Membranous proliferative glomerulonephritis. Antihypertensive and nephroprotective therapy. positive immunofluorescence for IgG, C3 and properdin

Membranous - proliferative glomerulonephritis (MPGN, mesangiocapillary glomerulonephritis) is a glomerulonephritis characterized by mesangial proliferation and thickening of the glomerular basement membrane. Statistical data. 5-20% of all cases of glomerulonephritis, from 30 to 40% of cases of nephrotic syndrome in children and adults. Men and women get sick equally often.

Code by international classification diseases ICD-10:

N00.2

Causes

Etiology. It can be idiopathic and secondary (with SLE, cryoglobulinemia, infection, damage to the glomeruli by drugs and toxins).

Pathomorphology. There are three (sometimes four) MPGN type. All forms are characterized by proliferation of mesangial cells, an increase in the volume of the mesangial matrix, and thickening of the basement membrane. Type I (idiopathic) is characterized by an intact basement membrane, subendothelial immune deposits, and positive immunofluorescence for IgG, C1q, C4, C2, and properdin. Type II (dense deposit disease) - intramembranous deposits and positive immunofluorescence for IgG, C3 and properdin. Type III - combined signs of membranous glomerulonephritis (fragmentation of the basement membrane) and type I MPGN. Type IV - subendothelial and subepithelial deposits.

Symptoms (signs)

Clinical picture. Nephrotic syndrome- mixed form (with arterial hypertension, erythrocyturia, azotemia). In 1/3 of patients, rapidly progressive renal failure develops with edema and severe arterial hypertension.

Diagnostics

Laboratory data. Hypocomplementemia.

Diagnostic tactics. Mixed form nephrotic syndrome with relatively rapid development renal failure always suspicious of MPGN. The diagnosis is verified by biopsy.

Treatment

TREATMENT

Diet (see Chronic glomerulonephritis).

Treatment primary disease(HBV - and HCV - infections, etc.).

Immunosuppressive therapy.. GCs are usually ineffective.. For proteinuria<3 г/сут и нормальной СКФ иммунодепрессивная терапия не показана.. При нефротическом синдроме: преднизолон в дозе 1 мг/кг внутрь или в сочетании с циклофосфамидом (хлорамбуцилом, азатиоприном) ежедневно в течение 2 мес или в виде пульсов 1 р/мес в течение 1-2 лет.. 3 - компонентная схема: цитостатики, антикоагулянты и антиагреганты (дипиридамол в дозе 400-600 мг/сут или ацетилсалициловая кислота в дозе 250-320 мг/сут); тем не менее преимущества в контролируемых исследованиях не доказаны.. Циклоспорин 3-5 мг/кг/сут в сочетании с низкими дозами преднизолона (данные неконтролируемых исследований).

Flow. Progressive to chronic renal failure, remissions are rare. The 10-year survival rate is no more than 50%, the prognosis is better with type I. Recurrence of the disease is possible in the transplanted kidney.

Reduction. MPGN is membranous proliferative glomerulonephritis.

ICD-10. N00.2 Acute nephritic syndrome, diffuse membranous glomerulonephritis

MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS

Membranoproliferative GN (MPGN) is a disease and, at the same time, a morphological variant of glomerular lesion, including heterogeneous pathological conditions with various pathogenetic mechanisms of development: deposition of immune complexes, chronic thrombotic microangiopathy, chronic graft rejection, etc. The histological picture is characterized by glomerular hypercellularity, expansion of the mesangial matrix, thickening of the capillary wall.

Pathogenetically, MPGN initially differs from other variants of chronic glomerulonephritis by the presence in most patients hypocomplementemia.

There are primary (idiopathic) and secondary variants of MPGN. Previously, primary MPGN was divided into 3 types. Currently, only type I with subendothelial deposits is classified as MPGN. Due to differences in pathogenesis, the nature of histological changes, course and prognosis (including after kidney transplantation), BPD (previously classified as MPGN type II) is now removed from the MPGN group and assigned to the group of C3 glomerulopathies (without Ig deposits) . Type III does not differ significantly from type I MPGN, both in morphological picture and in clinical course and prognosis, and therefore was excluded.

