Glomerulonephritis is inflammatory disease that affects the renal glomeruli and other tissues of the kidneys. Since from normal functioning renal glomeruli depends on the primary purification of blood from toxins, the transition of the disease to chronic stage gradually leads to kidney failure and the rapid accumulation of toxic substances in the body.

Treatment chronic glomerulonephritis is prescribed individually depending on the identified stage of the disease, its form and possible complications (if comorbidities). Complex therapy includes a number of medications, compliance correct mode and a strict diet.

Medical course of treatment

A patient with chronic glomerulonephritis is prescribed treatment after diagnosis and identification of the form of the disease. But before the start of the course of treatment, the doctor identifies foci chronic inflammation and is rehabilitating them. These foci can be:

• advanced caries;
• inflammation of the tonsils (tonsillitis);
• inflammation of the adenoids;
• chronic sinusitis and other inflammatory processes in the patient's body.

Against the background of such processes, autoimmune kidney damage occurs, therefore successful treatment CGN without elimination of foci of chronic inflammation is impossible.

The main treatment regimen includes the following drugs:

1. Antibiotics are used to fight infection. They are selected individually depending on the sensitivity of the pathogen to the drug and its tolerance to patients.
2. Non-steroidal anti-inflammatory drugs (indomethacin, ibuprofen): suppress the immune damage of the kidneys, which improves their condition.
3. Antiplatelet agents and anticoagulants (dipyridamole, ticlopidine, heparin) - thin the blood and improve its fluidity. In the inflammatory process, blood clots form in the vessels of the renal glomeruli, which interfere with normal blood circulation. These drugs prevent the formation of blood clots that clog blood vessels.
4. Immunosuppressants - suppress activity immune system and stop the destructive processes in the glomeruli. There are steroid (hormonal) and cytostatic. Cytostatic include: cyclophosphamide, chlorambucil, cyclosporine, azathioprine. As a hormonal drug, prednisolone is mainly used.
5. Medicines that lower blood pressure (captopril, enalapril, ramipril). Complications of chronic glomerulonephritis are expressed not only in renal failure and poor blood filtration, but also in other side effects. On the basis of delayed withdrawal excess fluid from the body in patients often observed an increase blood pressure. It also contributes to the violation hormonal background associated with malfunctioning of the adrenal glands. In such cases, the only way to lower blood pressure is medication.
6. Diuretics (hypothiazide, furosemide, uregit, aldactone) - help rid the patient's body of excess fluid and prevent deterioration of patency in the renal tubules.

In addition to these drugs, the patient may be prescribed other medications, depending on the individual symptoms of the disease.

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Treatment of chronic glomerulonephritis requires patients to comply with a sparing regimen. They are contraindicated:

• overwork (both mental and physical);
• hypothermia;
• night shifts at work;
• finding and working in stuffy rooms or in hot shops;
• excessive physical exercise;
• cold weather work outside.

Patients with glomerulonephritis are advised to sleep during the day or lie down for about 1.5 hours, if the work schedule allows. People with this disease should be more strict about the treatment of any concomitant diseases. For example, signs common cold do not call healthy person panic and desire to immediately visit the nearest pharmacy. But a patient with chronic glomerulonephritis, even with a cold, must observe strict bed rest and use antibacterial drugs that do not have a toxic effect on the kidneys (only as prescribed by a doctor).

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Nutrition for CGN

Regardless of the form of chronic therapeutic diet for patients based on:

• reducing salt intake;
• use a large number calcium and potassium;
• reduced sodium intake (found in mineral waters);
• use vegetable fats and complex carbohydrates in an increased amount;
• limiting the amount of fluid you drink to 0.8-1 l;
• reduction in the diet of animal protein;
• reducing the calorie content of food to 3500 kcal per day.

Patients with normal blood pressure can consume 2-3 g of salt per day, but with high pressure salt must be completely abandoned.

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Foods and dishes allowed by the diet

The list of permitted products includes:

• bread, pancakes or pancakes, but without salt;
• lean beef or trimmed pork, rabbit meat, turkey, veal, lamb, chicken, boiled tongue;
• milk, sour cream, cottage cheese, cream, kefir;
• rice, barley and corn grits;
• pasta of any kind (without salt);
• fruits and berries in any form;
• fruit and vegetable sauces and gravies, as well as tomato sauces and sauces from dairy products;
• vegetable and fruit soups with the addition of a small amount of sour cream, cooked only in butter;
• lean boiled fish (after pre-boiling it can be baked or lightly fried);
• egg yolks (no more than 2 pieces per day, but with the condition of reducing meat, cottage cheese and fish in the diet);
• salads from fresh vegetables and fruits, but without pickles;
• jelly, honey, sweets, jelly, jam, fruit ice cream;
• tea, fruit and vegetable juices, weak coffee, vitamin decoction of wild rose.

When cooking, it is allowed to use for taste citric acid, vanillin, cinnamon and vinegar.

Glomerulonephritis - a disease, usually of an immune nature, affecting both kidneys. The name of the disease comes from the word "glomerulus". This is the main part renal tissue. Translated from Greek word"glomerulus" means a glomerulus, and in the nephron - the structural unit of the kidney - there is an accumulation of the smallest blood vessels densely woven together.

Any acute glomerulonephritis, not cured within a year, is considered to have passed into chronic . The probability of such a transition is especially high in case of untimely or insufficient effective treatment and the presence in the body of foci chronic infection. For example, dental caries, sinusitis, cholecystitis, chronic tonsillitis, etc. Unfavorable conditions contribute to the development of chronic glomerulonephritis. living conditions when indoors for a long time there is a low temperature, as well as hard physical work.

It should be remembered that sometimes acute glomerulonephritis that has begun can turn into subacute malignant extracapillary glomerulonephritis with a rapidly progressive course. However, the chronic form of the disease is not necessarily a continuation of acute glomerulonephritis, it is often an independent primary disease. Chronic glomerulonephritis sometimes lasts for many years and leads to kidney shrinkage and death of the patient from chronic renal failure.

Causes of glomerulonephritis

Glomerulonephritis occurs most often after tonsillitis, SARS, pneumonia and other infectious lesions. In addition, the cause of the disease can be various viruses, in particular hepatitis B, rubella, herpes, infectious mononucleosis and adenoviruses. Perhaps the appearance of the disease after the introduction of vaccines and sera, as well as after hypothermia, trauma, stress. But in many cases, the factor that initiated the development of the disease remains unknown.

Symptoms and course of chronic glomerulonephritis

The following clinical forms of chronic glomerulonephritis are distinguished:

Nephrotic form Primary nephrotic syndrome is the most common. Unlike pure lipoid nephrosis, it is characterized by a combination of nephrotic syndrome with signs inflammatory lesion kidneys. The disease can have symptoms of only nephrotic syndrome for a long time before signs of glomerulonephritis appear. In chronic renal failure, the severity of nephrotic syndrome decreases, but blood pressure increases significantly.

Relatively common latent form The disease is manifested in most cases only by a mild urinary syndrome without an increase in blood pressure and the appearance of edema. It can last for 10-20 years or more, but in the end it still leads to the development of uremia - poisoning of the blood (and through it - of the whole organism) constituent parts urine.

Hypertonic form occurs in 20% of patients with chronic glomerulonephritis. Most often, this form of the disease is the result of the development of a latent form of acute glomerulonephritis. long time symptoms are dominated by pronounced hypertension, and urinary syndrome little expressed. Blood pressure under the influence various factors can change a lot during the day. Hypertrophy of the left ventricle of the heart develops, an accent of the II tone over the aorta is heard, changes in the fundus of the eye are observed in the form of neuroretinitis. However, as a rule, hypertension still does not become malignant, and blood pressure, especially diastolic, does not reach high values.

At mixed form both nephrotic and hypertensive syndromes are present.

Hematuric form occurs in 6-10% of cases of chronic glomerulonephritis. With this form of the disease, blood is present in the urine. The need to isolate the disease in separate form due to the fact that in some cases chronic glomerulonephritis can manifest itself without other signs and general symptoms.

All forms of chronic glomerulonephritis can periodically give relapses, very reminiscent or completely repeating the picture of the first attack of acute glomerulonephritis. Especially often, exacerbations occur in autumn and spring and occur within 1-2 days after exposure to an external irritant (most often streptococcal infection) on the body.

In any form of chronic glomerulonephritis, if appropriate measures are not taken, the disease passes into its final stage - a secondary wrinkled kidney.

Diagnosis of chronic glomerulonephritis

During diagnosis chronic glomerulonephritis must be distinguished from acute glomerulonephritis, hypertension, congestive kidney, focal nephritis, nephrolithiasis, tuberculosis of the kidneys, amyloid-lipoid nephrosis and primary wrinkled kidney.

In chronic glomerulonephritis, unlike hypertension, in the case history there is often evidence of a previous acute form of the disease. In addition, with chronic glomerulonephritis, edema and urinary syndrome appear from the very beginning of the development of the disease, and with hypertension first, blood pressure rises, and edema and urinary symptoms join it later.

When recognizing an exacerbation of the latent form of chronic glomerulonephritis in relation to acute glomerulonephritis, you need to ask the patient in detail and make comparative analysis urine. The revealed changes will play a serious role in the diagnosis. It is also important to study the morphological study of the kidney tissue obtained from the biopsy.

Latent and hypertensive forms of chronic glomerulonephritis should be distinguished from similar forms chronic pyelonephritis . In chronic glomerulonephritis, indicators characterizing the function of the glomeruli change earlier and to a greater extent, and in pyelonephritis, the function of the tubules.

You can check the functional state of the kidneys with the help of radioisotope methods studies such as renography and scintigraphy, as well as ultrasound and x-ray studies.

Basic principles of treatment chronic glomerulonephritis the same as acute. However, the nature of therapy depends on the specific form of the disease. With severe hypertension, edema and uremia, strict bed rest must be observed. Even at the very feeling better the patient should spend at least 10 hours a day in bed. In this case, you need to avoid cold, wear warm clothes and shoes. Significant physical activity must be completely eliminated.

At chronic renal failure resort to hemodialysis - non-renal blood purification, peritoneal dialysis - the method of replacement renal therapy or a kidney transplant.

There is a known case when a patient with renal insufficiency, strictly following a diet and leading healthy lifestyle life, regularly visited the sauna. By this he cleansed the body - with sweat they stood out harmful products metabolism.

At mixed form Chronic glomerulonephritis is recommended to use natriuretics, as they have a good diuretic and hypotensive effect. When using hypothiazide and other saluretics, it must be borne in mind that potassium is excreted from the body along with urine. Too much loss of this trace element can lead to its lack in the body and, as a result, to the development of hypokalemia with its characteristic general weakness (including muscle weakness) and a violation of the contractility of the heart. Therefore, potassium chloride solution should be taken simultaneously with diuretics.

With a long time not falling edema against the background of a decrease in the total amount of protein in the blood plasma, intravenous drip administration of a 6% solution of polyglucin can be recommended. It increases the colloid osmotic pressure of blood plasma, promotes the movement of fluid from tissues into the blood and causes diuresis. Polyglucin is more effective in combination with prednisolone or diuretics.

Mercury diuretics should not be used in renal edema. They can cause toxicity of the epithelium of the channels and glomeruli of the kidneys, which, despite an increase in urination, leads to a decrease in the filtration function of the kidneys. For the treatment of renal edema, purine derivatives such as theophylline, aminophylline and others are ineffective.

During treatment hypertonic form chronic glomerulonephritis can be prescribed drugs that lower blood pressure used in the treatment of hypertension: reserpine, reserpine with hypothiazide, adelfan, trirezide, kristepin, dopegit. However, when taking them, large fluctuations in blood pressure and its sharp drop. This can worsen the state of renal blood flow and reduce the filtration function of the kidneys.

Diet for chronic glomerulonephritis

During the treatment of patients with chronic glomerulonephritis great importance has a diet that is prescribed depending on the form and stage of the disease. With nephrotic and mixed forms of damage, the intake of sodium chloride into the patient's body should not exceed 1.5-2.5 g per day. In this regard, pickles should be completely abandoned, and ordinary food should not be salted.

With a normal excretory function of the kidneys, which is indicated by the absence of edema, the food should contain a sufficient amount of animal protein, rich in complete phosphorus-containing amino acids. Such nutrition normalizes the nitrogen balance and compensates for the loss of protein. However, at the first sign of uremia, foods containing a significant amount of protein are excluded. In the diet, only those that contain a lot of carbohydrates remain.

