2 months, sometimes (especially in GN associated with systemic diseases) longer maintenance therapy is required, even for several years, which can cause severe side effects.
At the same time, therapy every other day causes fewer side effects than daily corticosteroid therapy, even when the dose of corticosteroids for alternating therapy is 2-3 times higher than with daily intake.
In this regard, the best tactic for maintenance therapy of corticosteroids is considered to be a decrease in daily dose to the smallest possible level, and then switching to an alternating regimen using a 2-fold dose of daily intake.
If to suppress the activity of GN or maintain normal function kidneys require unacceptably high doses of corticosteroids, and if side effects of corticosteroid therapy appear quickly, then it is advisable to prescribe cytostatic drugs.
This allows you to use lower doses of corticosteroids and thus reduce the risk of side effects.
Side effects of corticosteroids can be acute (euphoria, depression, insomnia, increased appetite, corticosteroid psychosis, fluid retention, decreased glucose tolerance) and chronic (obesity, myopathy, striae, skin atrophy, hirsutism, cataracts, growth retardation, osteoporosis, aseptic necrosis and bone fractures, acne and opportunistic infections).

The former disappear after the abolition of GCS therapy, the latter can persist for a long time.
Abrupt withdrawal of corticosteroids after their long-term use leads to a life-threatening adrenal crisis, which is associated with suppression of the function of the hypothalamic-pituitary-adrenal system during long-term use of corticosteroids and indicates the need replacement therapy. Signs of an upcoming adrenal crisis are malaise, fever, muscle and headache, sweating, and hypotension with warm extremities due to dilatation of the peripheral vessels.

Cytostatic drugs
Indicated for long-term pathological processes, in the presence of hypertension, with initial signs of PN, as well as in the detection of diseases in which hormone therapy is doubtful or its previous use was ineffective, as well as in cases of complications of this therapy.
Usually, side effects in the treatment of cyclophosphamide are short-term, disappearing after stopping treatment (nausea, vomiting, diarrhea, alopecia and infections that develop during leukopenia), and long-term (gonadal insufficiency with the possibility of subsequent infertility, which patients should be warned about, hemorrhagic cystitis, teratogenic effects, tumors and chronic infections).

At cumulative doses up to 200 mg/kg, the likelihood of severe side effects small, but it increases significantly at doses above 700 mg/kg.
In this regard, when deciding on the long-term treatment of patients with cyclophosphamide (especially young men), it is necessary to warn about possible complications.
At very high doses, a syndrome of inappropriate ADH secretion may develop.

In the treatment of nephritis, a cytostatic is prescribed orally and in the form of pulse therapy.
Dose for oral administration - 2-2.5 mg / kg per day.
In severe kidney damage (like rapidly progressive GN) with systemic vasculitis, you can start with a dose of 3.5-4 mg / kg per day.
The goal of therapy is to reduce the number of leukocytes in the peripheral blood to approximately 3500 cells / μl (but not lower than 3000 cells / μl), the content of neutrophils should be 1000-1500 cells / μl.
The number of leukocytes decreases within a few days or weeks.
During this period of induction of immunosuppression, it is very important to check the number of leukocytes in peripheral blood at least every other day, so that if the number of leukocytes drops to the lower acceptable level, the dose of the drug can be reduced or canceled.
Since the level of leukocytes has stabilized, their content should be monitored at least once every 2 weeks. Over time, the dose of cyclophosphamide necessary to maintain white blood cells at the proper level has to be reduced.
If prednisolone (which protects the bone marrow from suppression) is prescribed simultaneously with cyclophosphamide, then when the dose of prednisolone is reduced, the dose of cyclophosphamide should also be reduced.

In / in pulse therapy with cyclophosphamide is considered more effective and at the same time has fewer side effects than conventional oral administration. Doses of 0.5-2.0 g/m2 of body surface are used, giving a drop in the level of leukocytes to a maximum of 2000-3000 cells/µl, which occurs between the 8th-12th day, then the leukocytes return to normal approximately at the 3rd week.

Pulses are used every 3 months, the duration of treatment is 2 years or more.
It has been established that the frequency of complications from the bladder with this regimen (1 pulse per 3 months) is significantly reduced.
This is probably due to the fact that the duration of contact of toxic metabolites of cyclophosphamide with the bladder wall is reduced to approximately 36 hours every 3 months, and the total dose of the drug over these 3 months is also reduced.

Infections, both large and small (for example, herpes zoster), occur, especially during the period of maximum fall in the number of leukocytes. Amenorrhea is a serious problem, although its frequency decreased somewhat with this option prescribing the drug (45 instead of 71%, which is observed with long-term oral therapy).

New regimens for the use of cyclophosphamide have been proposed, in particular, an increase in the pulse rate up to 1 time per month in the initial phase of therapy.
The effectiveness of treatment can be judged not earlier than after 6 months, if there are signs of improvement, continue treatment for another 3 months; in the future - if it is necessary to continue treatment, the intervals between pulses should be increased to 2-3 months.
The risk of side effects depends on the total dose of the drug.

When conducting pulse therapy with cyclophosphamide, the following conditions must be met:
- to prevent severe bone marrow suppression, the dose of the drug should correspond to the level of GFR, since cyclophosphamide metabolites are excreted by the kidneys: with normal GFR - 15 mg / kg of the patient's body weight (or approximately 0.6-0.75 g / m2 of body surface), with GFR less than 30 ml / min - 10 mg / kg (or about 0.5 g / m2).
The drug is administered intravenously in 150-200 ml of isotonic sodium chloride solution for 30-60 minutes;
- strict control of the level of leukocytes is necessary on the 10th and 14th day after pulse therapy: if the level of leukocytes falls below 2000 cells / μl - reduce the next dose by 25%, if the level of leukocytes is more than 4000 cells / μl - increase the next dose of cyclophosphamide by 25% (up to 1 g/m2); - to prevent nausea and vomiting, serotonin receptor antagonists are recommended: cerucal 10 mg 3 times a day, ondansetron (zofran) 4-8 mg orally 3-4 times every 4 hours (as an alternative, navoban or latraya); can be combined with a single dose of dexamethasone 10 mg orally;
- to prevent the toxic effect of cyclophosphamide metabolites on the mucous membrane of the bladder: stimulation frequent urination (increased consumption fluids inside) and the intake of mesna, which binds in bladder toxic metabolites (4 times every 3 hours, the total dose corresponds to 80% of the dose of cyclophosphamide).

Chlorbutin. Assign at a dose of 0.1-0.2 mg / kg per day, the half-life is 1 hour, and it is completely metabolized.
Chlorbutine acts more slowly than cyclophosphamide and the associated bone marrow suppression develops less rapidly and is more reversible. Side effects include gastrointestinal disturbances and gonadal failure.
More rare side effects: pulmonary fibrosis, seizures, dermatitis, and toxic liver damage.
Tumors develop less frequently than with cyclophosphamide treatment.
In young men, cyclophosphamide (less gonadotoxic than chlorbutin) is preferred at a dose of less than 2 mg/kg; in women and elderly men - chlorbutine (ovaries are less sensitive to the toxic effects of alkylating drugs) at a dose of 0.15 mg / kg.

Azathioprine is taken at a dose of 1-3 mg / kg per day, and the dose is selected in such a way as to maintain the number of leukocytes in the blood at least 5000 cells / μl.
The main side effect is bone marrow suppression, especially neutropenia with the development of infections.
Other complications include anemia, thrombocytopenia, hepatitis, dermatitis, stomatitis, alopecia, gastrointestinal disturbances, and an increased risk of tumors, especially skin cancer and lymphomas. In general, compared with cyclophosphamide, azathioprine has a less active effect on kidney inflammation and causes fewer severe complications. In patients with signs of renal insufficiency, azathioprine is not recommended to be administered together with allopurinol, which blocks its inactivation.

Selective immunosuppressants.
The representative is cyclosporine A (CsA).
The results of the studies confirm that CsA may be an alternative treatment for patients with GN with steroid-resistant or steroid-dependent NS.
Before treatment, a kidney biopsy is mandatory: interstitium sclerosis, tubular atrophy, or vascular damage prevent the appointment of CsA.
In patients older than 60 years, the drug increases the risk of developing tumors. The initial dose of CsA per day for adults is 5 mg/kg, for children - 6 mg/kg.
Depending on the morphology of GN, a decrease in proteinuria is usually observed within 1-3 months.
Mandatory monitoring of kidney function: an increase in creatinine by 30% relative to the original requires a dose reduction of CsA by 30-50%. The most serious side effects are nephrotoxicity, which is dose dependent and usually reversible, and development arterial hypertension that is associated with spasm of the afferent glomerular arteriole. Other side effects are hypertrichosis, gingival hypertrophy (with the latter, azithromycin helps, and possibly metronidazole).