At hypertonic form chronic glomerulonephritis, it is recommended to limit the intake of sodium chloride to 3-4 g per day; at the same time, there should be enough proteins and carbohydrates in the food. The latent form of the disease does not provide for significant restrictions in the nutrition of patients. But food should be complete, varied and rich in vitamins.

In general, with all forms of chronic glomerulonephritis, vitamins A, B and C can be included in the diet. It should be remembered that a long-term salt-free and protein-free diet not only does not prevent the development of the disease, but also has a bad effect on general well-being sick.

The drinking regimen of a sick person depends on the state of the excretory function of the kidneys. With satisfactory indicators, it is useful to drink weak tea from the red root (forgotten kopek), sweetened water with lemon and blackcurrant juice. If the patient has frequent vomiting, he loses a lot of sodium chloride, and a small additional amount is introduced into the diet table salt.

In addition to taking medication and dieting, constant skin care is also necessary. During chronic glomerulonephritis due to the release of urea occurs pruritus, numerous scratches appear. In addition, patients with uremia often develop bedsores, and therefore precautionary measures must be taken.

Treatment of chronic glomerulonephritis with folk remedies

Patients with chronic glomerulonephritis are encouraged to use the same plants as in the acute form of the disease. They are prescribed during the period of partial or complete remission, when the dose of glucocorticoids is reduced. Continuous medication based vegetable fees can last from 2 to 6 months. Then a cyclical intake of 2-3 months is shown with a break of 2 weeks. Fees need to be changed periodically. With stable remission, preventive courses can be carried out for 20-30 days 3-4 times during the year.

Folk recipes for the treatment of chronic glomerulonephritis

Here are the recipes for some herbal preparations used in chronic glomerulonephritis:

At hematuric form chronic glomerulonephritis, you need to take 2 parts of the horsetail herb, 3 parts of the herb kidney tea, common yarrow and tripartite succession, large plantain leaves and stinging nettle, calendula officinalis flowers. Grind the plants, mix thoroughly. Pour 1 tbsp. l. mixture with a glass of boiling water and insist for an hour. Strain the finished infusion and take 1/3 cup 4 times a day.

You can also take in equal proportions the herb of the five-lobed motherwort, wormwood and the initial drug, as well as the flowers of the calendula officinalis. Grind everything, mix. Pour 1 tbsp. l. collection with a glass of water, boil for 10 minutes, then, covered with a lid, leave for 4 hours. Strain the resulting infusion and take 3 tbsp. l. 4 times a day.

In chronic glomerulonephritis, such a collection helps well. Take 3 parts of the root of the field harrow and birch leaves and 4 parts of flaxseed. Grind everything, mix. Pour 1 tbsp. l. mixture with 2 cups of boiling water and infuse for 2 hours. Strain the infusion and take 1/3 cup 3 times a day.

In half a liter of milk, put 3 tbsp. l. parsley roots, boil for 20 minutes, cool, strain and drink throughout the day. In the morning on an empty stomach, you should drink a glass of beetroot or carrot juice.

Bath infusions and decoctions for glomerulonephritis

These infusions and decoctions are used during bath procedures. They are drunk, splashed on hot stones to inhale the steam, or used simultaneously for both procedures. Here are some recipes for such infusions and decoctions used to treat chronic glomerulonephritis.

Take 2 parts of the herb of lemon balm, flowers of white lamb and small-leaved linden, 1 part of flowers of calendula officinalis and parsley fruits. Grind everything, mix. Pour 1 tbsp. l. mixture in a preheated thermos, pour 1 liter of boiling water and insist for 12 hours. Strain the finished infusion and drink it warm in 3 divided doses during bath procedure.

Take 5 parts of flax seeds, 2 parts of birch leaves, 1 part of stinging nettle leaves and wild strawberries. Grind everything, mix. Pour 1 tbsp. l. mixture with a glass of water and boil in a water bath for 10 minutes. Cool the finished broth, strain and drink warm in 1-2 doses during a visit to the steam bath.

Take 2 parts of lemon balm herb, 1 part of oregano herb, black currant leaves and calendula officinalis flowers. Grind everything, mix. Pour into a thermos 1 tbsp. l. mixture, pour a glass of boiling water and insist for 12 hours. Strain the finished infusion, add 2 tbsp. l. honey and drink warm in 2-3 doses during a visit to the steam bath.

Take in equal proportions the buds of black poplar, the herb of tricolor violet and the initial drug, the leaves of the bearberry. Grind everything, mix. Pour 1 tbsp. l. mixture in a preheated dish, pour a glass of boiling water and insist, wrapped, for half an hour. Then strain the infusion and drink warm in several doses during a visit to the bath.

Take 3 parts of parsley fruit and bearberry leaves, 2 parts of blood-red hawthorn leaves and five-lobed motherwort herb, 1 part of common hop cones. Grind everything, mix. Pour 1 tbsp. l. mixture with a glass of boiling water, heat in a water bath at a low boil for 15 minutes, then leave for 45 minutes. Cool, strain and drink the decoction warm during the bath procedure.

Take in equal proportions the herb of stinging nettle, a series of tripartite, common yarrow and kidney tea, calendula officinalis flowers, cinnamon rose hips and large plantain leaves. Grind everything, mix. Place 1 tbsp. l. mixture in a preheated thermos, pour a glass of boiling water and insist for three hours. Then strain the infusion and drink warm in 2-3 doses during the bath procedure.

Take 2 parts of common lingonberry leaves, St. John's wort herb and black elder flowers, 1 part of Icelandic moss and elecampane root. Grind everything, mix. Pour 1 tbsp. l. mixture with a glass of boiling water and keep in a water bath at a low boil for 15 minutes. Then 45 minutes to insist, strain and drink while visiting the steam bath.

Take in equal proportions the herb St. John's wort, medicinal sage, oregano and highlander bird. Grind everything, mix. Pour 1 tbsp. l. mixture with a glass of boiling water and keep in a water bath at a low boil for 20 minutes. Then 40 minutes to insist, strain. Dilute the decoction in 2 liters warm water and little by little splash on the hot stones in the steam room, trying to inhale the resulting steam deeper. The same decoction can be taken orally during the bath procedure 1/4 cup 4 times with an interval of 10-15 minutes.

Take in equal proportions flax seeds, grass shepherd's bag and Hypericum perforatum, calamus root. Grind everything, mix. Pour 1 tbsp. l. mixture in a preheated thermos, pour 1 cup boiling water and insist for 3 hours. Then strain the infusion, dilute it in 3 liters of warm water and gradually splash it onto hot stones, inhaling the steam deeply. The infusion can also be drunk: it is recommended to drink one glass of warm infusion in 3 doses during the bath procedure.

Take 2.5 parts of parsley seeds and couch grass rhizomes, 2 parts of blood-red hawthorn fruits and five-lobed motherwort herbs, 1 part of common hop cones. Grind everything, mix. Pour 1 tbsp. l. mixture with a glass of boiling water and keep in a water bath at a low boil for 20 minutes. Then 40 minutes to insist, strain. Dilute in 2 liters of warm water and periodically splash a little on hot stones, inhaling deeply the resulting steam.

During the bath procedure, you can drink black radish juice with honey. The solution should be prepared based on 1 glass of juice 1 tbsp. l. honey and drink in the bath at one time. You can also squeeze celery juice and drink 1/4 cup during the bath procedure.

Prevention of chronic glomerulonephritis

The basis for the prevention of chronic glomerulonephritis is the timely elimination of foci of infection in the body. This can be the removal of the tonsils, the cure of caries, chronic tonsillitis, otitis media, sinusitis, etc. Prevention is also treatment intestinal infections. In addition, it is important to prevent severe hypothermia and exposure to humid air.

Patients with chronic glomerulonephritis prefer to live in an area with a dry and warm climate. People who have had acute glomerulonephritis should be under dispensary observation. They are prohibited from long business trips, night shifts, work with toxic and other harmful substances. With satisfactory general condition and the absence of complications, patients can be offered Spa treatment in Central Asia or south coast Crimea.

- it's a complicated matter. This disease is considered very common, since among all therapeutic pathologies its frequency reaches 2%. The disease can affect people at any age, but is more common between 20 and 40 years of age. It develops most often when acute glomerulonephritis is not cured in time, although there are cases when the disease immediately becomes chronic.

Bacteria and viruses can provoke pathological changes in the kidneys, which are often brought into this organ by blood from other parts of the body affected by infectious processes.

Determination of symptoms and treatment in chronic glomerulonephritis should be carried out exclusively), since self-medication with this disease can be fraught with extremely unpleasant consequences.

Symptoms of chronic glomerulonephritis

The main symptom of this disease is a violation of the normal activity of the kidneys lasting more than 1 year (both organs are affected). Usually, the symptoms of the disease begin to appear so gradually and slowly that a person for a long time does not even suspect that he has dangerous disease and therefore remains without appropriate treatment for a long time, which aggravates the situation.

The most characteristic general symptoms for this disease:

• swelling (especially in the legs);
• dyspnea;
• persistent increase in blood pressure;
• pallor and swelling of the face, which is characterized by a special term - "nephritic face".

The remaining manifestations of the disease in a chronic form, as a rule, are hidden from the patient himself. They are associated with changes in the composition of blood and urine, water-salt balance, disturbances in the structure of blood vessels in the organ and filtration processes in the urinary system.

With the chronicity of the disease, two stages are distinguished:

1. Stage of renal compensation. During this period, the function of nitrogen excretion in the kidneys is sufficient. Symptoms such as a slight ingress of protein and blood into the urine appear, a pronounced urinary syndrome is possible.
2. The stage of renal decompensation - the urinary syndrome is less significant, the nitrogen excretion function of the urinary organs is insufficient.

During chronic form may be various options, therefore, physicians distinguish several varieties of the disease, each of which has its own characteristics of symptoms, the most pronounced symptoms and a set pathological changes that occur in the body of a sick person.

Chronic minimal glomerulonephritis is characterized by a violation of the small processes of podocytes. Loosening and swelling of the tissue, thickening of the basement membranes occur in separate loops of nephrons.

By external symptoms, it is impossible to distinguish this variety, correct diagnosis only possible with electron microscopy.

Membranous - the walls of the renal tubules diffusely thicken. The reason is the deposition of complexes of the immune system on the surface of the vessels. In this case, the kidney increases in size and has a smooth surface. Often this type of disease is associated with allergic reactions in the body to drugs or to processes that occur in the presence of tumors.

Mesangial - accompanied by changes in the cells of the mesangium during the deposition of immune complexes on the surface of the vessels. The kidneys at the same time have a dense texture.

Focal - pathological changes and the deposition of hyaline substance does not occur in the entire volume of the renal tissue, but only in individual foci or segments.

In addition, doctors distinguish varieties of the disease according to the speed of development of its symptoms:

• rapidly progressive - develops within 2-5 years;
• slowly progressive - develops over more than 10 years.

Symptoms of various forms of the disease

Depending on which of the symptoms appear during the development of the disease, the following forms of chronic glomerulonephritis are distinguished:

• Latent - manifested by urinary syndrome, occurs in almost half of patients. It does not cause swelling or increased blood pressure. As symptoms appear hematuria, leukocyturia, proteinuria (that is, blood, leukocytes and protein are detected in urine tests). As a rule, this kind of disease develops for a long time (up to 20 years).
• Hypertension - accompanied by an increase in blood pressure. It occurs in approximately one in five patients. The pressure can rise very intensively, up to 200/120 mm Hg. Art., and during the day its fluctuations are possible. Accompanied given form illness and other symptoms: changes in the structure of the fundus of the eye (neuroretinitis), cardiac asthma, which is provoked by insufficiency of the left ventricle of the heart. The disease manifests itself for a long time and is fraught with an onset.

• Hematuric - pronounced macrohematuria is manifested, that is, blood enters the urine in such quantities that it can be seen by a change in color, without special clinical research. Such a symptom can lead to the development of anemia due to constant blood loss. This symptomatology occurs in about one in twenty patients.
• Nephrotic - occurs in every fourth patient and is accompanied by nephrotic syndrome. It manifests itself with such symptoms: protein excretion in the urine, a violation of water metabolism, as a result of which edema develops not only external, but also internal (accumulation of a large amount of fluid in the pleura, pericardium). Blood is found in the urine, blood pressure may increase. With this type of disease, renal failure occurs quickly enough, which negatively affects the patient's condition.
• Mixed - accompanied by the manifestation of nephrotic-hypertensive syndrome, in which symptoms of both of the above forms of the disease are observed.

In this way, this pathology kidneys in a chronic form can manifest different symptoms, which determine the features of the disease, its course, treatment and possible complications in the future.

Diagnostics

Diagnosis of chronic glomerulonephritis always includes comprehensive examination. In order to correctly diagnose this disease, it is necessary to collect a very large amount of information about the patient, about his current condition, about all infectious and noncommunicable diseases that were in the past. During the examination, the patient is assigned:

• Clinical and biochemical analysis of urine. The presence of chronic glomerulonephritis is indicated by the results of tests in which protein is observed in the urine, shaped elements blood (in particular, leukocytes, erythrocytes), protein, cylinders. Together with pathological changes in biochemical composition urine changes and its specific gravity.
• Blood tests. With such an ailment in the blood, the amount of protein changes, the ratios in the number of different fractions of protein compounds. Studies show an increase in the number of antibodies to streptococcus (referred to as ASL-O in the test results) and a decrease in the content of the components of the complement system C3 and C4. With this disease, the indicators of several types of immunoglobulins in the blood (IgA, IgM, IgG) increase.

• Zimnitsky's test - laboratory research urine, in which urine is collected within one day in 8 containers (each container contains urine excreted in three hours). By this survey it is possible to determine the change in urine production during the day (the ratio of night and daytime urination), its total, density. In addition, you can compare the amount of fluid consumed and excreted.
• Rehberg's test is a study of kidney function, in which their filtering ability is revealed. For examination, daily urine and blood serum taken from a vein are required at the same time. Determine the amount of creatinine in the blood and excreted urine.
• Excretory urography is an X-ray image that covers the area from top edge kidney to border urethra. On this image, you can determine the position, shape and size of organs, the structure of their tissues, the presence of stones.

• Renography is a study that uses a special radioactive substance(technetium-99). It is injected into the kidneys and with the help of a gamma camera, which is installed next to the organ, the excretion process is recorded. By the nature of this process, it is possible to determine the rate of urine excretion from the patient's body.
• with this disease, pathological changes in the structure of the renal tissue: its sclerotization and decrease in volume.
• A biopsy of the renal tissue is performed to determine changes in the histological structure of the kidney. A tissue sample is taken with a special needle that is inserted through the back muscles. The procedure is very complicated, therefore, it is performed exclusively in stationary conditions and use local anesthesia. To exclude complications and the correct implementation of the manipulation, the biopsy is monitored using ultrasound.

In addition to these basic studies, the attending physician may prescribe other examinations, based on what concomitant symptoms develop in the patient. It can be ultrasound of other organs, ECG. With simultaneous deterioration of vision, consultation with an ophthalmologist and examination of the fundus are necessary.

Based on the results of the examinations, the doctor conducts differential diagnosis glomerulonephritis and other diseases that may present with the same symptoms.

Among these diseases:

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

As a rule, the diagnosis of the chronic form of glomerulonephritis is not difficult task, but difficulties may arise with latent, hematuric and hypertensive varieties of the disease.

In the case when these studies show a typical picture of a violation of the renal tissue and related changes in the internal environment of the body, a diagnosis of "chronic glomerulonephritis", or CGN, is established. After completing the diagnosis, they begin to choose the tactics of treating the patient.

Treatment

Is it possible? With a timely visit to the doctor and the fulfillment of all prescriptions, it is possible to ensure that the disease stops recurring. Many factors are very important in this matter: individual characteristics organism, neglect of the disease, the degree of damage to the organs of the urinary system, approaches to treatment.

Treatment of the disease depends on what factors led to these pathological changes.

It can provoke chronic kidney disease acute form(if it is not treated on time and correctly), hereditary predisposition, immune shifts in the body (for example, allergies, the effects of vaccination, autoimmune diseases).

Perhaps the influence of hypothermia, a general weakening of the body due to the action of unfavorable environmental factors, malnutrition. All this must be taken into account when developing treatment tactics, otherwise the root cause of the disease will constantly prevent effective elimination Problems.

Without appropriate therapy, the disease can lead to very serious consequences, including renal failure, kidney dystrophy, hemorrhages from its blood vessels and others dangerous states. In chronic glomerulonephritis, the treatment is very complex, includes several components, each of which is extremely important for maintaining the human body and eliminating the problem.

Corticosteroid therapy

This is the basis of pathogenetic therapy for this disease. Data medications are prescribed in a dose that is determined by the doctor based on the patient's condition. As a rule, gradually the dosage of corticosteroids is gradually increased. Treatment is carried out in courses, which, if necessary (during exacerbations), should be repeated periodically. The scheme of reception is developed in each separate case individually. With progressive azotemia, sclerosis of the renal glomeruli, their atrophy and high blood pressure, corticosteroids hormonal preparations contraindicated.

In some cases, during treatment with corticosteroids, the patient exacerbates inflammation in the foci of infection in other organs. Then there is a need for simultaneous reception antibacterial drugs(if the infection is bacterial) or appropriate therapy for other infectious agents.

Immunosuppressive Therapy

With chronic glomerulonephritis, changes in the patient's immune system play a very serious role. Specific substances are formed in his body (antibodies that are produced in response to antigens, fractions of the complement system C3 and C4). These compounds are deposited on the delicate tissues of the renal glomeruli and lead to their destruction. As a result, the blood circulation of organs and the processes of urination are disturbed. Therefore, the treatment of chronic glomerulonephritis must necessarily include an impact on the immune processes in the body.

Immunosuppressants in some cases can replace corticosteroid hormonal drugs or be used simultaneously with them. There are conditions in which this therapy needs to be stopped, therefore, constant monitoring of the patient's well-being is necessary.

Drugs that suppress the immune system have different adverse reactions, among which there is an effect on the state of the optic nerve.

Therefore, while taking these funds, constant monitoring by an ophthalmologist is necessary.

Anti-inflammatory therapy

It is aimed at eliminating inflammatory processes in the organs of the urinary system. Anti-inflammatory drugs anesthetize and lower the temperature, reduce the release of protein from the blood into the urine. If corticosteroids and anti-inflammatory drugs are used at the same time, in some cases it is possible to reduce the dosage of hormones.

Anticoagulant therapy

When there are such changes in which the risk of blood clotting increases. In particular, this is the deposition of fibrin on the walls of the glomeruli and arterioles. Anticoagulants are taken to normalize blood clotting and prevent complications. In addition, they are able to have other effects: reduce inflammation and allergic reactions.

As a result of such therapy, the filtering function of the kidneys improves, protein excretion into the urine decreases, and the ratio of different fractions of protein substances in the blood serum normalizes.

Antihypertensive therapy

Since with glomerulonephritis, in particular, with its hypertensive form, blood pressure rises, it is necessary to normalize it. To this end, the doctor prescribes drugs that reduce pressure indicators. Moreover, such therapy must be selected with great care: the patient is negatively affected not only high blood pressure, but also his a sharp decline, as well as sharp drops. Therefore, it should be reduced gradually.

Drugs that have a diuretic effect not only lower blood pressure, but also increase the outflow of fluid from the body, which prevents the development severe edema. For example, with a mixed form of the disease, natriuretics are prescribed, which are characterized by such double action. But medicines with a diuretic effect, which are based on purine derivatives, are ineffective in eliminating edema caused by impaired renal function.

Diet

Nutritional modification is also an integral part of treatment. this disease. A diet for chronic glomerulonephritis is necessary to normalize the composition of blood serum so that the urinary system can cope with the processes of urination and urination.

Very close attention need to pay attention to the amount of salt consumed. With mixed and nephrotic forms of the disease, salt intake should be minimal. The patient is satisfied with the amount of sodium chloride that is initially present in food, so the dishes are not salted at all during cooking.

If a patient has developed a chronic hypertensive type of the disease, the amount of salt in his food should be about 3-4 g per day, and the content of proteins and carbohydrates should be normal.

If there are no edemas provoked by a violation of the renal filtering ability, the amount of protein in the food should be sufficient so that enough protein substances enter the body, because they are intensively lost in the urine.

With glomerulonephritis, as with any other disease, it is very important that the patient's nutrition is balanced, correct.

Food must contain everything necessary substances, because with their lack, the human condition will worsen, the likelihood of complications will increase.

Among the vitamins, especially valuable in this case are A, C and group B.

If at any stage of the treatment of the disease it became necessary to limit the intake of salt or protein compounds, such a diet should not last long. Prolonged shortage of these vital important substances also negatively affects human health, so nutrition during the entire period of therapy should be adjusted from time to time depending on changes in functional state kidneys.

Other features of treatment

It is noticed that the climate in the patient's place of residence has a special effect on the course of the disease. Doctors advise during treatment to be in a dry and warm climate, where there is no chance of exposure to cool, moist air and further hypothermia.

If the patient's health is not critical (there is no heart failure, excessive edema, uremia), he can go to a spa treatment. The best places for recreation are Central Asia or the Crimea (South Coast).

Thus, if chronic glomerulonephritis is suspected, diagnosis should be started as soon as possible, without waiting for the onset dangerous consequences for the patient's body.

Once the diagnosis is established, appropriate treatment must be carried out. It is very important that the patient follow all the doctor's instructions and adhere to a sparing regimen, including nutrition. Neglect of such appointments can aggravate the condition.

Glomerulonephritis is a disease in which the kidney tissue is damaged. In this disease, the renal glomeruli are primarily affected, in which the primary filtration of blood occurs. The chronic course of this disease gradually leads to the loss of the ability of the kidneys to perform their function - to cleanse the blood of toxic substances with the development of renal failure.

What is a renal glomerulus and how do the kidneys work?

The blood entering the kidneys through the renal artery is distributed inside the kidney along the smallest vessels, which flow into the so-called renal glomerulus.

What is a renal glomerulus?
In the renal glomerulus, the blood flow slows down, as through a semipermeable membrane, the liquid part of the blood with electrolytes and dissolved in the blood organic matter seeps into the Bowman's capsule (which, like a wrapper, envelops the renal glomerulus from all sides). From the glomerulus, the cellular elements of the blood with the remaining amount of blood plasma are excreted through the renal vein. In the lumen of the Bowman's capsule, the filtered part of the blood (without cellular elements) is called primary urine.

What is Bowman's capsule and renal tubules (loop of Henle)?
But in addition to toxic substances, many useful and vital substances are dissolved in this urine - electrolytes, vitamins, proteins, etc. In order for everything useful for the body to return to the blood, and all harmful to be excreted in the final urine, the primary urine passes through the tube system (the loop of Henle, the renal tubule). It takes place permanent processes the passage of substances dissolved in the primary urine through the wall of the renal tubule. After passing through the renal tubule, primary urine retains in its composition toxic substances(which need to be removed from the body) and loses those substances that are not subject to removal.

What happens to urine after it has been filtered?
After filtration, the final urine is excreted through the renal tubule into the renal pelvis. Accumulating in it, urine gradually flows into the lumen of the ureters into the bladder.

It is accessible and understandable about how the kidneys develop and work.

What happens with glomerulonephritis in the kidneys?

Glomerulus of the kidneys is mainly affected in glomerulonephritis.

1. Because of inflammatory response the wall of the vessels of the glomeruli, the following changes occur:

• The wall of the vessels of the renal glomerulus becomes permeable to cellular elements
• Microthrombi are formed, which clog the lumen of the vessels of the glomeruli.
• The blood flow in the vessels of the affected glomeruli slows down or even stops.
• Blood cells enter the lumen of the Bowman's capsule.
• Blood cells in the lumen of Bowman's capsule clog its lumen.
• Blood cells clog the lumen of the renal tubules.
• The entire process of filtering blood and primary urine in the affected nephron is disrupted (nephron is a complex: renal glomerulus + Bowman's capsule + renal tubules).

1. Due to impaired blood flow in the renal glomerulus, the lumen of its vessels becomes empty and is replaced by connective tissue.
2. As a result of blockage of the renal tubules by blood cells, their lumen becomes empty and the walls stick together with the replacement of the entire nephron with connective tissue.
3. The gradual "death" of nephrons leads to a decrease in the volume of filtered blood, which is the cause of renal failure.
4. Kidney failure leads to the accumulation of toxic substances in the blood, and necessary for the body substances do not have time to return the remaining nephrons of the kidneys to the blood.

Causes of chronic glomerulonephritis

From the foregoing, it becomes clear that the cause of the disruption of the kidneys is developing in the renal glomeruli inflammatory process. Now briefly about the causes of inflammation of the renal glomeruli.