Combined treatment regimens.
Among the combined treatment regimens, the most common regimens for the treatment of corticosteroids with cytostatics, as well as the so-called 4-component regimen.
GCS + cytostatic.

GCS in combination with various cytostatics can be administered orally, as well as parenterally.
For example, pulse therapy with methylprednisolone is carried out, followed by oral administration of prednisolone and cytostatics, pulse therapy with cyclophosphamide and methylprednisolone.

The following combined pulse therapy schemes are possible: on the 1st day, 800-1200 mg of cyclophosphamide and 1000 mg of methylprednisolone or prednisolone are administered intravenously, on the next two days - only methylprednisolone or prednisolone.

A peculiar regimen with alternating corticosteroids and cytostatics was proposed by C. Ponticelli et al.
During the first 3 days of the 1st month of treatment, methylprednisolone (1000 mg each) is administered intravenously, the next 27 days - methylprednisolone daily orally at a dose of 0.4 mg / kg, i.e. 28 mg with a body weight of 70 kg; During the 2nd month of treatment, the patient takes only chlorbutin at a sufficiently high dose - 0.2 mg / kg per day, i.e. 14 mg with a body weight of 70 kg.
This 2-month cycle is repeated 3 times, the total duration of treatment is 6 months. The 4-component scheme includes the appointment for 8 weeks of prednisolone at a dose of 60 mg / day, azathioprine at 2 mg / kg / day, dipyridamole at 10 mg / kg / day, heparin at a dose that causes a doubling of thrombin time.
Then, during the year, treatment with azathioprine and dipyridamole is continued at the same doses, and heparin is replaced with phenylin (at a dose that causes a doubling of prothrombin time).

Other (non-immune) treatments for nephritis.
Over the past decade, the possibility of a non-immune effect on the progression of GN has significantly expanded in accordance with new ideas about non-immune mechanisms of progression.

At the present stage, we can talk about four methods of nephroprotective therapy, the effect of which on the progression of GN has been proven or is being studied.
These are ACE inhibitors, heparin, dipyridamole, lipid-lowering drugs.

The influence of other non-immune treatments (modern non-steroidal anti-inflammatory drugs, etc.) is also discussed.
ACE inhibitors (ACE inhibitors) inhibit the conversion of inactive angiotensin I to angiotensin II.
In addition, ACE destroys kinins - tissue vasodilating hormones.
ACE inhibition blocks the systemic and organ synthesis of angiotensin II and accumulates kinins in the circulation and tissues.
Essentially, any antihypertensive therapy has a beneficial effect on the course of GN.
However, the effect of ACE inhibitors in GN is not limited to lowering systemic blood pressure.
The antiproteinuric effect of ACE inhibitors may be due to a decrease in systemic blood pressure and expansion of efferent arterioles, as well as changes in the permeability of the glomerulus to macromolecules.
This effect of ACE inhibitors depends on the dose of the drug, the duration of treatment and low sodium intake. In most patients, a significant and sustained reduction in proteinuria is observed only after several weeks of treatment.

Long-acting ACE inhibitors (enalapril, lisinopril, ramipril) are more effective.
The antiproteinuric effect of ACE inhibitors is manifested by restricting sodium intake, and is enhanced by its sharp restriction.
With poor tolerance of a low-salt diet, it can be replaced by taking diuretics.

Thus, ACE inhibitors (captopril, enalapril, ramipril, fosinopril, etc.) are the drugs of choice for hypertensive variants of nephritis.
In addition, the indication for the appointment of ACE inhibitors in CGN is the presence of proteinuria (in the absence of high GN activity requiring immunosuppression).
Essentially, to slow the progression of the disease, ACE inhibitors are indicated for all patients with CGN who do not have contraindications to their appointment. To obtain the maximum antiproteinuric effect of an ACE inhibitor, treatment should begin with small doses of the drug (for example, 2.5-5.0 mg of enalapril) and gradually increase the dose to the maximum tolerated (10-20 mg), regularly monitoring serum creatinine and potassium levels, risk the increase of which is especially high in patients with initially reduced kidney function.

Efficiency can be assessed only after several months of continuous treatment.
Complications of therapy with ACE inhibitors in nephrological practice: an increase in the level of not only serum creatinine (usually transient in the first 1-2 weeks of treatment), but also serum potassium, hypotension, urticaria, Quincke's edema, cough, leukopenia (the latter more often when taking captopril containing SH -rpyny).
Contraindications: severe PI (serum creatinine above 5-6 mg / dl), hyperkalemia, stenosis of the renal arteries of both kidneys, severe heart failure.
In these situations, ACE inhibitors can lead to a rapid decline in kidney function.
Care should be taken when prescribing these drugs to elderly patients with chronic GN.
ACE inhibitors are contraindicated in pregnant women.

Angiotensin II receptor blockers (losartan, irbesartan, etc.) have general effects similar to ACE inhibitors (with the exception of antikinin), but their nephroprotective capabilities have not yet been clearly proven.

Heparin is a heterogeneous mixture of glycosaminoglycans with a molecular weight of 1 to 40 kDa, which have different anticoagulant activity.
Fragments and fractions of heparin with a molecular weight of more than 10 kDa, containing more than 18 sugar residues, bind to antithrombin III and inhibit almost all blood coagulation factors, mainly thrombin and factor Xa.
In nephrological practice, heparin began to be used in the late 60s. in connection with its ability to suppress the processes of intravascular, including intraglomerular, coagulation.
Heparin implements an antithrombotic effect, affecting not only plasma, but also vascular factors thrombosis.
So, it inhibits adhesion and aggregation of platelets; has a profibrinolytic effect, increasing the secretion of tissue-type plasminogen activators from the endothelium of the vascular wall into the bloodstream, affects the rheological properties of blood, contributing to an increase in blood flow in the vessels. In addition, heparin stimulates the synthesis vascular wall endogenous anticoagulant - heparan sulfate.
Influence on the processes of thrombosis is not the only property of heparin that justifies its use in nephrological practice. It has been established that it has a diuretic and natriuretic effect, in the mechanism of which the leading role belongs to the suppression of aldosterone production by heparin.
Heparin has a hypotensive effect, associated both with stimulation of the release of cGMP and nitric oxide (NO), and with a decrease in the production of endothelin by endothelial and mesangial cells of the kidneys.
In addition, it has an antiproteinuric effect, being a polyanion and stimulating the synthesis of negatively charged heparan sulfate, restoring the negative charge lost by the basement membrane and reducing its permeability to protein molecules. Heparin affects lipid metabolism disorders, which are an independent factor in damage to the renal tissue, and has an anti-complementary effect that prevents the formation of immune complexes.

Unfractionated heparin is prescribed subcutaneously at a dose of 15,000-40,000 IU / day, in rare cases - 50,000-60,000 IU / day.
Usually the daily dose is divided into 3-4 injections; the dose is considered adequate if 4-5 hours after subcutaneous injection the blood clotting time increases by 2-3 times compared to the initial one, and the activated partial thromboplastin time - by 2 times.
To achieve diuretic and hypotensive effect a heparin dose of 25,000-30,000 IU/day is usually sufficient.
Usually the course of treatment with heparin is 6-8 weeks; if necessary, treatment can be continued up to 3-4 months.
In order to avoid reactive hypercoagulability (rebound action), which is especially dangerous when heparin is suddenly discontinued, the drug should be discontinued slowly (within 6-8 days), gradually reducing the single dose, but not reducing the number of injections.
After the end of treatment, it is recommended to take indirect anticoagulants (phenylin) for 2-3 months.

Side effects. Despite the many-sided properties of heparin, its effective use difficult due to high frequency side effects, mainly bleeding.
With medium doses of heparin (15,000-20,000 units / day) hemorrhagic complications occur in 5-10% of patients, at high doses (more than 40,000 IU / day) - in 10-30% of cases.
In addition to bleeding, treatment may be complicated by allergic reactions (rash, headache, myalgia, fever); sometimes there is a syndrome of selective hypoaldosteronism with hyperkalemia; osteoporosis, thrombocytopenia, sometimes with thrombosis may develop. Low molecular weight heparins. IN recent decades synthesized heparins with low molecular weight (LMWH), including for oral administration, have a number of advantages over conventional unfractionated heparin.

Low molecular weight (1-8 kDa) heparin fractions bind to antithrombin III, predominantly inhibit coagulation factor Xa and practically do not inhibit thrombin.
It is this property of low molecular weight fractions of heparin that can explain their antithrombotic effect without pronounced anticoagulant and hemorrhagic activity. The action of LMWH does not depend on baseline antithrombin III in plasma, they have better bioavailability, are rapidly absorbed from the depot, and have a longer half-life.
LMWH is administered 1-2 times a day s / c or / m. Monitoring of LMWH therapy is carried out on the basis of anti-Xa-factor activity, although it is not necessary to determine it, especially at low doses of the drug (50-60 anti-Xa units per 1 kg of body weight per day).
In the treatment of LMWH, fewer injections per day are required, laboratory monitoring of therapy is facilitated, which makes it possible to prescribe them on an outpatient basis and on an outpatient basis. long term. Dipyridamole is used for GN in combination with other drugs, such as acetylsalicylic acid, heparin and immunosuppressants, and as monotherapy. Dipyridamole is indicated in high doses - 225-400 mg and even 600 mg / day. Due to possible headaches, it is better to start treatment with a small dose, gradually increasing it (25 mg / day every 3-4 days).
Lipid-lowering therapy.
A lipid-lowering diet containing less than 200 mg/day of cholesterol is shown, in which total fats provide less than 30%, and polyunsaturated fatty acid- about 10% of the total calories, and allows you to reduce cholesterol by 15-20%.
Patients do not tolerate more severe, especially prolonged, restriction. More effective in the correction of hyperlipidemia was vegetarian diet(soy with the addition of essential amino acids), which also slightly reduces proteinuria.
The nephroprotective effect of normalizing the level of blood lipids is especially clearly manifested in hypercholesterolemia. It is necessary to maintain cholesterol levels within 120mg/dL(<100mL/dL).

Statins, in addition to lipolytic action, inhibit LDL peroxidation, reduce the formation of their modified forms, which reduces the penetration of monocytes into the vascular wall.

Non-steroidal anti-inflammatory drugs (NSAIDs), which were widely used in nephrology in the 70-80s. XX century, have a pronounced antiproteinuric property (can reduce proteinuria by 50% or more). The action of the drugs is explained by a decrease not only in the permeability of glomerular capillaries for protein molecules, but also in the pressure inside the capillaries, as well as a decrease in the filtration surface of the latter.
The antiproteinuric effect of indomethacin is especially pronounced. However, the use of NSAIDs in nephrology, especially such as metindol or brufen, is futile.
Too frequent complications (side effects), such as increased blood pressure, abdominal pain, increased heartburn, worsening kidney function.

The anti-inflammatory, analytical and antipyretic effect of NSAIDs is associated with their ability to inhibit COX-2, while the most common side effects (damage to the gastrointestinal tract, kidneys, impaired platelet aggregation) are associated with suppression of COX-1 activity.
This created the theoretical prerequisites for the creation of a new class of NSAIDs with the ability to selectively inhibit COX-2, the use of which can make treatment with these drugs safer.

In this regard, attention is drawn to the drug nimesulide (nise), which was developed back in 1985 and has now become widely used in many countries of the world.
Nimesulide has an original structure and is one of the first NSAIDs to show high selectivity for COX-2. In short, a new effective drug has appeared, the use of which, perhaps, will relieve the doctor of fear for the usual complications. Dosage for adults - 100 mg 2 times a day.

For the treatment of nephrotic syndrome (glomerulonephritis and FGS), several reports analyze the efficacy of mycophenolate mofetil (celcept) (250 and 500 mg tablets), a potent, selective, non-competitive and reversible inhibitor of inosine monophosphate dehydrogenase that inhibits de novo synthesis of guanosine nucleotides.
It has a more pronounced cytostatic effect on lymphocytes than on other cells, since the proliferation of T- and B-lymphocytes is very dependent on the synthesis of de novo purines, while other types of cells can switch to bypass metabolic pathways.
Highly effective in the prevention of organ rejection and the treatment of refractory organ rejection in patients undergoing allogeneic kidney transplantation.
For the treatment of refractory rejection, a daily dose of 3 g (1.5 g 2 times a day) is recommended.
Selcept should be administered simultaneously with standard therapy with cyclosporine and corticosteroids.
In / in the introduction of y-globulin (daily at the same dose for 5 days, the total dose of 2 g / kg of body weight) and monoclonal antibodies. The usefulness of these treatments for patients with severe disease is not yet clear, but they may be effective in patients with skin and neurological symptoms of the disease.

It seems promising to use drugs from the group of prostaglandins in any form of GN. There is already good experience with a 3-week infusion of PgEl (aprostadil).
After such a short course, creatinine clearance significantly increased, and serum creatinine concentration significantly decreased.

Hemosorption is rarely used.
When it is carried out, due to the contact of blood with sorbents, toxic substances are removed; in addition, the sensitivity to cytostatic and glucocorticosteroid drugs changes (usually increases). A particularly good effect is observed in patients with membranous nephropathy, even without the use of other active methods.
The effectiveness of sorbents in other forms of GN is less obvious (special sorbents are used).

Lymphorrhea is usually carried out by draining the thoracic duct, after which up to 2-5 liters of lymph are removed (rarely 10).
This leads to a sharp rejuvenation of the lymphoid germ and activation of morphogenesis processes in the kidney.
Treatment is indicated for patients with NS, especially in the absence of the effect of other types of therapy.
This treatment is contraindicated with a decrease in kidney function (even only with a decrease in glomerular filtration with a normal level of plasma creatinine).

Tactics of treatment of individual forms of glomerulonephritis.

Rapidly progressive glomerulonephritis.
The administration of cyclophosphamide (3 mg/kg/day for 8 weeks) stops the ongoing synthesis of anti-GBM antibodies.
This therapy is supplemented by plasmapheresis with an exchange of up to 4 liters daily for 14 days. Such a combination should be started as early as possible, this leads to a rapid clearing of the bloodstream from AT.
The presence of crescents with fairly intact glomeruli, small tubulo-interstitial lesions, a moderate increase in creatinine (< 440 ммоль/л) диктует раннюю активную цитостатическую терапию, применение пульсов метилпреднизолона (1,0 г в/в калельно в течение 30 мин) 3-5 дней в сочетании с приемом преднизолона внутрь 1 мг/кг/день. Имеются данные, что такая терапия может снизить уровень креатинемии и задержать применение диализа.
For ANCA(+) patients, monthly pulses of cyclophosphamide are shown.
With naturally concomitant hypertension, preference is given to ACE inhibitors. With galloping PN, hemodialysis can be used. The rest is symptomatic therapy.

Mesangiocapillary glomerulonephritis.
Treatment of MzKGN should be differentiated.
In cases of severe course, the attitude should be the same as for RPGN. For this option, the intensive care courses described above are good. A variant of the usual course with regular exacerbations without a noticeable decrease in kidney function requires prolonged therapy with corticosteroids and / or cytostatics.
Courses of pulse therapy are suitable, followed by long-term intake (up to 1.5 years) of maintenance doses or the initially traditional treatment regimen with prednisone at 1.5-2 mg/kg of the patient's weight.
Any of these options should be supplemented by many months of therapy with aspirin (0.5-1.0 g / day) and dipyridamole (75-250 mg / day). This combination maintains the stored function for a long time.
Combinations with hepatitis B or C are often mentioned in the literature in connection with MgCHN, so different options for interferon therapy may be appropriate.
Mesangial-proliferative glomerulonephritis should be treated carefully, and in the absence of special indications (NS, high AH, etc.), be limited to chimes.
Such a recommendation is based on the benign course of this form of GN, which is known for its low sensitivity to drugs and the high probability of spontaneous remission.

More severe forms of IgA nephropathy are successfully treated with cyclophosphamide (6 months), dipyridamole at a dose of 400–600 mg/day, and warfarin, an indirect anticoagulant, at a dose of 5 mg/day (36 months).
When relapses of IgA nephropathy are associated with a possible infection, 10-day courses of antibiotics (tetracycline) are recommended on the first day of exacerbation.
Sometimes improvement in the course of lgA nephropathy occurs after tonsillectomy.

Antibacterial therapy should only be used if there is evidence of an association with infection.
In other situations, it is better to look for luck by using less allergenic agents.
By the way, when detecting in the kidney tissue (during immunohistological examination) AT to viruses, a good effect was noted from the use of interferons. Some patients with MzPGN have steroid-resistant NS, an early increase in blood pressure, and the rapid onset of azotemia. In such patients, it is necessary to apply the treatment regimen for RPGN (see above).
With an uncomplicated course of acute glomerulonephritis in the first days, it is advisable to completely exclude table salt, restrict liquid, prescribe ascorbic acid, calcium gluconate, and, if necessary, correct electrolyte disorders.
And only with a prolonged course, persistent hypertension, it is necessary to prescribe corticosteroids, antihypertensive drugs, diuretics.
In the first days of the disease, the appointment of antibiotics is justified.

Unfortunately, patients rarely see a doctor on the first day, and after a week or two, the prescription of antibiotics becomes meaningless.

All of the above are serious generally accepted provisions that pass from one monograph to another.
But all of them are focused on a highly qualified specialized nephrology clinic.
But there are few of them, the vast majority of doctors work in non-specialized medical institutions.

Naturally, this provision prompted many nephrologists to look for an acceptable form of an algorithm for managing patients with GN for a practical physician.
Such proposals are more than enough.
But all of them, by virtue of their inevitable artificiality, are open to criticism.
We will offer our lightweight version of the GN treatment regimen.