1. Common infectious diseases

• angina, tonsillitis
• scarlet fever
• infective endocarditis
• septic conditions
• pneumococcal pneumonia
• typhoid fever
• meningococcal infection
• parotitis(piggy)
• chicken pox(chickenpox)
• infections caused by coxsackieviruses

1. Rheumatic and autoimmune diseases:

• systemic lupus erythematosus (SLE)
• systemic vasculitis
• Schönlein-Henoch disease
• hereditary pulmonary-renal syndrome

1. Vaccination and transfusion of blood components

1. Substance intoxication:

• Poisoning by organic solvents
• alcoholic drinks
• mercury poisoning

1. radiotherapy, radiation sickness

Types and symptoms of chronic glomerulonephritis

downstream and clinical manifestations allocate the following types:

1. Latent- the most common (accounts for about 45% of all cases of chronic glomerulonephritis). Appears unexpressed external symptoms : moderate swelling and increased blood pressure. More manifested by data laboratory examination: general analysis urine reveals elevated level proteins, erythrocytes and leukocytes.

2. Hematuric- a rare form (makes no more than 5% of total number patients). Manifested by the following outward signs: pink or red urine. In the general analysis of urine an increased number of altered erythrocytes is detected.

3. Hypertensive- a common form (about 20% of the total incidence). Manifested by the following external symptoms: a constant increase in blood pressure, an increase in the volume of daily urine excreted, nocturnal urge to urinate. In the general analysis of urine come to light increased content protein and altered erythrocytes, urine density is slightly below normal or within the lower limit of normal.

4. Nephrotic- a common form (about 25%). The disease manifests itself as follows outward signs: high blood pressure, severe swelling, reduced amount of daily urine excreted. Laboratory signs v general urinalysis: increased density urine, increased protein content in the urine; blood chemistry reveals: a decrease in total protein (mainly due to albumin), an increase in blood cholesterol.

5. Mixed (nephrotic-hypertonic)- characterized by symptoms of the two forms described above: nephrotic and hypertensive.

Methods for diagnosing chronic glomerulonephritis

For the diagnosis of all types of chronic glomerulonephritis, the following types of examinations are used:

Type of diagnostics	Why is it appointed?
General urine analysis	This analysis reveals changes in the following indicators: urine density, the presence of protein and cylinders, the presence of leukocytes and erythrocytes, urine color.
Biochemical analysis blood	This analysis examines the following indicators: general level blood protein, blood albumin, creatinine, urea, cholesterol and all fat fractions (lipidogram).
Kidney biopsy and microscopy of the biopsy	This research method allows you to explore tissue changes in the structure of the glomeruli of the kidneys and reveals various morphological forms of glomerulonephritis. In many ways, the histological form of glomerulonephritis is a criterion for the appointment of adequate treatment.

Stages of chronic glomerulonephritis

Stage of compensation initial stage(compensation stage) the functional activity of the kidneys is not changed.

Stage of decompensation- associated with the progression of the disease with impaired renal function (stage of decompensation). Stage with impaired renal function and the development of chronic renal failure.

External signs

Laboratory signs

The accumulation of nitrogenous compounds in the blood, accompanied by the following symptoms: headache, nausea, vomiting A significant increase in blood pressure: associated with water retention in the body, electrolyte imbalance and hormonal disorders. Increased amount excreted daily urine (polyuria). This process is associated with the inability of the kidneys to concentrate urine. Polyuria is accompanied by the following symptoms: dry skin, constant thirst, general weakness, headache.

General urine analysis Increased urinary protein Decreased density of urine The presence of casts in the urine (hyaline, granular) Erythrocytes in the urine: often significantly higher than normal.

Uremia- severe degree of renal failure. At this stage of the disease, the kidneys completely lose their ability to maintain normal composition blood.

Diagnosis of chronic glomerulonephritis

Laboratory signs of acute glomerulonephritis:
General urine analysis :
Urine color: pink, red, meat slop color Changed erythrocytes: present, many Cylinders: erythrocyte, granular, hyaline Urine density: increased / decreased or normal (depending on the stage of the disease) Protein: found to be significantly higher than normal (symptom is characteristic of all types of disease)
Zimnitsky's test:
Increase/decrease in daily urine output Increase / decrease in the density of urine The parameters of the Zimnitsky test depend on the stage of chronic glomerulonephritis and the form of the disease.
Blood chemistry :
Reduced blood protein levels (due to a decrease in albumin) Detection of C reactive protein Increased blood cholesterol levels Detection of sialic acids An increase in the level of nitrogenous compounds in the blood (typical for advanced stages of the disease)
Immunological study blood:
an increase in the titer of antisteptolysin O (ASL-O), increased antistreptokinase, increased antihyaluronidase, increased antideoxyribonuclease B; increase in gamma globulins of total IgG and IgM decreased levels of complement factors C3 and C4

Treatment of chronic glomerulonephritis

Type of treatment	Target	Practical Information
Sanitation of foci of chronic inflammation	Eliminate the source of chronic inflammation, which is a trigger factor for autoimmune kidney damage	Removal carious teeth Removal of chronically inflamed tonsils, adenoids. Treatment of chronic sinusitis
Bed rest	Reduce the burden on the kidneys. Physical activity accelerates metabolic processes, which lead to the acceleration of the formation of nitrogenous compounds toxic to the body.	The patient is advised to stay with recumbent positions Do not get out of bed unless absolutely necessary.
Diet	Violation of the kidneys leads to a change in the electrolyte balance of the blood, loss needed by the body nutrients and the accumulation of harmful toxic. An adequate diet can reduce the adverse effects of the above factors.	Table number 7 Power features: Reduce salt intake Limit fluid intake Consumption of foods rich in potassium and calcium poor in sodium Limiting animal protein intake Diet Enrichment vegetable fats and complex carbohydrates.
Anticoagulants and antiplatelet drugs	Improved blood flow. With inflammation in the renal glomeruli, conditions are created for the formation of blood clots in their vessels and blockage of their lumen. The drugs of this group prevent this process.	Dipyridamole at a dosage of 400-600 mg / day Ticlopidin at a dosage of 0.25 g 2 r / day Heparin at a dosage of 20 - 40 thousand units / day. Course duration - 3 to 10 weeks. Dosage and duration of treatment is determined by the attending physician based on the data laboratory tests and the course of the disease.
Non-steroidal anti-inflammatory drugs	There is evidence that indomethacin and ibuprofen affect the activity of the immune response. Suppression of immune damage to the kidneys leads to an improvement in the condition of the kidneys.	Indomethacin Appointed by a course of several months On the initial stage appointed daily dose in 25 mg. After a few days (with good tolerability of the drug), the dosage is gradually increased to 100-150 mg per day.
Immunosuppressants	Means that suppress the activity of the immune system have a beneficial effect in glomerulonephritis. By reducing the activity of the immune response, these drugs suppress the destructive processes in the renal glomeruli.	Steroid drugs: Prednisolone is used in an individual dosage, calculated according to the formula 1 mg / kg / day for 6-8 weeks, after which the dosage of the drug is reduced to 30 mg / day with a gradual decrease in dosage until complete cancellation. Periodic pulse therapy as prescribed by the attending physician (prescription of short-term high doses of steroid drugs). Cytotoxic drugs: cyclophosphamide at a dosage of 2-3 mg / kg / day chlorambucil at a dosage of 0.1-0.2 mg / kg / day cyclosporine at a dosage of 2.5-3.5 mg / kg / day azathioprine at a dosage of 1.5-3 mg / kg / day
Drugs that lower blood pressure	With the development of kidney failure, there may be fluid retention in the body, as well as a change in the concentration of hormones produced by the kidneys. These changes often lead to a persistent increase in blood pressure, which can only be reduced with medication.	captopril at a dosage of 50-100 mg / day enalapril at a dosage of 10-20 mg / day ramipril at a dosage of 2.5-10 mg / day
Diuretics	The obstructed blood flow in the inflamed glomeruli of the kidneys, the accumulation of blood cells in the renal tubules requires activation of the fluid flow in the nephron. Therefore, diuretics can have a positive effect in glomerulonephritis.	hypothiazide at a dosage of 50-100 mg furosemide at a dosage of 40-80 mg uregit at a dosage of 50-100 mg aldactone at a dosage of 200-300 mg / day
Antibiotics	In the event that a patient with glomerulonephritis has a chronic focus of infection (chronic sinusitis, sinusitis, endometritis, urethritis, tonsillitis), it is necessary to sanitize it with antibacterial drugs.	In each case, the type of antibiotic is selected by the attending physician individually, depending on the following factors: type of chronic inflammation Sensitivity to the antibiotic of the causative agent of an infectious disease Tolerability of the drug by the patient.

Health prognosis for chronic glomerulonephritis

In the absence of treatment, the disease steadily leads to the loss of functionally active nephrons by the kidneys with the gradual onset of renal failure.

At active treatment with the suppression of the activity of the immune system, the course of the disease improves significantly, renal failure does not develop or the timing of its onset is significantly delayed.

There is evidence of complete remission (successful cure of the disease) during treatment with suppression of immune activity.

What are the features of chronic glomerulonephritis in children?

General features glomerulonephritis in childhood:

• The clinical picture of the disease can vary greatly.
• Chronic glomerulonephritis is the most common cause of chronic renal failure in children (except newborns).
• Up to 40% of all cases of hemodialysis and kidney transplantation in children are performed for chronic glomerulonephritis.

The main causes of chronic glomerulonephritis in children:

• In most cases, the causes are unknown. The disease develops as primary chronic, that is, before that the child had no acute glomerulonephritis.
• The role of irrational therapy of chronic foci of infection (sick teeth, inflamed tonsils), severe hypovitaminosis, hypothermia and malnutrition during acute glomerulonephritis is not excluded.
• A certain role is played by slow current infectious processes Key words: cytomegalovirus infection, hepatitis B, parainfluenza, etc.
• congenital disorders structures of the kidney tissue.
• Hereditary immunodeficiencies(decreased function of the immune system due to genetic disorders).

The main forms of chronic glomerulonephritis in children:

• nephrotic (edematous-proteinuric);
• hematuric;
• mixed.

Features of the nephrotic form of chronic glomerulonephritis in children:

• The disease develops acutely after hypothermia, tonsillitis, acute respiratory infection, vaccinations, or without visible reasons.
• The main symptoms are swelling and the presence of protein in the urine.
• The disease proceeds for a long time, periods of improvement are replaced by new exacerbations. Gradually, chronic renal failure develops.

Features of the hematuric form of chronic glomerulonephritis in children:

• Usually there are no complaints - the child feels fine.
• A small amount of erythrocytes and protein is found in the urine. Sometimes such changes persist for 10-15 years without any symptoms.
• Many children are found chronic tonsillitis(inflammation of the tonsils) and other chronic foci of infection.
• Swelling, back pain, headache, may occur periodically fatigue, stomach ache .
• In some children, the disease is accompanied by anemia, pallor, and increased blood pressure.
• If symptoms persist for a long time, there is a risk of chronic renal failure.

Features of the mixed form of chronic glomerulonephritis in children:

• Characterized by a combination of impurities of blood and protein in the urine, edema, increased blood pressure.
• Manifestations of high blood pressure: headaches and dizziness, lower back pain, lethargy, irritability, blurred vision, sometimes convulsions.
• Often there is anemia, pallor.
• The disease is severe, chronic renal failure develops very early.

The principles of diagnosis of chronic glomerulonephritis in children are the same as in adults. Treatment is prescribed strictly individually, depending on the form of the disease, the presence of chronic renal failure, complications, concomitant diseases.

How is it carried out dispensary observation children with chronic glomerulonephritis?

Dispensary observation is carried out until the child is transferred to an adult clinic:

• Chronic pyelonephritis. A disease in which inflammation mainly develops in the pelvis, calyx, tubular system of the kidneys.
• Amyloidosis. A disease in which the metabolism of proteins and carbohydrates is disturbed in kidney cancer

  Is it possible to drink alcohol with glomerulonephritis?

  Alcohol consumption negatively affects the state of all organs and systems, and the kidneys are no exception. Alcohol can aggravate the course of chronic glomerulonephritis, so it is recommended to completely abandon it. The taboo also applies to carbonated drinks.
  

  Is it possible to eat watermelons with glomerulonephritis?

  People suffering from chronic glomerulonephritis can eat watermelons. But since they contain a lot of liquid, it is recommended maximum amount consumed watermelons is determined depending on the form and stage of the disease. Consult with your doctor. Sometimes with chronic glomerulonephritis it is even recommended to arrange unloading "watermelon" days.
  latent form- the prognosis is favorable;
• hematuric and hypertonic form- the prognosis is serious;
• mixed and proteinuric form- the prognosis is unfavorable.

Chronic glomerulonephritis is a chronic immune inflammatory disease of the kidneys with a long-term persistent or recurrent urinary syndrome (proteinuria and / or hematuria) and a gradual deterioration of renal functions. Chronic glomerulonephritis is one of the main causes of CRF requiring program hemodialysis or kidney transplantation.

CLASSIFICATION

Classification of chronic glomerulonephritis in Lately has undergone a significant transformation. If earlier the classification was based on the clinical picture of the disease, now all over the world chronic glomerulonephritis is classified according to pathomorphological changes detected during histological examination kidney biopsy. To make a diagnosis according to pathomorphological criteria, a puncture biopsy of the kidney is necessary, which, however, is not always possible. In this regard, both classifications are still used, although preference is given to pathomorphological.

CLINICAL CLASSIFICATION

In our country, the clinical classification of chronic glomerulonephritis by E.M. Tareeva (1958, 1972, pl. 33-1).

Table 33-1. Clinical classification of chronic glomerulonephritis

Clinical forms*

Latent (chronic glomerulonephritis with isolated urinary syndrome)

Hematuric

Hypertensive

Nephrotic

Mixed (nephrotic syndrome in combination with hypertension)

Phases

Aggravation

Remission

stages chronic renal insufficiency

MORPHOLOGICAL CLASSIFICATION

According to pathomorphological features, they are distinguished the following forms chronic glomerulonephritis* (based on the classification of V.V. Serov et al., 1978, 1983, as well as later additions).

* It is believed that any of these pathomorphological forms can occur in both acute and chronic forms. Acute glomerulonephritis is most often represented by a diffuse proliferative variant, rapidly progressive glomerulonephritis - glomerulonephritis with "crescents". All other options are more characteristic of chronic glomerulonephritis, which is why we present the pathomorphological classification in the chapter on chronic glomerulonephritis.

Diffuse proliferative (discussed in chapter 30 "Acute glomerulonephritis").

With "Crescents" (discussed in Chapter 31 "Rapidly Progressive Glomerulonephritis").

Mesangioproliferative.

Membrane-proliferative (mesangiocapillary).

Membraneous with minimal changes.

Fibrillar-immunotactoid.

Fibroplastic.

For more information about each form of glomerulonephritis, see below in the section "Pathomorphology and pathogenesis of individual forms."

EPIDEMIOLOGY

It is noted in 5-10% of cases of idiopathic nephrotic syndrome in adults. Berger's disease is a hematuric variant with IgA deposits; predominantly develops in young men; one of the most common glomerulopathies.

Occurs equally often in men and women. Membranoproliferative glomerulonephritis accounts for 15% of cases of idiopathic nephrotic syndrome in children and 30% of cases of this syndrome in adults.

Membranous glomerulonephritis is usually noted at the age of 30-50 years, twice as often in men. It is found in 30-40% of cases of nephrotic syndrome in adults and in 5% of cases of nephrotic syndrome in children.

The peak frequency occurs at the age of 6-8 years. This morphological form causes nephrotic syndrome in children in 80% of cases.

Focal segmental glomerulosclerosis is the cause of 10-15% of cases of nephrotic syndrome in children and 15-25% of cases in adults.

Less than 1% of all cases of glomerulonephritis in adults.

ETIOLOGY

The etiology of chronic glomerulonephritis is presented in Table. 33-2.

Table 33-2. Etiology of chronic glomerulonephritis

Mesangioproliferative glomerulonephritis

IgA nephropathy (it is considered as a monosyndromic variant hemorrhagic vasculitis adults), chronic viral hepatitis B, Crohn's disease, Sjögren's syndrome, ankylosing spondylitis, adenocarcinomas of the gastrointestinal tract

Membrano-proliferative (mesangiocapillary) glomerulonephritis

idiopathic Secondary in SLE, cryoglobulinemia, chronic viral (hepatitis C virus) or bacterial infections, damage to the glomeruli of drugs by toxins

membranous glomerulonephritis

Cancers of the lung, intestines, stomach, breast and kidney (paraneoplastic glomerulonephritis), non-Hodgkin's lymphoma, leukemia, SLE (lupus glomerulonephritis), viral hepatitis B, syphilis, filariasis, malaria, schistosomiasis, exposure to drugs (gold and mercury preparations, penicillamine)

Glomerulonephritis With minimal changes

Acute respiratory infections, vaccination; sometimes occurs after the manifestation of an atopic phenotype (associated with HLA B12 Ag), when taking NSAIDs, rifampicin or interferon alfa; Fabry disease, diabetes mellitus, lymphoproliferative pathology (Hodgkin's lymphoma). In most cases, the cause remains unidentified.

focal segmental glomerulosclerosis

idiopathic Secondary: sickle cell anemia, renal transplant rejection, cyclosporine toxicity, surgical excision parts of the renal parenchyma, chronic vesicoureteral reflux, heroin use; congenital (nephron dysgenesis, later stages Fabry disease) defects; HIV infection (collapsing nephropathy)

Fibrillar-immunotactoid glomerulonephritis

Often associated with lymphoproliferative diseases ( chronic lymphocytic leukemia, Hodgkin's lymphoma)

fibroplastic glomerulonephritis

Outcome of most glomerulopathies

PATHOGENESIS

The same mechanisms are involved in the development and maintenance of immune inflammation as in acute glomerulonephritis. After the initiating damaging factors are triggered, the cells of the inflammatory infiltrate and the cells of the glomerulus secrete various mediators. Complement activation occurs, cytokines TNF-α, IL-1 and IL-6, γ-IF), growth factors (platelet and transforming growth factors-β), somatomedins, chemokines are produced, proteolytic enzymes and oxygen radicals are released, the coagulation cascade is activated, proinflammatory prostaglandins.

Proliferation and activation of mesangial cells play a key role in the processes of accumulation and changes in the structure of the extracellular matrix, which end in sclerosis of the glomerulus.

However, non-immune factors are also important for the further progression of glomerulonephritis.

Changes in hemodynamics (intraglomerular hypertension and hyperfiltration) occupy a leading place among the non-immune mechanisms of progression of chronic glomerulonephritis. An increase in intraglomerular pressure is facilitated by systemic hypertension, adaptive hypertrophy and hyperfunction of the remaining nephrons, a concomitant decrease in the tone of arterioles (more afferent than efferent) with the creation of a transcapillary pressure gradient. Against the background of high intraglomerular pressure, the permeability of the glomerular filter increases, which is accompanied by the deposition of various blood plasma macromolecules in the tissues of the nephron. Under the influence of intraglomerular hypertension, the renin-angiotensin-aldosterone system is activated. It has been established that angiotensin II promotes the synthesis of transforming growth factor-β, and the latter, in turn, stimulates the production of extracellular matrix. On the other hand, angiotensin II, directly or through the production of transforming growth factor-β, stimulates the expression of a plasminogen activator inhibitor, which leads to a decrease in local renal production of plasmin, which suppresses the formation of extracellular matrix components. This is one of the important mechanisms for the development of glomerulosclerosis and tubulointerstitial fibrosis.

There was a direct correlation between the progression of chronic glomerulonephritis and the presence of tubulointerstitial changes. In their development, proteinuria is of great importance, primarily with the release of albumin, transferrin. Excessively filtered proteins cause activation and release of vasoactive and inflammatory factors by tubular epithelium cells, among which chemokines, MCP-1, are of great importance ( M onocyte C hemoattractant P rotein-1 - monocytic chemotactic protein-1), RANTES ( R regulated upon A activation N normal T-cell E expressed and S ecreted - a factor that regulates the activation of normal T-cell expression and secretion) and endothelin. These factors cause an inflammatory interstitial response, marked accumulation of fibroblasts, and increased production of extracellular matrix, leading to an increase in tubulointerstitial fibrosis. Establishing the role of proteinuria in the development of tubulointerstitial fibrosis, which is the pathomorphological basis of renal failure, has played important role in the development of a nephroprotective strategy (see below).

Hyperlipidemia accompanying nephrotic syndrome contributes to the development of glomerulosclerosis. Lipid peroxidation products have a toxic effect on nephron cells, cause mesangial proliferation, and stimulate collagen synthesis.

Intercurrent recurrent infections urinary tract can play decisive role in deterioration of renal functions.

Recently, much attention has been paid to the role of obesity in the pathogenesis of chronic renal failure. Obesity is considered not only as an unfavorable "non-immune" factor in the progression kidney disease but also as an independent etiological factor kidney damage. In the early stages of obesity, a state of relative oligonephronia develops (deficit in the mass of nephrons in relation to increased body weight), which leads to an increased filtration load of the glomeruli (hyperfiltration). Hyperfiltration is initiated and maintained by metabolites and hormones of the adipose tissue itself, primarily leptin, through the activation of intrarenal hormones (anotensin II, endothelin) and the expression of transforming growth factor-β receptors on nephrocyte membranes with the development of glomerulo- and tubulointerstitial fibrosis.

PATHOMORPHOLOGY AND PATHOGENESIS OF INDIVIDUAL FORMS

Pathological examination of the renal biopsy is of great importance for diagnosis, treatment and prognosis.

MEsangioproliferative glomerulonephritis

Mesangioproliferative glomerulonephritis is characterized by mesangial enlargement due to mesangial cell proliferation and monocyte infiltration. For the activation and proliferation of mesangial cells, platelet-derived growth factor and transforming growth factor-β are most important.

IgA nephropathy is a form of mesangioproliferative glomerulonephritis with deposition of immune complexes containing IgA in the mesangium. In the development of IgA nephropathy, dysregulation of the synthesis or structure of IgA is important - a glycosylated isotype of IgA 1 is found in glomerular deposits. Abnormal IgA glycosylation is thought to help immune complexes containing IgA avoid clearance by cells of the reticuloendothelial system and promote their deposition in the glomeruli of the kidneys.

MEMBRANO-PROLIFERATIVE (MESANGIOCAPILLARY) GLOMERULONEPHRITIS

The main signs are the proliferation of mesangial cells and the expansion of the volume of the mesangial matrix with a diffuse increase in vascular loops, creating a picture of lobulation of the glomerulus, as well as a thickening of the basement membrane. The proliferation of mesangial cells is due to the influence of growth factors: epidermal growth factor, platelet growth factor; thrombospondin. The combination of damage to the glomerular membrane and mesangial proliferation causes the development of signs of nephrotic and nephritic syndromes. On ultrastructural examination, two main types of mesangiocapillary nephritis are distinguished: type 1 (with a subendothelial location of immune complexes) and type 2 ("dense deposit disease") with the detection of dense deposits within the basement membrane of the glomeruli. Approximately 30% of cases of mesangiocapillary nephritis type 1 are associated with infection with the hepatitis C virus.

MEMBRANOUS GLOMERULONEPHRITIS

Membranous glomerulonephritis is characterized by diffuse thickening of the glomerular basement membrane with the formation of subepithelial protrusions surrounding immune complex deposits. Immune deposits deposited under epithelial cells (podocytes) significantly disrupt their functions, which manifests itself massive proteinuria. Gradually, the basement membrane expands, bifurcates and "absorbs" immune deposits, forming the so-called "spikes". Sclerotic processes develop, capturing the collecting ducts and interstitium. Most probable cause development of this variant of glomerulonephritis is considered "molecular mimicry" and loss of tolerance to autoantigens. Circulating complement-fixing antibodies combine with antigen on podocyte processes to form in situ immune complexes. Complement activation leads to the formation of a membrane attack complex (C5b-C9) with damage to podocytes.

GLOMERULONEPHRITIS WITH MINIMAL CHANGES

Glomerulonephritis with minimal changes - with light microscopy and immunofluorescent examination, no pathological changes are detected, however, with electron microscopy, a fusion (smoothing) of the small legs of podocytes is found throughout the glomerular capillaries, which causes a loss of the negative charge of the glomerular basement membrane and, usually, a "large" proteinuria. Immune deposits are not found. Glomerular damage is associated with circulating permeability factors - lymphokines, due to an impaired T-cell response. In some patients, transformation into focal segmental glomerulosclerosis is observed.