This part of the material is for those who are alone with the patient today, and the Nephrological Center is "far away". (In any other case, it is necessary to immediately refer the patient to a specialized department for consultation and treatment!).

We accept the condition: the impossibility of a biopsy.
So, a doctor who encounters a nephrological patient for the first time can diagnose one of the following variants of a nephrological disease (the proposed scheme is very similar to the clarifications to the WHO scheme, but, in our opinion, it is simpler):
- newly diagnosed (acute - according to the accepted scheme) nephritic syndrome;
- newly diagnosed nephrotic syndrome;
- rapidly progressive nephritic syndrome;
- recurrent nephritic syndrome;
- recurrent nephrotic syndrome.

A number of diseases can be behind the listed syndromes.
Acute nephritic syndrome.
AGN is possible, as well as all the forms of GN mentioned above.
It is possible that systemic diseases, also manifested by nephropathy, are hidden behind such a nephritic syndrome.
Since, in most cases, a rapid decline in kidney function, as a rule, is not detected for the first time in nephritic syndrome, it is possible not to rush with active therapy (especially pathogenetic). Symptomatic therapy is quite appropriate.

Newly diagnosed NS is a much more alarming condition.
If LN is excluded, which is extremely difficult to diagnose without a biopsy, this syndrome can hide all the named forms of GN, including RPGN.
Tactics - active short-term pathogenetic therapy, supported by symptomatic.

Rapidly progressive nephritic syndrome.
The criterion of severity - a decrease in kidney function - is recorded no earlier than after a few weeks.
It is tactically correct, without wasting time to establish an accurate diagnosis, to start pulse therapy (see above).

Recurrent nephritic and nephrotic syndromes are most likely to be caused by any form of CGN.
It must be remembered that nephritic is more characteristic of MzPGN, and both of these syndromes are more characteristic of MN and MzKGN.
If there is no rapid decline in kidney function, then it is not necessary to start active treatment already in the emergency room. You can observe the patient, find out his "past", conduct the maximum possible examination. So that the patient does not feel "disadvantaged", symptomatic therapy should be prescribed.

The situations described are quite real, and a doctor (not a nephrologist) may encounter them. We have given recommendations, but only for the first steps.

We take nephrological disease too seriously to justify such a simplistic approach.
The patient must be referred to a specialized nephrology department (or an outpatient nephrology center).
Moreover, time does not endure with reduced kidney function.

A few specific recommendations.
First. If there is no 100% certainty in the presence of GN, then the treatment with corticosteroids and cytostatics should be postponed.
In the presence of NS, it is best to carry out a full-fledged anticoagulant therapy with a clear control of blood clotting. Scheme - 20,000 IU of heparin per day in two injections.
At the end of the course of heparin therapy (usually it lasts no more than 5 weeks), switch to long-term use of antiplatelet agents (chimes). If edema does not decrease within 5-6 days after the start of the course, then diuretics should be added - in the absence of a sufficient effect, plasmapheresis can be resorted to.
AH requires adequate antihypertensive therapy, taking into account already prescribed diuretics.

Second. The condition is the same, but kidney function is reduced.
If there is a terminal PN - see the subsection on the treatment of uremia.
At the initial stages of decompensation, the effect of improving kidney function is possible with the appointment of ACE inhibitors at a dose of 0.005 g 2 times a day per os. It is possible to achieve an improvement in the excretory function of the kidneys, an increase in plasma flow, vasodilation, normalization of the IOC, and potassium metabolism.

Third. With confidence in the diagnosis of GN, the presence of NS is a sufficient reason for prescribing GCS therapy, preferably with a “pulse”.
If kidney function is reduced, then the presence of nephrosclerosis is likely.
In such cases, it is more reliable to use cytostatics, also with a “pulse”.
The severity of hypertension is a reason to think about the mechanism of the latter.
Depending on the predominance of renin or sodium pressor influence, therapy with either ACE inhibitors or natriuretics is chosen. Under all circumstances, statin therapy is indicated for courses of up to 3-6 months. (10 mg/24 h).
This treatment significantly restores endothelial dysfunction and also prevents the formation of glomerulosclerosis.
With poor urinary syndrome and hypertension, the already mentioned ACE inhibitors, antiplatelet agents are justified.

Fourth. If the previous examination of the patient gave an established diagnosis of IgA nephropathy with detected AT against viral antigens, then you can try to conduct a short course of treatment with rheoferon.

Fifth. It seems promising to use drugs from the PG group for any form of GN. As mentioned above, it is advisable to use a three-week infusion of PGE1 (aprostadil).

Sixth. If after the appointment of different drugs there is no obvious effect, then the patient can be released for 2-3 weeks.
In a third of patients, the symptoms of the disease will gradually fade away, since in some part of the patients remission occurs spontaneously, despite treatment or its absence.

Seventh. When prescribing corticosteroids and cytostatics, preference should be given to the method of pulse therapy and, if possible, long-term multi-month therapy with these drugs should be avoided.

The applied prolonged regimens of traditional pathogenetic therapy do not affect the duration of survival of patients with glomerulonephritis, only a certain improvement in the quality of life is possible.

Glomerulonephritis - acquiredkidney disease among women , men and children, proceeding in a peculiar way, depending on the causes, methods of treatment.

More often, pathology is detected in the glomeruli of the kidneys (glomeruli), but it can also capture the renal tubules and tissues. According to statistics, the disease is often detected in children under 12 years of age, but it also happensglomerulonephritis in adults.

Medical encyclopedias provide detailed information aboutwhat is glomerulonephritis, which clinical formsdiagnosed in what cause illness. If the terminology makes it difficult to understand, what's happened glomerulonephritis, may be considered picture with the anatomical structure of the kidney, in order to understand which parts are affected and why it is dangerous kidney disease.

Classification of glomerulonephritiscomplicated by a number of significant factors. According to the course of the disease, suchforms of glomerulonephritis:

• acute. Occurs suddenly, proceeds rapidly, usually this type in cure t forever a, but occasionally a transition to a chronic form is possible;
• chronic. This is the state when acuteprimary glomerulonephritispassed into the chronic stage, periodically suchinternal illnesses give relapses;
• subacute - dangerous for life a pathology that is rapidly progressing and characterized by a malignant character. Serious complications andconsequences of the diseasein 80% of cases lead to a fatal outcome.

Classification of glomerulonephritisBy symptoms, the following types can be distinguished:

• nephrotic. Characterized by the presence puffiness at normal pressure;
• hematuric. In laboratory tests of urine, protein and blood are detected, edema no, BP is normal;
• hypertensive. Urination is unchanged, there is no blood and protein in the analysis of urine. Mainsigns of glomerulonephritisassociated with increased pressure, which is steadfastly held;
• mixed. All the symptoms that provoke the above are manifestedtypes of glomerulonephritis;
• latent. Edema with glomerulonephritisof this form are insignificant, the pressure is slightly elevated. Considering how secretiveglomerulonephritis definitionThe diagnosis is based on the results of a urinalysis (blood and protein will be detected).

According to the mechanism of development, which exhibits a specificglomerulonephritis classificationidentifies the following types:

• primary - an independent disease;
• secondary glomerulonephritis- pathology occurs against the background of systemic pathologies (lupus erythematosus, arthritis, etc.).

Separately, it is necessary to highlight post-streptococcal glomerulonephritis in an acute form, which begins after a streptococcal infection. This is a serious pathology that gives life-threatening complications.

At diagnosis glomerulonephritis typesthe pathologies listed above are provoked by autoimmune and inflammatory causes. Autoimmune risk factors occur when the patient's immunity after past illnesses does not work adequately, perceiving kidney cells as foreign. Causeglomerulonephritis causesof the following type: hypothermia, chronic infection in the body, heredity, vitamin deficiency, carriage of streptococci.

Causes of glomerulonephritisinflammatory nature - these are past diseases: tonsillitis, typhoid fever, tuberculosis, rubella, herpes, chicken pox and influenza.

Symptoms of glomerulonephritis

At the appointment with the nephrologist, the patient should describe all his complaints in detail, and the doctor will listensymptoms of glomerulonephritisand draw conclusions about the need for additional diagnostics, further treatment strategies. Must be said treating doctor about such ailments:

• headache;
• severe fever;
• nausea, occasionally - vomiting;
• weakness and drowsiness.

Listed clinical manifestationsare considered common, but there are also specific signs of acute glomerulonephritis:

• swelling of tissues, including internal edema;
• increase in pressure. Such a picturerenal glomerulonephritisprovokes even those who have never complained of pressure;
• urine becomes cloudy, acquires a pinkish tint due to blood particles, the amount of urine excreted decreases.

When diagnosed with chronicglomerulonephritis symptoms and treatmentare somewhat different. The pathology itself proceeds with restraint, the patient's health during the period of remission does not suffer. When an exacerbation occurs, all the signs of the acute form listed above are present.

How is glomerulonephritis diagnosed?

If you suspectglomerulonephritis formsdiseases are determined after the diagnosis is accurately established. Despite the brightness of the clinical picture, similar symptoms can be detected in other diseases. That's whydiagnosis of glomerulonephritisshould be complex. The range of activities includes the following:

• survey (if we are talking about a child, then the doctor receives the necessary information from the parents). Important information - this is the first time such aformulation of the diagnosisor kidney disease has occurred in the past. Next, the doctor finds out if relatives have a similar disease, whether the patient had infectious diseases in the recent past, all this is necessary to suggest the cause that caused the pathology;
• a medical history is made. The doctor finds out when the symptoms appeared, how severe they are, whether the patient was taking symptomatic medications and how they helped;
• inspection. The doctor assesses the presence of puffiness, measures the patient's pressure, can visually assess the changed color of urine;
• analyses. If you suspectglomerulonephritis diagnosisincludes a urine test for protein and blood, a blood test for leukocytes and ESR, blood biochemistry for protein and cholesterol, as well as an immune analysis if an autoimmune cause of the disease is suspected;
• hardware diagnostics. An ultrasound is performed, which reveals an increase in the size of the kidneys and other characteristics of the organ.

Before, how to treat glomerulonephritis, the doctor may refer the patient to a rheumatologist, cardiologist, ophthalmologist, infectious disease specialist, and other specialists as needed.

Treatment of glomerulonephritis

Acute glomerulonephritis being treated in about 4 weeks. If we consider the mainprinciples of treatment of glomerulonephritis, the first step is to focus on bed rest. This disease requires maximum adherence to bed rest, as far as possible. For those who want cure pathology forever, such a requirement will not seem excessive.

Definitely will be appointed antibiotics from the group of penicillins and macrolides - only such therapy will be effective. Since often the clinical picture includes swelling, it is logical to imagine thatdiuretics, the doctor will select the most effective and safe diureticdrugs for glomerulonephritis.

After the acute phase is stopped,glomerulonephritis treatmentcontinue taking antihistamines, the doctor adds anticoagulants to them to improve blood circulation. If the patient's condition is serious, they will be prescribed cytostatics and hormonal agents.

Complicated at diagnosisglomerulonephritis treatmentcan be prescribed in the form of hemodialysis - such a procedure for cleaning the blood of toxins is indicated if the patient's condition is life-threatening. At diagnosisglomerulonephritis symptoms treatment- the prerogative of the doctor, self-medication is unacceptable!

Dietary nutrition for kidney disease

An important part of therapy is medical diet. Without dietary correction, treatment with any means will be ineffective and time consuming. Treatment andprevention of glomerulonephritisnecessarily begin with a diet that unloads the kidneys. The following foods are prohibited:

• sweet apples and apricots;
• potatoes and white cabbage in any form;
• fresh grapes and raisins;
• dairy products, including cottage cheese.

In addition to the listed products, with a diagnosisglomerulonephritis preventionincludes the rejection of fried foods, pickled, salted and smoked foods. During the period of exacerbation of chronic pathology and the treatment of acute glomerulonephritis, it is advisable to eat steamed dishes.

It is better to refuse coffee and strong tea, instead, include rosehip broth and pumpkin juice in the diet. The first will remove puffiness, remove excess fluid from the body, and the second will cleanse the blood of toxic substances and increase the body's defenses.

Traditional medicine recipes

It is forbidden to independently make a decision on treatment with certain herbs - the pathology can be serious, pose a threat to life. Only a doctor can give recommendations on connecting traditional medicine recipes to the basic treatment, since plants affect the kidneys in different ways, and some can cause an exacerbation of the disease. Herbal decoctions and tinctures can only be taken as an additional therapy, without violating the schedule for taking the main medications prescribed by the doctor. The advantages of plants are that they can be taken longer, used not only for treatment, but also for the prevention of disease. Below are proven recipes that you can discuss with your doctor:

• elderberry infusion. It will take 1 tbsp. dried elderberry flowers, the raw material is placed in a thermos, poured with a glass of boiling water and left overnight. The next morning, the remedy is filtered and taken in 3 divided doses during the day. The infusion is drunk before meals for half an hour. The course lasts about a month, by which time the disease should recede;
• infusion of corn stigmas and cherries. It will take 1 tsp. corn stigmas and a similar amount of cherry tails. The raw material is placed in a thermos, 0.5 liters of boiling water is poured and the night is infused. Ready infusion take a quarter cup before each meal. The course lasts until the symptoms of glomerulonephritis disappear;
• infusion of flax seeds and other herbs. In a thermos you need to fill up 4 tbsp. flax seeds, 3 tbsp. dried birch leaves and 3 tbsp. crushed root of the field harrow. Herbs pour 0.5 liters of boiling water and leave for 2 hours. Ready infusion is taken in a third of a glass 3 times a day. The course is a week.

To boost the body's immune system and live a long and happy life without glomerulonephritis, you can take 1 tsp daily. medicinal drug. It is prepared like this: a glass of honey is mixed with 1 tbsp. ground walnuts, 1 tbsp. ground hazelnuts and chopped zest of one lemon. All components are mixed, the mixture is stored in a glass container with a lid in the refrigerator.

You should always remember that in the early stages of glomerulonephritis completely curable so every effort must be made to heal this and other diseases.

Complications of glomerulonephritis

Doctors immediately warn people treated from glomerulonephritis, that neglect of one's health can provoke a relapse or the onset of other diseases.

For example, if a woman is lived without caring about your healthcomplications of glomerulonephritisin which case they will be serious.

The healthier the body, the less pronounced will be the consequences of kidney pathologies.

Among the main complications are the following:

• pulmonary edema. The manifestation of suchcomplications of acute glomerulonephritishappens in patients with hypertension, heart disease;
• acute renal failure. The kidneys stop working against the background of poststreptococcal glomerulonephritis;
• eclampsia. A person's blood pressure rises sharply, seizures of epilepsy and convulsions, a hypertensive crisis are possible;
• uremia. In this caseacute glomerulonephritis complicationsgives out in the form of serious intoxication of the whole organism;
• the transition of the disease to a chronic form.

Usually diagnosed with acuteglomerulonephritis prognosisfavorable, and a reason for panic and a question to the doctor - how many live with glomerulonephritis– simply not. A timely diagnosis and competent medical care will quickly raise the patient to his feet.

Reversal of renal damage can be achieved primarily through an etiological approach to treatment, however, such treatment of glomerulonephritis is possible only in a few patients. Etiological treatment is the use of antibiotics for poststreptococcal nephritis and nephritis associated with subacute infective endocarditis; antiviral drugs for virus-associated glomerulonephritis; specific treatment of syphilitic and malarial, paratuberculous nephritis with release from immune complexes and complete cure; tumor removal in paraneoplastic nephrotic syndrome; discontinuation of the corresponding drug that caused drug nephritis; persistent abstinence in alcoholic nephritis, exclusion of allergenic factors in atopic nephritis.

The possibility of reverse development with the timely elimination of the etiological factor is quite real, as evidenced by our observations of patients with nephritis caused by subacute infective endocarditis, paraneoplastic nephritis, paratuberculous IgA nephritis, etc.

Pathogenetic treatment of glomerulonephritis

To lead to the reverse development of glomerulonephritis, to stop or slow down its progression can be pathogenetic treatment of glomerulonephritis, aimed at certain links of pathogenesis: immune processes, inflammation, intravascular coagulation. To a certain extent, antihypertensive therapy, and in some cases, diuretic therapy, also belongs to the pathogenetic one.

Most of the pathogenetic therapy of nephritis (glucocorticoids, cytostatics, including selective, heparin, plasmapheresis) has a wide range of action, interferes with homeostatic processes, often causes severe complications, which allows us to call them methods of "active" or "aggressive" therapy of nephritis. The appointment of active therapy is indicated at those stages of nephritis, when the role of immunoinflammatory processes or intravascular coagulation processes in the progression of the disease is obvious.

A comprehensive assessment of the clinical manifestations and morphological picture of the disease is the best approach to determining the degree of activity of the process and the severity of nephrosclerosis.

Treatment for glomerulonephritis is as follows:

• with high activity of glomerulonephritis, especially glomerulonephritis with nephrotic syndrome, immunosuppressive therapy is necessary. Only in the presence of contraindications to active therapy or the impossibility of its implementation for any reason, they are limited to symptomatic treatment, as well as the appointment of ACE inhibitors and statins;
• at the first appeared nephrotic syndrome, especially without hematuria and hypertension, treatment of glomerulonephritis with glucocorticoids is indicated. With subsequent relapses, treatment is started with glucocorticoids (if the first episode of glucocorticoid treatment was effective), then cytostatics or cyclosporine are prescribed;
• with progressive forms of nephritis (with a rapid increase in creatinine levels), large doses of glucocorticoids and cytostatics are prescribed orally and / or in the form of pulses;
• in latent nephritis with proteinuria > 1 g/day, ACE inhibitors are indicated;
• there is no single tactic for hematuric forms (see "Treatment of IgA Nephropathy").