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

Individual glomeruli (focal changes) are involved in the process, sclerosis of individual segments occurs in them (segmental changes); the rest of the glomeruli are intact. In the pathogenesis of focal segmental glomerulosclerosis, humoral permeability factors, as well as molecular mechanisms, are important. In familial forms of focal segmental glomerulosclerosis, mutations in the genes of several podocyte proteins (podocin, α-actin, nephrin) have been identified, with impaired expression and function of which a defect in the barrier properties of glomerular capillaries and the development of proteinuria are associated with these and some sporadic forms of focal segmental glomerulosclerosis. Sclerosis is accelerated by hyperfiltration and increased intraglomerular pressure, which contribute to excessive accumulation of extracellular matrix. Transforming growth factor-β, angiotensin II, reactive oxygen radicals, endothelins, inhibitors of cyclin-dependent kinase p21 and p27 are considered as modulators of this process. Frequent sign, in most cases preceding focal segmental glomerulosclerosis, - single "gentle" synechia of capillaries with a glomerular capsule. Subsequently, hyaline material appears in individual glomerular capillaries in the form of single or multiple spherical deposits, usually associated with the glomerular capsule. Foci of collapse and atrophy of the tubules in combination with stromal sclerosis are pathognomonic. The difficulty of morphological diagnosis of focal segmental glomerulosclerosis as an independent form is that the development various types glomerulonephritis may result in similar changes. What matters is the assessment of the dynamics morphological changes. Immune deposits are usually not found; in some cases, segmental luminescence of IgM is noted.

Allocate the so-called collapsing nephropathy, characterized by significant damage to podocytes and a pronounced collapse of the capillary loops of the glomeruli in the affected segments. The collapsing form of focal segmental glomerulosclerosis is the most common variant of kidney damage in HIV-infected people (marker - detection in podocytes and tubular cells of the HIV genome using PCR) and people who use heroin.

fibrillary-immunotactoid glomerulonephritis

On light microscopy, changes range from mesangial expansion and basement membrane thickening to proliferative glomerulonephritis and extracapillary crescents. Typical changes are detected by electron microscopy - extracellular amyloid-like fibrillar inclusions in the mesangium or capillary wall; they are distinguished from amyloid by a larger diameter, in addition, they do not stain with Congo red.

Fibroplastic glomerulonephritis is characterized by a significant severity of fibrotic processes: adhesions (synechia) of the vascular lobules with the capsule are formed, capillary loops of the glomerulus are sclerosed. Sclerosis of the glomerular capillaries is due to the progressive accumulation in the mesangium and beyond of the extracellular matrix synthesized by mesangial cells under the influence of transforming growth factor-β. If the integrity of the capillary walls is violated, plasma components penetrate into the extracapillary space, and the resulting fibrin provokes the development of sclerotic changes. In general, fibroplastic changes are the final link in the "damage-inflammation-fibrosis" chain.

CLINICAL PICTURE

The clinical picture of chronic glomerulonephritis varies significantly depending on the clinical and morphological variant.

CLINICAL PICTURE DEPENDING ON THE CLINICAL OPTION

CHRONIC GLOMERULONEPHRITIS WITH ISOLATED URINARY SYNDROME (LATENT FORM)

This form accounts for up to 50% of all cases of chronic glomerulonephritis. The disease proceeds unnoticed by the patient (edema and hypertension are absent). The study reveals proteinuria (no more than 1-2 g / day), microhematuria, leukocyturia, cylindruria (hyaline and erythrocyte cylinders). The relative density of urine is not changed. Perhaps a primary latent and secondary latent course (with partial remission of another clinical form of chronic glomerulonephritis). In turn, latent chronic glomerulonephritis can transform into nephrotic or hypertensive forms. The development of CRF against the background of the latent form is slow (for 10-15 years or more).

HEMATURIC FORM

Changes in the urine - microhematuria and usually unexpressed proteinuria (less than 1.5 g / day). Extrarenal symptoms (edema, hypertension) are absent. CKD develops slowly.

HYPERTONIC FORM

The course is long, before the development of chronic renal failure takes 20-30 years. The clinical picture is dominated by symptoms of increased blood pressure (headaches; visual disturbances - a veil, flashing "flies" before the eyes; characteristic changes fundus; pain in the precordial region; signs of left ventricular hypertrophy). Hypertension is initially intermittent and well tolerated by patients. The urinary syndrome is minimally expressed - slight proteinuria, sometimes microhematuria, cylindruria. Unlike hypertension, these changes in the urine in chronic glomerulonephritis are observed from the very beginning of the disease. AH gradually becomes stable and resistant to drug therapy, and in the terminal period often becomes malignant. Against the background of a significant increase in blood pressure, the development of acute left ventricular failure is possible.

NEPHROTIC FORM

This form is characterized by the development of nephrotic syndrome - daily proteinuria above 3.5 g / day (more precisely, more than 3.5 g / 1.75 m 2 in 24 hours), hypoalbuminemia, hyperlipidemia followed by lipiduria, hypercoagulation, edema. The key symptom is massive (“big”) proteinuria associated with kidney filter damage, i.e. basement membrane and podocytes. Other manifestations of nephrotic syndrome are derived from proteinuria and can be expressed to varying degrees.

Thus, the higher the level of proteinuria, the lower the content of albumin in the blood. The consequence of hypoalbuminemia is a decrease in plasma oncotic pressure, which leads to the appearance of edema. A decrease in intravascular fluid volume leads to activation of the renin-angiotensin-aldosterone system, as well as an increase in tone. sympathetic department vegetative nervous system. There is a release of antidiuretic hormone and inhibition of the synthesis of atrial natriuretic factor. The combination of neurohumoral mechanisms leads to a delay in the body of salts and water.

Urinary excretion of transferrin explains the microcytic hypochromic anemia associated with nephrotic syndrome.

Urinary loss of cholecalciferol-binding protein leads to vitamin D deficiency and, consequently, to hypocalcemia and secondary hyperparathyroidism.

Urinary excretion of thyroxine-binding protein is accompanied by a decrease in the concentration of thyroxine in the blood.

Hypoalbuminemia significantly changes the pharmacokinetics of drugs transported by the blood in a protein-bound state, which significantly increases the risk of side and toxic effects of drugs in conditions of nephrotic syndrome.

Hyperlipidemia may result from urinary loss of a protein that regulates lipid homeostasis; in addition, with a decrease in plasma oncotic pressure, there is an increase in the synthesis of LP by the liver. In most patients, the concentration of triglycerides, total cholesterol, LDL increases, and in severe nephrotic syndrome - VLDL. Changes in lipid metabolism can contribute to atherosclerotic vascular changes (the development of myocardial infarction in patients with long-term nephrotic syndrome has been noted) and non-immune progression of glomerulopathy.

The tendency to hypercoagulability is associated with the excretion of antithrombin III in the urine, changes in the concentrations of proteins C and S, hyperfibrinogenemia due to increased synthesis of fibrinogen by the liver, combined with a weakening of fibrinolysis processes. In addition, in conditions of nephrotic syndrome, hyperaggregation of platelets is noted.

The tendency to hypercoagulability in nephrotic syndrome determines the increased risk of renal vein thrombosis and PE. The probability of thrombosis of the renal veins is highest in conditions of nephrotic syndrome with membranous and membrane-proliferative glomerulonephritis, as well as in amyloidosis. Renal vein thrombosis (as a complication of nephrotic syndrome) can be acute (abdominal pain develops, gross hematuria, left-sided dropsy of the testicular membranes, GFR decreases) or chronic (malosymptomatic, often difficult to diagnose).

In addition to a large amount of protein, erythrocytes, leukocytes (mainly lymphocytes) and cylinders can be found in the urine in a small amount. An increase in ESR and anemia are also characteristic.

MIXED FORM

This form suggests a combination of nephrotic syndrome and hypertension. It is usually noted in secondary chronic glomerulonephritis (for example, in SLE, systemic vasculitis). It has poor prognosis: CRF develops over 2-3 years.

TERMINAL GLOMERULONEPHRITIS

This form is considered as the final of any glomerulonephritis (the allocation of this form is not recognized by all authors). The clinical picture corresponds to CRF and eliminates the differences between the forms of chronic glomerulonephritis that led to its development. Recently, the term " chronic illness kidneys" (CKD - C chronic K idney D isease) for all forms of kidney damage with an indication of the stage of CRF, which is justified by the solution of common tactical tasks: renal replacement therapy and kidney transplantation.

CLINICAL PICTURE DEPENDING ON THE MORPHOLOGICAL FORM

MEsangioproliferative glomerulonephritis

Mesangioproliferative glomerulonephritis manifests as an isolated urinary syndrome, acute nephritic or nephrotic syndromes.

IgA nephropathy (Berger's disease) is the most common clinical variant (50-60% of all cases), observed mainly in people under 25 years of age, with a predominance in men. Characterized by episodes of gross hematuria with pain in lumbar region associated with nasopharyngeal or gastrointestinal infections. Unlike acute post-infectious glomerulonephritis, the time of onset kidney symptoms coincides with the influence of provoking factors. Proteinuria is insignificant, so there is no edema or they are mild. BP is within the normal range. Approximately 30% of cases (usually in people older than 25 years, regardless of gender) have persistent microhematuria with concomitant proteinuria varying degrees expressiveness. In 10% of patients, acute nephritic or nephrotic syndromes may develop.

In most cases, the course is benign, however, in 20-40% of patients, progression to the final stage of chronic renal failure is noted in terms of 5 to 25 years.

MEMBRANO-PROLIFERATIVE (MESANGIOCAPILLARY) GLOMERULONEPHRITIS

Membrano-proliferative glomerulonephritis (mesangiocapillary) often begins with acute nephritic syndrome (like acute glomerulonephritis); approximately 50% of patients develop nephrotic syndrome. Possible isolated urinary syndrome with hematuria. Severe hypertension, hypocomplementemia and anemia are characteristic, cryoglobulinemia is possible, especially in patients chronic hepatitis C. The course is steadily progressive, and a rapidly progressive variant is also observed.

MEMBRANOUS GLOMERULONEPHRITIS

In 80% of cases it is manifested by nephrotic syndrome and more often than in other cases, it is complicated by the development venous thrombosis including renal vein thrombosis.

GLOMERULONEPHRITIS WITH MINIMAL CHANGES

In the foreground in the clinical picture - nephrotic syndrome. Hypertension and renal failure are rare, the process tends to resolve spontaneously. Proteinuria is massive, mainly due to albumin, but small amounts of IgG and α 2 -macroglobulin are detected. Gradually, the selectivity of proteinuria disappears, and it becomes non-selective. In 20-30% of cases, microhematuria is noted.

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

In almost 70% of cases, persistent nephrotic syndrome is observed. In the urinary sediment, erythrocytes and leukocytes are found. AG - important component clinical picture. The development of chronic renal failure is natural, in 20% of patients kidney failure noted at the onset of the disease. A severe progressive course is characterized by a collapsing form of focal segmental glomerulosclerosis associated with HIV infection.

fibrillary-immunotactoid glomerulonephritis

It is manifested by severe proteinuria, in 50% of cases - nephrotic syndrome. Most patients have hematuria, hypertension, and impaired renal function. In some cases, monoclonal gammopathy is found. The course is progressive.

fibroplastic glomerulonephritis

In 43% of cases, nephrotic syndrome persists. Characterized by chronic renal failure, associated with the loss of functional properties of sclerotically altered nephrons.

All these clinical variants and morphological forms of chronic glomerulonephritis differ in the duration of the course, the rate of formation of renal failure, and the tendency to relapse the activity of the process. Consideration should be given to the importance of identifying an exacerbation, which sometimes manifests itself as a picture of rapidly progressive glomerulonephritis, which requires an urgent decision on the issue of more active treatment (see Chapter 31 "Rapidly progressive glomerulonephritis").

COMPLICATIONS

Complications of chronic glomerulonephritis - renal failure, left ventricular failure against the background of hypertension, stroke, intercurrent infections (including urinary tract infections), thrombosis, nephrotic crisis. The latter is characterized by fever, abdominal pain, migratory erythema erysipelas, and the development of hypovolemic shock. The pathogenesis of nephrotic crisis continues to be studied, importance give activation of the kallikrein-kinin system, DVS. Special mention should be made of possible complications of active immunosuppressive therapy - cytopenias (agranulocytosis, etc.), infections (including "steroid tuberculosis"), osteoporosis, hemorrhagic cystitis, hyperglycemic conditions.

DIAGNOSTICS

Diagnosis of chronic glomerulonephritis is based on the definition of the leading syndrome - isolated urinary, acute nephritic, nephrotic syndromes, hypertension syndrome. Additional sign consider symptoms of CKD.

SYNDROME DIAGNOSIS

NEPHROTIC SYNDROME

Nephrotic syndrome is most often noted in glomerulonephritis with minimal changes, membranous glomerulonephritis (both primary and secondary), focal segmental glomerulosclerosis, diabetic glomerulosclerosis, amyloidosis of the kidneys.

ACUTE SYNDROME

Acute nephritic syndrome is a combination of hematuria, proteinuria, hypertension and, often, decreased renal function. Possible with rapidly progressive glomerulonephritis, mesangiocapillary glomerulonephritis, mesangioproliferative glomerulonephritis, exacerbation of lupus nephritis.