Currently, the following groups of drugs are used to treat nephritis: glucocorticoids, cytostatics, ACE inhibitors, anticoagulants, antiplatelet agents, lipid-lowering drugs; in some situations, the method of "mechanical" immunosuppression - plasmapheresis - is of great importance.

Glucocorticoids and the treatment of glomerulonephritis

Glucocorticoids have been one of the main means of pathogenetic therapy of nephritis for several decades.

Mechanisms of action

Glucocorticoids have both anti-inflammatory and immunosuppressive effects, interfering, on the one hand, with the function of all inflammatory cells and the formation of humoral inflammatory factors, and, on the other hand, with the immune response, and more in the cellular than in the humoral.

The main mechanisms of action of glucocorticoids, leading to the suppression of the inflammatory response and the immune response, are:

• redistribution of inflammatory cells and the immune system from the bloodstream to other organs of the immune system, which reduces their entry into the focus of inflammation and thereby inhibits the development of the inflammatory response;
• suppression of the production of many mediators involved in the implementation and persistence of the immune response and inflammation (cytokines, arachidonic acid metabolites, active oxygen radicals, proteolytic enzymes, etc.), as well as a decrease in the sensitivity of inflammatory and immune cells to these mediators (suppression of the synthesis of membrane receptors for cytokines, increased production of receptor antagonists, etc.).

Influence on the inflammatory response

Glucocorticoids interfere with all stages of the inflammatory response. The degree of anti-inflammatory activity of glucocorticoids is associated with their concentration at the site of inflammation, and therefore depends on the dose and route of administration.

Glucocorticoids disrupt the adhesion of neutrophils to the capillary endothelium, inhibit the influx of macrophages, affect their function, block the release of cytokines (IL-1, IL-6, TNF-a, etc.), and also suppress the production of certain proteolytic enzymes by macrophages (collagenase, elastase, plasminogen activator); at the same time, glucocorticoids inhibit the antitumor and antimicrobial activity of macrophages.

In addition, when administered intravenously at high doses, glucocorticoids alter the chemical structure of the glomerular basement membrane, with a consequent decrease in proteinuria.

Impact on the immune response

In humans, glucocorticoids cause transient lymphopenia, inhibit the presentation of antigen to T cells by macrophages, and the activation of T-lymphocytes (due to a decrease in the production of IL-2) - helper, suppressor and cytotoxic subpopulations.

Unlike T cells, B cells are less sensitive to glucocorticoids. The effect of glucocorticoids on the production of antibodies depends on the dose: low ones do not affect it, while high ones can reduce the level of immunoglobulins (due to suppression of the activity of T-helpers).

When administered intravenously in high doses, glucocorticoids have a more pronounced effect on T cells: suppression of the production of a number of cytokines that increase the permeability of the glomerular basement membrane; decreased vascular permeability caused by immune complexes.

From a clinical standpoint, it is important to remember that lower doses of glucocorticoids are required to suppress the migration of leukocytes to sites of inflammation and cellular immune response, and higher doses of glucocorticoids are required to suppress the functional activity of leukocytes and humoral immunity.

Indications for the appointment of glucocorticoids in nephritis

General indications for the appointment of glucocorticoids in nephritis are:

• pronounced activity of the renal process;
• the presence of nephrotic syndrome without severe hypertension and hematuria (morphologically - minimal changes in the glomeruli, mesangioproliferative and membranous nephritis).

Treatment is less promising for focal segmental glomerulosclerosis, mesangiocapillary glomerulonephritis and diffuse glomerulosclerosis in the outcome of any variant of glomerulonephritis.

Particular indications for individual clinical and morphological variants of glomerulonephritis will be discussed below.

Methods (schemes) of glucocorticoid therapy for nephritis

There are various ways (modes) of the use of glucocorticoids in glomerulonephritis. To achieve effective concentrations of glucocorticoids in areas of immune inflammation and edema in the renal tissue, where blood flow is significantly reduced, 2 methods of administering glucocorticoids are effective - long-term daily administration of high and moderately high doses of glucocorticoids (prednisolone) orally and intravenous administration of ultra-high doses (so-called pulses) of glucocorticoids (methylprednisolone or prednisolone).

Daily high-dose oral prednisone

Depending on the severity of glomerulonephritis, prednisolone in high doses can be given orally in 2-3 doses (the main part in the morning) or once in the morning. In the first case, with a fractional intake of prednisolone, better control of renal inflammation is achieved, but the immediate side effects develop more often and are more pronounced. Therefore, some authors recommend at the first opportunity (clinical signs of improvement) to transfer the patient from a fractional to a single dose. Then, when a positive effect is achieved, the daily dose is slowly reduced to the lowest possible maintenance dose.

Taking high doses of prednisolone every other day

When taking glucocorticoids every other day, significantly less than with daily intake, the function of the hypothalamic-pituitary-adrenal system is suppressed. In this case, the dose of prednisolone, which the patient takes every other day once in the morning, is equivalent to a double daily dose of daily intake. This method is used most often in pediatric practice, less often in adults. Efficiency is close to the generally accepted scheme, but side effects are less common, children do not have growth retardation. This alternating regimen is especially indicated for maintenance therapy.

Pulse therapy with methylprednisolone

For rapid achievement Very high concentrations plasma glucocorticoids intravenous pulses of methylprednisolone have been used for many years to treat renal allograft rejection crises. The number of complications, as a rule, was small. A similar approach is used to treat rapidly progressive crescentic glomerulonephritis and other severe forms of glomerulonephritis that occur without crescent formation (eg, diffuse proliferative glomerulonephritis in patients with systemic lupus erythematosus). The procedure consists in intravenous drip administration over 20-40 minutes of 0.5-1.5 g of methylprednisolone (or prednisolone, somewhat less effective in this situation), which is repeated 2 more times in subsequent days to reach a total dose of 3-4 g of the drug . With almost 30 years of experience with this method of administering glucocorticoids (since 1977), we consider it relatively in a safe way for rapid control of severe glomerular inflammation. The method is contraindicated in patients with severe hypertension, as well as with myocarditis or severe cardiomyopathy.

Supportive care

After a course of treatment with high doses (most often within 2 months), the dose is reduced (usually within the same period, and more slowly in systemic diseases) to maintenance (10-20 mg / day). The timing of maintenance therapy is determined empirically, usually 2 months, sometimes (especially with glomerulonephritis associated with systemic diseases) longer maintenance therapy is required, even for several years, while taking the drug every other day causes fewer side effects than daily glucocorticoid therapy, in including when the dose of glucocorticoids for alternating therapy is 2-3 times higher than with daily intake. In this regard, the best tactic for maintenance therapy with glucocorticoids is considered to be a decrease in the daily dose to the lowest possible level, and then switching to an alternating regimen using a 2-fold dose of daily intake.

If unacceptably high doses of glucocorticoids are required to suppress the activity of glomerulonephritis or maintain normal kidney function, if side effects of glucocorticoid therapy appear quickly, then it is advisable to prescribe cytostatic drugs. This allows the use of lower doses of glucocorticoids and thus reduces the risk of side effects.

Side effects of glucocorticoids

Undesirable effects of glucocorticoids can occur quickly (euphoria, depression, insomnia, increased appetite, corticosteroid psychosis, fluid retention, reduced glucose tolerance) and some time after the start of treatment (obesity, myopathy, striae, skin atrophy, hirsutism, cataracts, growth retardation , steroid diabetes, osteoporosis, aseptic necrosis and bone fractures, acne and opportunistic infections). The former disappear after the abolition of glucocorticoid therapy, the latter may persist for a long time.

Abrupt withdrawal of glucocorticoids after their long-term use leads to a life-threatening adrenal crisis. Signs of an upcoming adrenal crisis are malaise, fever, muscle and headache, sweating, and hypotension with warm extremities due to dilatation of the peripheral vessels.

Cytostatic (cytotoxic) drugs and treatment of glomerulonephritis

Alkylating agents (cyclophosphamide and chlorbutine)

Cyclophosphamide (CFA) and chlorbutine are alkylating compounds that, when taken orally, are absorbed in the intestine and then converted to active metabolites in the liver. The main mechanism of action of these metabolites is the cross-linking of nucleic acids, which disrupts the process of transcription of information necessary for protein synthesis and, accordingly, cell division.

Cyclophosphamide

The half-life of cyclophosphamide is 6 hours, and it is lengthened with the simultaneous administration of allopurinol. In very high doses, cyclophosphamide inhibits the division of all cells in the body, with the clinically most important consequences of bone marrow suppression. When taken orally at doses that reduce the level of leukocytes in the blood to 3000 cells / μl (the number of neutrophils is 1500 cells / μl), the immune response to new antigens (mediated by both T- and B-cells) is suppressed. At these doses, cyclophosphamide has less effect on inflammation, can suppress fibroblast proliferation and thus the development of fibrosis, but its main effect is suppression of the immune system.

Taking cyclophosphamide by mouth

Cyclophosphamide is usually taken orally at a dose of 2-2.5 mg / day. In case of severe kidney damage (by the type of rapidly progressive glomerulonephritis) with systemic vasculitis, you can start with a dose of 3.5-4 mg / day). It is assumed that the number of leukocytes in the peripheral blood will decrease to approximately 3500 cells / μl (but not lower than 3000 cells / μl), while the content of neutrophils should be 1000-1500 cells / μl. The number of leukocytes decreases within a few days or weeks. During this period of induction of immunosuppression, it is very important to check the number of leukocytes in the peripheral blood at least every other day, so that if the number of leukocytes falls below an acceptable level, the dose of the drug can be reduced or canceled.

Since the level of leukocytes has stabilized, their content should be monitored at least once every 2 weeks. Over time, the dose of cyclophosphamide necessary to maintain white blood cells at the proper level has to be reduced. If prednisolone (which protects the bone marrow from suppression) is prescribed simultaneously with cyclophosphamide, then when the dose of prednisolone is reduced, the dose of cyclophosphamide should also be reduced.

Side effects of cyclophosphamide treatment

Side effects during treatment with cyclophosphamide can be short-term, disappearing after stopping treatment (nausea, vomiting, diarrhea, alopecia and infections that develop during leukopenia), and long-term (gonadal insufficiency with the likelihood of subsequent infertility, which patients should be warned about; hemorrhagic cystitis, teratogenic effect, tumors and chronic infections). At a cumulative dose up to 200 mg/kg, the likelihood of severe side effects is small, but it increases significantly at a cumulative dose above 700 mg/kg. In this regard, when deciding on long-term treatment with cyclophosphamide, patients (especially young men) should be informed about possible complications. At very high doses, a syndrome of inappropriate ADH secretion may develop.

Intravenous cyclophosphamide pulse therapy

A group of nephrologists led by J. Balow and A. Steinberg ( national institutions health, USA), in the early 1980s, proposed for the treatment of patients with lupus glomerulonephritis "pulse therapy" of cyclophosphamide, which is currently considered to be highly effective and at the same time has fewer side effects than conventional oral cyclophosphamide. Doses of 0.5-2.0 g/m 2 body surface were used, causing a drop in the level of leukocytes to a maximum of 2000-3000 cells/µl, which occurs between the 8th-12th day, then the leukocytes return to normal approximately on the 3rd week. Pulses were used every 3 months, the duration of treatment was 2 years or more. It has been established that the frequency of complications from the bladder with this regimen (1 pulse per 3 months) is significantly reduced. This is probably due to the fact that the duration of contact of toxic metabolites of cyclophosphamide with the bladder wall is reduced to approximately 36 hours every 3 months and the total dose of the drug over these 3 months is also reduced. Infections, both severe and less severe (for example, herpes zoster), continued to be observed, especially during the period of maximum fall in the number of leukocytes. Amenorrhea remained a serious problem, although its incidence decreased slightly (45% instead of 71%, which is observed with long-term oral therapy).

In subsequent years, in our and several other centers, new regimens for the use of cyclophosphamide were proposed, in particular, an increase in the pulse rate up to 1 time per month in the initial phase of therapy in the treatment of lupus, as well as chronic idiopathic glomerulonephritis. The effectiveness of treatment can be judged not earlier than after 6 months. If there are signs of improvement - continue treatment of glomerulonephritis for another 3 months; in the future - if it is necessary to continue treatment, the intervals between pulses should be increased to 2-3 months. The risk of side effects depends on the total dose of the drug.

When conducting pulse therapy with cyclophosphamide, the following conditions must be met:

• to prevent severe bone marrow suppression, the dose of the drug should correspond to the level of GFR, since the metabolites of cyclophosphamide are excreted by the kidneys (the drug is administered intravenously in 150-200 ml of isotonic sodium chloride solution for 30-60 minutes):
  • with normal CF - 15 mg / kg of the patient's body weight (or approximately 0.6-0.75 g / m 2 of the body surface);
  • with CF less than 30 ml / min - 10 mg / kg (or about 0.5 g / m 2).
• strict control of the level of leukocytes is necessary on the 10th and 14th day after pulse therapy: if the level of leukocytes drops to 4000 cells / μl - increase the next dose of cyclophosphamide by 25% (up to 1 g / m 2);
• to prevent nausea and vomiting, serotonin receptor antagonists are recommended: cerucal 10 mg 3 times a day, ondansetron 4-8 mg orally 3-4 times every 4 hours (as an alternative, navoban or latran); can be combined with a single dose of dexamethasone 10 mg orally;
• to prevent the toxic effect of cyclophosphamide metabolites on the bladder mucosa: stimulation of frequent urination (increased oral fluid intake) and taking mesna, which binds toxic metabolites in the bladder (4 times every 3 hours, the total dose corresponds to 80% of the dose of cyclophosphamide).

With the help of mathematical modeling methods, prognostic signs were revealed that allow us to presume the patient's sensitivity to therapy with ultra-high doses of cyclophosphamide, thereby avoiding the unreasonable prescription of immunosuppressants. The results of the analysis carried out in 44 patients with glomerulonephritis indicate that:

• treatment of glomerulonephritis with ultra-high doses of cyclophosphamide is satisfactorily tolerated by the majority (89%) of patients with chronic glomerulonephritis;
• by the end of treatment, a positive effect was recorded in almost 50% of patients previously resistant to oral methods of immunosuppressive therapy;
• a good long-term result can be expected in patients with a normal creatinine level and a disease duration of not more than 2 years. The accuracy of the prognosis (especially with elevated creatinine levels and disease duration of more than 2 years) increases with a kidney biopsy: higher efficiency can be assumed with MR, MPGN and MCGN, lower - with focal segmental glomerulosclerosis and sclerosing variant of glomerulonephritis. However, the degree of activity of the immunoinflammatory process is of decisive importance: for all morphological variants, survival is higher with a high morphological activity index;
• to achieve the effect (in patients potentially sensitive to cyclophosphamide), long-term treatment of glomerulonephritis (at least 6.0 g of cyclophosphamide for 6 months or more) is necessary. Undertreatment dramatically worsens the prognosis, especially with elevated creatinine levels;
• a positive response of the patient by the end of the course of treatment (complete or partial remission) is an indicator of a good long-term prognosis;
• the lack of an immediate response makes a good prognosis unlikely.

Chlorbutin

Assign at a dose of 0.1-0.2 mg / kghsut). The half-life is 1 hour; it is completely metabolized. Chlorbutine acts more slowly than cyclophosphamide, and the associated bone marrow suppression develops less rapidly and is often reversible. Side effects include gastrointestinal disturbances and gonadal failure. More rare side effects are pulmonary fibrosis, seizures, dermatitis, and toxic liver damage. Tumors develop less frequently than with cyclophosphamide treatment.

In young men, cyclophosphamide (less gonadotoxic than chlorbutin) is preferred at a dose of

Antimetabolites and treatment of glomerulonephritis

Azathioprine

Azathioprine, an analog of the purine base hypoxanthine, is a derivative of 6-mercaptopurine. Azathioprine metabolites inhibit the enzymes required for DNA synthesis, therefore suppressing any immune response that requires cell division. Azathioprine is taken at a dose of 1-3 mg / mg / kghsut), and the dose is selected in such a way as to maintain the number of leukocytes in the blood at least 5000 cells / μl. The main side effect is bone marrow suppression, especially neugropenia with the development of infections. Other complications include anemia, thrombocytopenia, hepatitis, dermatitis, stomatitis, alopecia, gastrointestinal disturbances, and an increased risk of tumors, especially skin cancer and lymphomas.

In general, compared with cyclophosphamide, azathioprine acts less actively on renal inflammation, but causes less severe complications. In patients with signs of renal insufficiency, azathioprine is not recommended to be administered together with allopurinol, which blocks its inactivation.

Selective immunosuppressants and treatment of glomerulonephritis

Cyclosporin A

Cyclosporine A, a cyclic polypeptide of fungal origin, was synthesized in 1980. It is eliminated from the body by the liver through the biliary tract. The effect of cyclosporin A on the immune response is due to the suppression of not only the activity of T-helpers at the time of antigen presentation, but also the production of interleukin-2, the proliferation of cytotoxic T-cells, and indirectly (through the suppression of T-cells) activation of B-cells. Cyclosporine A has no effect on an already developed antibody response.