ARTERIAL HYPERTENSION

Hypertension in combination with proteinuria and minimal changes in urinary sediment occurs, in addition to chronic glomerulonephritis, with diabetic nephropathy, kidney damage as part of hypertension. In the latter case, hypertension significantly outpaces the onset of renal symptoms; more often than with glomeruloneritis, hypertensive crises occur.

URINARY SYNDROME

The urinary syndrome usually consists of symptoms of hematuria, proteinuria, leukocyturia with lymphocyturia, cylindruria, and their combinations (Table 33-3).

Table 33-3. Causes of isolated hematuria

. Hematuria. Based on these reasons, isolated hematuria is an indication for excretory urography, cystoscopy and selective angiography. In most nephrological diseases, hematuria is combined with proteinuria.

. Proteinuria may be associated with inflammatory (glomerulonephritis) or non-inflammatory (diabetic nephropathy, amyloidosis) glomerular or tubulointerstitial lesions various etiologies(see chapter 36 "Tubulointerstitial nephropathies"). In the latter case, proteinuria is never massive. Filling proteinuria is distinguished - a special variant, more often "large" proteinuria, associated with multiple myeloma with the presence of paraprotein in the blood (hyperproteinemia). There is also benign proteinuria (occurs with a feverish reaction, hypothermia, emotional stress accompanies heart failure and obstructive sleep apnea syndrome). The term "benign" reflects a favorable prognosis for kidney function. Orthostatic proteinuria occurs only in an upright position; it is commonly seen in adolescents, may be constant or intermittent, and has a favorable prognosis.

. Leukocyturia with glomerulonephritis, it often has the character of lymphocyturia (more than 20% of leukocytes in the urinary sediment are lymphocytes).

KIDNEY BIOPSY

Needle biopsy of the kidney is performed to determine the morphological form of chronic glomerulonephritis, which is necessary for an adequate choice of treatment tactics. This procedure contraindicated in the following cases.

Having a single functioning kidney.

Hypocoagulation.

An increase in venous pressure in big circle circulation - with right ventricular failure.

Suspicion of renal vein thrombosis.

Hydro and pyonephrosis.

Polycystic kidney disease.

Aneurysm of the renal artery.

Disturbances of consciousness.

Suspicion of a malignant neoplasm.

DIFFERENTIAL DIAGNOSIS

Chronic glomerulonephritis must be differentiated from chronic pyelonephritis, acute glomerulonephritis, nephropathy of pregnancy, chronic tubulointerstitial nephritis of various etiologies, alcoholic kidney damage, amyloidosis and diabetic nephropathy, as well as kidney damage in systemic diseases connective tissue(primarily SLE) and systemic vasculitis, multiple myeloma, thrombosis of the renal and inferior vena cava (see "Complications" above).

Chronic pyelonephritis is characterized by asymmetry of the lesion, changes in the pyelocaliceal system, exacerbations with fever and chills, bacteriuria, neutrophiluria (with glomerulonephritis in the urine sediment - lymphocytes, microbial flora is absent).

In acute glomerulonephritis, there is often a connection with the transferred streptococcal infection, however, unlike IgA nephropathy, the exposure is 10-14 days. Characterized by acute onset and spontaneous recovery. Usually children and young people get sick.

Chronic tubulointerstitial nephritis is manifested by violations of tubular functions: proteinuria (not reaching the values ​​characteristic of nephrotic syndrome), polyuria, a decrease in relative density and a violation of urine acidification, hyperproteinemia, etc.

If amyloidosis is suspected, the detection of background pathology (chronic inflammation, primarily - rheumatoid arthritis; multiple myeloma; Mediterranean familial fever). The persistence of normal or enlarged kidney size and nephrotic syndrome in CKD increases the likelihood of amyloidosis (as well as diabetic nephropathy). Of decisive importance is tissue biopsy (detection of amyloid in the tissues of the kidney, gums, rectum, adipose tissue).

If the patient has diabetes or its complications (eg, diabetic retinopathy), scanty changes in urinary sediment, normal or slightly enlarged kidneys, the diagnosis of diabetic nephropathy is likely even without testing. needle biopsy kidneys.

Nephropathy of pregnancy: symptoms of kidney damage appear in the second half of the gestational period, accompanied by high blood pressure and other signs of pre- and eclampsia. special form severe preeclampsia - HELLP syndrome ( H emotion, E levated L iver enzymes, L ow P latelet), in which, along with hypertension and kidney damage, hemolysis, liver damage and thrombocytopenia develop.

The features of alcoholic nephropathy include persistent painless microhematuria in combination with minimal or moderate proteinuria, a persistent increase in the concentration of IgA in the blood and hyperuricemia.

Kidney damage in SLE (lupus nephritis) and systemic vasculitis is accompanied by signs systemic disease(articular and skin syndromes; detection of LE cells, hypergammaglobulinemia, autoantibodies, such as ANCA, etc.).

TREATMENT

Treatment for chronic glomerulonephritis includes:

Elimination of the etiological factor (including during exacerbation);

Elimination from the blood of the CEC and other factors of immune inflammation;

Conducting immunosuppressive therapy;

Reducing elevated blood pressure and other effects that reduce intraglomerular hypertension;

Correction of hyperlipidemia and hypercoagulability;

Reduction of edema;

Removal of products of nitrogen metabolism (hemodialysis and hemosorption).

With advanced CRF, chronic hemodialysis and kidney transplantation are indicated.

One of promising directions in nephrology recent years- development of nephroprotective therapy aimed at inhibiting the progression of kidney diseases by influencing the common non-immune links of their pathogenesis. Among the approaches to nephroprotection, important is the leveling of the nephrotoxic effects of proteinuria, which ultimately leads to remodeling of the tubolointerstitial tissue - tubulointerstitial fibrosis (see below).

GENERAL ACTIVITIES

It is necessary to avoid hypothermia, physical overexertion. Adverse temperature conditions(work in conditions of increased and low temperature environment). special care must be observed in the event of acute respiratory diseases or exacerbation of chronic foci of infection (tonsillitis, sinusitis, etc.). In these situations, bed rest is indicated, antibiotic therapy is performed.

A low-protein diet is recommended (positive effect on intraglomerular hypertension). The exception is cases of nephrotic syndrome with hypoalbuminemia below 30 g/l, when protein restriction is ineffective. A strict low-protein diet (0.3 g / kg per day) in patients with chronic renal failure is possible against the background of simultaneous administration of drugs essential amino acids and their ketoanalogues (for example, "Ketosteril" 10-12 tablets per day). In nephrotic syndrome rational hypocholesterol diet and food containing polyunsaturated fatty acid (sea ​​fish, sunflower oil).

IMMUNOSUPPRESSIVE THERAPY

This type of therapy involves the appointment of two groups of drugs - HA and cytostatics (both individually and in combination). The expediency of their use significantly depends on the morphological form of glomerulonephritis.

GCs are indicated in the presence of nephrotic syndrome or severe proteinuria with high probability development of nephrotic syndrome. Contraindications to the appointment of HA in chronic glomerulonephritis are considered high (poorly correctable) hypertension and chronic renal failure. The drugs of this group are most effective in mesangioproliferative glomerulonephritis and glomerulonephritis with minimal changes. With membranous glomerulonephritis, the effect is doubtful. With membranoproliferative glomerulonephritis and focal segmental glomerulosclerosis, GCs are less effective. Two routes of administration of HA are used.

◊ Orally: the average dose is in terms of prednisolone 1 mg / kg / day (usually it is prescribed for a period of 2 months) followed by a gradual decrease (5 mg / week to a dose of 30 mg / day, then 2.5-1, 25 mg/week until complete withdrawal).

◊ Pulse therapy involves intravenous drip of methylprednisolone at a dose of 1000 mg 1 time per day for 3 days in a row. Usually prescribed for severe nephrotic syndrome, rapid progression of the disease.

Cytostatics (cyclophosphamide 2-3 mg/kg/day, chlorambucil 0.1-0.2 mg/kg/day, cyclosporine 2.5-3.5 mg/kg/day) are indicated for active forms glomerulonephritis with a high risk of progression of renal failure, as well as in the presence of contraindications for the appointment of GC, the absence therapeutic effect or the development of pronounced side effects during their use (in the latter case, combined use is preferred, which allows to reduce the dose of HA). Preparations of this group are prescribed orally; cyclophosphamide also in the form of pulse therapy at 15 mg / kg (or 0.6-0.75 g / m 2 of body surface) intravenously monthly.

The combined use of GC and cytostatics is considered more effective than GC monotherapy. The Ponticelli scheme provides for alternating cycles of therapy with prednisolone (1 month duration) and chlorambucil (1 month duration) for 6 months. At the beginning of the monthly course of treatment with prednisolone, a three-day pulse therapy with methylprednisolone is performed, then prednisolone is prescribed at 0.4 mg/kg/day orally for the remaining 27 days. A monthly course of treatment with chlorambucil involves oral administration of the drug at a dose of 0.2 mg / kg / day.

Selective immunosuppressants: drugs from the calcineurin group - cyclosporine, an inhibitor of nucleotide synthesis - mycophenolate mofetil, an inhibitor of intracellular signal transmission from growth factor receptors - sirolimus. The greatest experience has been accumulated in relation to cyclosporine (see below - "Treatment of individual morphological forms"). Indications for cyclosporine therapy are frequent recurrences of GC-sensitive nephrotic syndrome (with glomerulonephritis with minimal changes) and GC-resistant nephrotic syndrome (with focal segmental glomerulosclerosis and membranous glomerulonephritis). Due to the possible nephrotoxic effect, the use of cyclosporine is limited in severe sclerotic changes with impaired renal function and severe hypertension.

ANTICOAGULANTS AND ANTIAGGREGANTS

The preparations of these groups of drugs are used as part of combined regimens for the hypertensive form of glomerulonephritis and chronic glomerulonephritis with isolated urinary syndrome and reduced kidney function. Dipyridamole is prescribed at a dose of 400-600 mg / day, clopidogrel - at a dose of 0.2-0.3 g / day.

COMBINATION THERAPY

It implies the appointment of a three-component scheme (cytostatics or GCs, antiplatelet agents, sodium heparin) or a four-component scheme (GCs, cytostatics, antiplatelet agents, sodium heparin with a switch to warfarin or phenindione).

ANTIHYPERTENSIVE AND NEPHROPROTECTIVE THERAPY

Ideally, it is necessary to compensate not only systemic arterial, but also intraglomerular hypertension. It is necessary to limit the intake of table salt to 3-5 g / day and observe bed rest with high blood pressure. but greatest effect provides drug therapy.

ACE inhibitors and AT1 angiotensin receptor blockers, in addition to lowering blood pressure, reduce intraglomerular capillary pressure, hyperfiltration and proteinuria. In addition, drugs of this group reduce the pro-inflammatory effects of proteinuria, preventing proteinuria-induced activation of the transcription factor NF-κ B in tubular epithelial cells and their release of chemokines into the interstitium, inhibit tubulointerstitial fibrosis through inhibition of the synthesis by macrophages and proliferating fibroblasts of the main profibrogenic cytokine - transforming growth factor - β and by reducing the formation of a plasminogen activator inhibitor, which inhibits the processes of proteolytic degradation of the extracellular matrix. In connection with these multilateral effects, ACE inhibitors and AT1 angiotensin receptor blockers are currently considered as the central link in the nephroprotective strategy. early start therapy ACE inhibitors and / or blockers of AT1 receptors of angiotensin to a greater extent contributes to the inhibition of the progression of chronic renal failure, and their appointment is justified even in situations not accompanied by hypertension.

◊ Of the ACE inhibitors, enalapril 5-20 mg / day in 1-2 doses is most often used, fosinopril 10-20 mg 1 time per day, trandolapril 2-8 mg 1 time per day, and from angiotensin AT1 receptor blockers - losartan 25-100 mg / day in 1-2 doses, valsartan 80-160 mg 1 time per day, irbesartan 150-300 mg 1 time per day. The dose of drugs is adjusted depending on the level of blood pressure, serum concentrations of creatinine and potassium. These two groups of drugs can be combined with each other to achieve a more pronounced antihypertensive and antiproteinuric effect.

◊ Contraindications for the appointment of ACE inhibitors: severe renal failure (hyperkalemia, serum creatinine concentration over 500-600 µmol/l), bilateral stenosis renal arteries.

◊ In case of hyperkalemia or poor tolerance of ACE inhibitors, they are prescribed in smaller doses in combination with slow-acting blockers calcium channels non-dihydropyridine series.