Greatest experience use of cyclosporine A accumulated during renal transplantation. IN last years it is used to treat steroid-resistant nephrotic syndrome, with doses lower than for renal transplantation to prevent nephrotoxicity. According to some data, unlike patients with a transplanted kidney, the effectiveness of cyclosporine A in patients with glomerulonephritis is not so clearly related to the concentration of the drug in the blood plasma.

Cyclosporine A may be an alternative treatment for patients with glomerulonephritis with steroid-resistant or steroid-dependent nephrotic syndrome. These are mainly patients with minimal changes (lipoid nephrosis) and focal segmental glomerulosclerosis, in the pathogenesis of which hyperproduction of lymphokines, suppressed by cyclosporine A, plays a role.

The frequency of positive results of treatment is about 80% with minimal changes, and 50% with FSGS. In our observations, the treatment of glomerulonephritis with cyclosporine A was accompanied by remission in 20 out of 25 patients with steroid-dependent and steroid-resistant nephrotic syndrome.

Before treatment, a kidney biopsy is mandatory: interstitium sclerosis, tubular atrophy, or vascular damage prevent the appointment of cyclosporine A. In patients older than 60 years, the drug increases the risk of developing tumors.

The initial dose of cyclosporine A per day for adults is 2.5-5 mg/kg, for children - 6 mg/kg. Depending on the morphology of glomerulonephritis, a decrease in proteinuria is usually observed within 1-3 months. The level of cyclosporine A in the blood does not always correlate with the effectiveness of treatment, but is useful for monitoring the accuracy of taking the drug by patients and detecting possible interactions of cyclosporine A with other drugs. Mandatory monitoring of kidney function: an increase in creatinine by 30% relative to the original requires a dose reduction of cyclosporine A by 30-50%.

The most serious side effects are nephrotoxicity, which is dose-dependent and usually reversible, and the development of arterial hypertension, which is associated with spasm of the afferent glomerular arteriole.

Other side effects are hypertrichosis, gingival hypertrophy (with the latter, azithromycin helps; possibly metronidazole).

Long-term ciclosporin nephrotoxicity is often difficult to assess clinically. Continuous use of cyclosporine for 12-38 months is accompanied by a significant increase in tubulo-interstitial fibrosis, and its severity in repeated biopsies correlates with the number of glomeruli with segmental sclerosis in the first biopsy, the level of creatinine at the time of the first biopsy, and also with a dose of cyclosporine exceeding 5 .5 mg/kg per day. The development of nephrotoxicity may not be clinically noticeable, since there is no direct correlation between the severity of structural damage and the state of renal function. To prevent nephrotoxicity, adequate fluid intake and the exclusion, as far as possible, of other nephrotoxic drugs, especially NSAIDs, are necessary, since in patients with hypovolemia, blockade of prostaglandin production can dramatically impair renal blood flow.

After discontinuation of cyclosporine A, a relapse of nephrotic syndrome is possible and steroid-dependent nerotic syndrome may become cyclosporine A-dependent. However, patients with complications of steroid therapy tolerate cyclosporine A fairly well.

Tacrolimus (FK-506) and mycophenolate mofetil

Currently, attempts are being made to use new immunosuppressants in nephrology - tacrolimus and mycophenolate mofetil.

Tacrolimus (FK-506), a calcineurin inhibitor, is similar in mechanism of action to cyclosporine A, relatively selectively suppresses CD4 T-helpers; perhaps slightly more suppresses the release of cytokines; an inhibitory effect on the production of vascular permeability factor is not excluded. In the experiment, the introduction of FK-506 prevented the development of autoimmune nephritis in rats.

Tacrolimus has the same spectrum of numerous side effects as cyclosporine A: acute and chronic nephrotoxicity, neurotoxicity, hypertension, hyperlipidemia, increased potassium and uric acid levels.

Mycophenolate mofetil, a derivative of mycophenolic acid, is an inhibitor of inosine monophosphate dehydrogenase, which depletes guanidine nucleotides in cells, selectively inhibits the proliferation of T- and B-lymphocytes, the production of antibodies and the formation of cytotoxic T-lymphocytes. In addition, it inhibits glycosylation of adhesive molecules, which may affect the influx of lymphocytes into inflammatory foci in rejected transplants. Used primarily in transplantology. Suppresses the proliferation of rat and human mesangial cells in tissue culture without the development of cell necrosis or apoptosis.

Mycophenolate mofetil causes a number of serious side effects from the gastrointestinal tract: nausea, vomiting, diarrhea, due to which it is necessary to reduce the dose of the drug or even cancel the treatment of glomerulonephritis. Leukopenia develops with the same frequency as with the appointment of azathioprine. The risk of developing opportunistic infections increases.

A new form of the drug (myfortic), soluble only in the intestine, causes fewer side effects from the gastrointestinal tract and opens the way to more widespread use this drug.

Clinical observations with glomerulonephritis are still few. So, F. Schweda et al. (1997) achieved remission in the treatment of tacrolimus in a young woman with minimal changes in the glomeruli and NS resistant to glucocorticoids and cyclosporine A for 20 months without visible side effects. M. Choi et al. (1997) used mycophenolate mofetil to treat 8 patients with steroid- or cyclosporine A-dependent nephrotic syndrome (with a different morphological basis) - the condition improved in 6 patients. The greatest experience was gained in controlled trials in patients with diffuse proliferative lupus nephritis, where mofetylamicophenolate was used as suppressive or maintenance therapy. The main conclusion of these studies is that mycophenolate mofetil is as effective as cyclophosphamide in inducing remission of nephritis, but increases the survival rate of patients due to fewer septic complications.

Combined regimens for the treatment of glomerulonephritis

Among the combined treatment regimens, the most common treatment regimens are glucocorticoids with cytostatics and the so-called 4-component regimen.

Glucocorticoids in combination with various cytostatics can be administered orally, as well as parenterally. So, for example, pulse therapy with methylprednisolone is carried out, followed by oral administration of prednisolone and cytostatics, pulse therapy with cyclophosphamide and methylprednisolone. The following combined pulse therapy regimens are used: on the 1st day, 800-1200 mg of cyclophosphamide and 1000 mg of methylprednisolone or prednisolone are administered intravenously, on the next two days - only methylprednisolone or prednisolone.

A peculiar regimen with alternating glucocorticoids and cytostatics was proposed by S. Ponticelli et al. (1984). During the first 3 days of the 1st month of treatment, methylprednisolone is administered intravenously (1000 mg each), for the next 27 days, methylprednisolone is administered orally daily at a dose of 0.4 mg/kg, i.e. 28 mg with a body weight of 70 kg; during the 2nd month of treatment, the patient takes only chlorbutin in a very high dose - 0.2 mg / kghsut), i.e. 14 mg with a body weight of 70 kg. This 2-month cycle is repeated 3 times; the total duration of treatment is 6 months.

Six-month therapy with methylprednisolone and chlorbutine ("PONTICELLI regimen")

A. Months 1st, 3rd, 5th

Methylprednisolone 1000 mg IV for 3 days followed by prednisolone inside, 0.5 mg / kghsut) - for 27 days.

B. Months 2nd, 4th, 6th

Chlorbutin - 0.2 mg Dcghsut) - within 30 days

Intravenous methylprednisolone - the dose may be reduced to 500 mg per pulse in patients weighing less than 50 kg.

Chlorbutin - the dose should be reduced to 0.1 mg / kgxday) at a leukocyte level of less than 5000 cells / mm 3 and completely canceled at a level of less than 3000 cells / mm 3.

Possible modifications

Chlorbutin is indicated at a dose of 0.1 mg / kg per day:

• in young men to prevent azoospermia;
• in patients who developed leukopenia after 1 month of treatment.

In 1968, P. Kincaid-Smith suggested combining immunosuppressants (prednisolone and cytostatics) with anticoagulants (heparin followed by its replacement with warfarin) and antiplatelet agents (dipyridamole 400 mg/day) in the treatment of rapidly progressive glomerulonephritis. In the future, this combination was called a 4-component scheme. Similar schemes are also used, where chlorbutin is prescribed instead of cyclophosphamide. In addition, a modified regimen was proposed: for 8 weeks, prednisolone was prescribed at a dose of 60 mg/day, azathioprine at 2 mg/kgxday), dipyridamole at 10 mg/kgxday), heparin at a dose that caused a doubling of thrombin time. Then, during the year, treatment of glomerulonephritis with azathioprine and dipyridamole at the same doses is continued, and heparin is replaced with phenylin (at a dose that causes a doubling of prothrombin time). Similar regimens without prednisolone are recommended.

In some patients with slowly progressive renal failure, aggressive treatment with corticosteroids and/or cytostatics may improve renal function. At the same time, patients with renal insufficiency are more sensitive to side effect immunosuppressants. In this regard, the treatment of glomerulonephritis should be used only if there is a real chance of getting improvement.