Of the blockers of slow calcium channels, drugs of the non-dihydropyridine series are preferable (verapamil 120-480 mg / day in 2-3 doses, diltiazem 180-360 mg / day in 2-3 doses). Blockers of slow calcium channels of the dihydropyridine series can reduce GFR, so they can be used in severe hypertension in combination with other drugs. Slow calcium channel blockers, in addition to antihypertensive effects, also have an antiproteinuric effect, although to a lesser extent than ACE inhibitors. The antiproteinuric effect of this group of drugs is associated mainly with a decrease in the severity of systemic hypertension and antiplatelet action.

Statins (inhibitors of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase) also have nephroprotective properties, and the anti-inflammatory effect of statins is no less important for the implementation of nephroprotection than their antilipidemic effect. Statins inhibit the expression of plasminogen activator inhibitor, increase the synthesis of tissue plasminogen activator. Prescribe simvastatin 20-40 mg/day, fluvastatin 20-80 mg/day, etc.

Currently, the possibility of using new classes of drugs for nephroprotective purposes, such as vasopeptidase inhibitors, endothelin-1 antagonists, anti-chemokine drugs (ATs that neutralize chemokines, antagonists of chemokine receptors), inhibitors of protein kinase that activates the transcription factor NF-κ B, etc. Some of them have already passed successful preclinical testing.

ANTIOXIDANT THERAPY

Antioxidants (eg, tocopherol, trimetazidine) have attracted the attention of many researchers, but convincing evidence of their effectiveness has not yet been obtained.

TREATMENT OF EDEMAS

With severe edematous syndrome, salt intake is limited and bed rest is prescribed. Furosemide is the most commonly used diuretic. Do not use hydrochlorothiazide (impairs kidney function); caution is needed with potassium-sparing diuretics (danger of hyperkalemia), guanethidine and minoxidil (sharp retention of sodium ions and decrease in GFR).

TREATMENT OF SELECTED MORPHOLOGICAL FORMS

In any form of chronic glomerulonephritis, bed rest, diet, symptomatic therapy (described above) are prescribed, if possible, the etiological factor (infection, tumor) is eliminated. Features of the treatment of individual morphological forms mainly relate to pathogenetic immunosuppressive therapy.

MEsangioproliferative glomerulonephritis

In slowly progressive variants, including patients with IgA nephropathy with episodes of gross hematuria and minimal proteinuria, there is no need for immunosuppressive therapy. In patients with a higher risk of progression (severe proteinuria or nephrotic syndrome, AH), HA is prescribed at a dose of 1 mg/kg/day for 2-3 months; in case of relapses, therapy with cytostatics is increased. It is possible to use three- and four-component schemes. However, the effect of active immunosuppressive therapy on the long-term prognosis (duration of renal function) in this form of glomerulonephritis remains unclear.

MEMBRANO-PROLIFERATIVE (MESANGIOCAPILLARY) GLOMERULONEPHRITIS

There is no convincing data on the advantage of any pathogenetic treatment for this form of glomerulonephritis. The importance of treating the underlying disease is undeniable. Hypertension control required; preference is given to ACE inhibitors. In the presence of nephrotic syndrome and a decrease in kidney function, combined therapy with GC and cyclophosphamide orally or in the form of pulses for at least 6 months is justified, it is possible with the addition of antiplatelet agents (dipyridamole) and anticoagulants (warfarin, phenindione).

MEMBRANOUS GLOMERULONEPHRITIS

Concerning use of immunosuppressive therapy the opinion is ambiguous. Many believe that immunosuppressants should only be used in patients with high proteinuria and/or renal insufficiency to avoid its progression, but there are also advocates. early use"aggressive" approaches. With monotherapy with GC, it is not possible to achieve remission, best results achieved with the combined use of HA and cytostatics, for example, according to the Ponticelli scheme with monthly alternation of methylprednisolone and chlorambucil. There is evidence of the successful use of pulse therapy with cyclophosphamide 1 g intravenously monthly in membranous glomerulonephritis. However, due to frequent spontaneous remissions, it is necessary in each specific situation weigh the benefits and harms of treatment with cytostatics. To date, it seems appropriate in patients with membranous glomerulonephritis without nephrotic syndrome (with its possible complications) and normal function kidneys to prescribe ACE inhibitors with antiproteinuric and nephroprotective purposes.

GLOMERULONEPHRITIS WITH MINIMAL CHANGES

Glomerulonephritis with minimal changes is treated with GC. 90% of children and 50% of adults with this form of glomerulonephritis go into remission within 8 weeks of treatment with prednisone. Prednisolone in adults is prescribed at 1-1.5 mg / kg for 4 weeks, then at 1 mg / kg every other day for another 4 weeks. With an increase in the duration of treatment up to 20-24 weeks, remission occurs in 90% of adult patients. Immunosuppressants - cyclophosphamide 2-3 mg / kg / day or chlorambucil 0.1-0.2 mg / kg / day are used in cases where GCs in an adequate dose are ineffective, and also if after long-term use they cannot be canceled due to the occurrence of relapses.

If attempts to prevent recurrence of nephrotic syndrome with the help of alkylating agents fail, cyclosporine is prescribed at 3-5 mg / kg / day (children at 6 mg / m 2). Long-term treatment, the dose of the drug begins to be reduced no earlier than 6-12 months after achieving remission; the minimum maintenance dose (usually 2.5-3.0 mg/kg) is sometimes taken even for 2 years. During treatment with cyclosporine, its concentration in the blood should be monitored. The occurrence of complications (hypertension, hyperkalemia, an increase in serum creatinine by 30% of the initial level or more) requires dose adjustment or discontinuation of the drug. The lack of effect of cyclosporine treatment with a sufficient concentration in the blood is assessed after 3-4 months of administration, after which the drug is canceled.

FOCAL SEGMENTAL GLOMERULOSCLEROSIS

Immunosuppressive treatment is not effective enough. A decrease in the severity of proteinuria is noted in 20-40% of cases with 8-week GC treatment, the effectiveness increases to 70% with a duration of therapy of 16-24 weeks. Patients with nephrotic syndrome are prescribed prednisolone 1-1.2 mg/kg daily for 3-4 months, then every other day for another 2 months, after which the dose is gradually reduced until the drug is completely discontinued. The effectiveness of cytostatics (cyclophosphamide, cyclosporine) is approximately 50-60%, with the combined use of cytostatics with GC, the frequency of subsequent exacerbations decreases. Cyclophosphamide can be used orally at 2-3 mg/kg/day or as pulse therapy intravenously at 1000 mg/day once a month. With resistance to GC, preference is given to cyclosporine (orally at 3-5 mg / kg / day), remissions are achieved in 25-50% of patients.

fibrillary-immunotactoid glomerulonephritis

Treatment of fibrillary-immunotactoid glomerulonephritis has not been developed. Data have been obtained on the effectiveness of kidney transplantation.

fibroplastic glomerulonephritis

Diffuse form of fibroplastic glomerulonephritis - rather contraindication than an indication for active immunosuppressive therapy, since the resolution of sclerotic processes does not occur in this case, and the resulting side effects drugs are quite serious.

TREATMENT OF CHRONIC GLOMERULONEFRITIS ACCORDING TO CLINICAL FORMS

Carried out when it is impossible to perform a kidney biopsy. For all clinical forms first of all, it is necessary to influence the etiological factor, if it can be established (infection, tumors, drugs). Even when obtaining data from a morphological study of kidney tissue, clinical criteria for assessing the severity and prognosis of glomerulonephritis are important for choosing adequate therapy.

CHRONIC GLOMERULONEPHRITIS WITH ISOLATED URINARY SYNDROME

In the latent form (without hypertension and unchanged kidney function), active immunosuppressive therapy is not indicated; conduct regular monitoring with control of blood pressure and creatinine levels in the blood. With proteinuria more than 1 g / day, ACE inhibitors are prescribed.

HEMATURIC FORM

Note the intermittent effect of prednisolone and cytostatics. Patients with isolated hematuria or hematuria associated with mild proteinuria are recommended long-term use ACE inhibitors (even with normal blood pressure) and dipyridamole.

HYPERTONIC FORM

An indispensable rule is the correction of hypertension, primarily with ACE inhibitors. It is necessary to strive to reduce the level of blood pressure to 120-125/80 mm Hg. With exacerbations (especially by the type of acute nephritic syndrome), cytostatics are used as part of a three-component scheme. GC can sometimes be prescribed as monotherapy at a dose of 0.5 mg / kg / day (in terms of prednisolone) orally or at the same dose as part of combined regimens.

NEPHROTIC FORM OF CHRONIC GLOMERULONEPHRITIS

The nephrotic form of chronic glomerulonephritis is considered as an indication for the appointment of prednisolone (methylprednisolone) orally and in the form of "pulse therapy", cytostatics, antiplatelet agents and anticoagulants. Diuretics and antihyperlipidemic drugs are used.

CHRONIC GLOMERULONEFRITIS OF MIXED TYPE

Chronic glomerulonephritis mixed type are treated actively with the use of three- or four-component schemes. Use antihypertensive drugs, diuretics.

SPA TREATMENT

The main therapeutic factor is the effect of dry and warm climate.

Indications: latent form of glomerulonephritis, hematuric form without gross hematuria, hypertensive form with blood pressure not higher than 180/105 mm Hg, nephrotic form in remission.

Contraindications: exacerbation of glomerulonephritis, severe renal dysfunction, high blood pressure, gross hematuria. Initial manifestations CRF is not considered a contraindication for spa treatment.

DISPENSERIZATION

Patients with chronic glomerulonephritis should be under the constant supervision of a therapist (nephrologist). Clinical examination rules for chronic glomerulonephritis are developed taking into account clinical classification.

. Latent and hematuric form. Frequency of visits - 2 times a year. Observed parameters: body weight, blood pressure, fundus, urinalysis according to Nechiporenko, general analysis and blood electrolytes, proteinogram, protein content in daily urine, serum creatinine concentration, urea, Reberg-Tareev test. Annual ultrasound of the kidneys. With hematuria, the patient is referred for a consultation with a urologist.

. Hypertensive form- the same research methods, however, observation should be carried out 1 time in 1-3 months.

. Nephrotic and mixed form. The volume of studies is the same, the frequency of observation is 1 time in 1-2 months. Special attention must be expressed edematous syndrome and electrolyte composition of the blood in connection with the use of diuretics.

Exacerbation of any form of chronic glomerulonephritis is considered an indication for hospitalization. In case of temporary disability (more than 2 months) without regression of symptoms of the disease, it is necessary to resolve the issue of disability.

FORECAST

Mesangioproliferative glomerulonephritis. Proteinuria reaching the threshold of nephrotic syndrome has an unfavorable prognostic value. IgA nephropathy has a benign course in most cases, but 20-40% of patients reach terminal stage HPN. Poor prognostic factors for IgA nephropathy: elderly age, male, proteinuria above the nephrotic threshold (3.5 g/day), impaired renal function at the onset of the disease, detection of extracapillary "crescents" or hyalinosis of the glomeruli, interstitial fibrosis during biopsy.

membranous glomerulonephritis. Nephrotic syndrome with membranous glomerulonephritis spontaneously disappears in 40% of patients, recurs in 40% and proceeds continuously with slow development of CRF in 20% of patients. Unfavorable prognostic factors: male gender, advanced age, persistent hypertension, severe proteinuria and hyperlipidemia, deterioration of renal function, late recognition of paraneoplastic genesis of glomerulonephritis. Complications include renal vein thrombosis and pulmonary embolism.

Membrano-proliferative (mesangiocapillary) glomerulonephritis in general has an unfavorable prognosis, since with this form pathogenetic therapy ineffective. To factors high risk progression include renal failure at the time of diagnosis, age over 50 years, hypertension, detection of extracapillary cellular "crescents" in the glomeruli of the kidneys.

Glomerulonephritis With minimal changes predictively evaluate favorably. Spontaneous remissions are observed in 30-40% of children, but in adulthood they are much more rare.

focal segmental glomerulosclerosis. Unfavorable prognostic factors indicating the possibility of rapid progression include hypertension in combination with persistent treatment-resistant nephrotic syndrome and thrombotic complications.

Fibrillar-immunotactoid glomerulonephritis progresses to the end stage of chronic renal failure in 1-10 years.

fibroplastic glomerulonephritis - a step to a secondarily wrinkled kidney and chronic renal failure; the reverse development of fibroplastic changes does not occur.

pregnant with glomerulonephritis constitute a risk group for complications during pregnancy and childbirth.