Epidemiology. MPGN used to be more common, but due to successful prevention and treatment of infectious diseases, the incidence of MPGN has decreased in the last decade in developed countries in Europe and North America. In general, the incidence of primary MPGN in economically developed countries is very low, while it remains high in developing countries. Idiopathic MPGN usually affects children and adolescents. MPGN I is more common. BPD is a rare disease, accounting for only 5% of all primary cases of MPGN. Just like MPGN I, it is typical for children and adolescents.

MPGN type I

Pathogenesis. MPGN type I, or now simply MPGN, develops as a result of the deposition of circulating immune complexes in the subendothelial space of the GBM and mesangium, which leads to the activation of complement through the classical pathway. Hypocomplementemia is characteristic. These processes lead to proliferation of mesangial cells and expansion of the mesangial matrix. Mesangial cells form cytoplasmic projections that pass under the endothelial cells and synthesize GBM material consisting of type IV collagen (like mesangium). Thus, the capillary wall of the glomerulus changes from three-layer to five-layer:

1) endothelial cell;

2) newly formed GBM;

3) cytoplasm of the mesangial cell;

4) initial GBM with deposits;

5) podocytes.

The glomeruli acquire a multicellular, lobulated appearance, the lumens of the capillary loops narrow. This process is diffuse in nature.

When stained with Jones stain, double basement membranes produce a typical “tram rail” appearance. With IF, granular luminescence of IgG, C3, and less commonly IgM occurs along the periphery of the capillary wall. MPGN is also characterized by damage to the tubules and interstitium. Inflammatory infiltration of neutrophils and mononuclear cells, macrophages is detected. Detection of MPGN in adults requires the exclusion of chronic antigenemia. More common is secondary MPGN associated with viral hepatitis B, C, bacterial endocarditis, SLE, Sjogren's syndrome, chronic lymphocytic leukemia, α1-antitrypsin deficiency, against the background of shunt nephritis. With viral hepatitis C, cryoglobulinemic GN develops, which is morphologically characterized, in addition to the MPGN variant, by the presence of capillary thrombi (cryoglobulins and immunoglobulins) and arteritis. In EM, deposits and masses in the lumens of capillaries are organized in the form of tubes or tactoid changes. With IF, the glow of IgM, C3, IgG not only along the periphery of the capillary loops, but also in the lumens of the capillaries, corresponding to capillary thrombi.

Clinical picture. MPGN manifests as nephritic syndrome, nephrotic syndrome, or a combination of both. At the onset of the disease, a third of patients have hypertension and renal failure. However, it can be difficult to distinguish it from OPIIGN. But APIGN is characterized by an improvement in its course with relief of the main symptoms of nephritic syndrome during the first weeks. In type I MPGN, symptoms are stable or become more severe. There are no spontaneous remissions of the disease; it is chronic and progresses to the development of ESRD within 5-10 years.

Treatment. MPGN is difficult to treat. However, in idiopathic type I MPGN, immunosuppressive therapy can slow progression. In children and adolescents, long-term treatment with PZ at a dose of 60 mg/m2 in an alternating course followed by a slow dose reduction with a total maximum treatment duration of up to 5 years in some cases led to a decrease in the level of proteinuria and an improvement in renal survival, although no subsequent randomized studies were conducted . In adults and children with MPGN with UA and a progressive decrease in GFR, oral cyclophosphamide or MMF is proposed as induction therapy, in combination with low doses of corticosteroids in alternating mode or daily (KDIGO, 2012). Other drugs of choice may be rituximab and, to a lesser extent, calcineurin inhibitors (increased hypertension, more rapid decline in renal function). Due to the small number of observations, it is difficult to draw conclusions regarding effectiveness. Many patients are prescribed maintenance therapy (symptomatic, diuretic, antihypertensive, nephroprotective).

In secondary MPGN, which develops against the background of infection (viral hepatitis B and C), systemic diseases (cryoglobulinemia, SLE, etc.), and tumor diseases, the histological changes do not differ from those in the idiopathic variant. Treatment requires the above-mentioned types of maintenance therapy in combination with treatment of the trigger factor for the development of MPGN - infection. In the presence of hepatitis C virus, combination antiviral therapy is used. In this case, the stage of CKD and patient tolerance of drugs should be taken into account. In patients with mixed cryoglobulinemia, nephrotic level PU and decreased GFR, it is recommended to prescribe antiviral therapy in combination with plasmapheresis, rituximab or CP in combination with GCS pulses (KDIGO, 2012).

Below is a medical history of the patient, who was observed from the onset of the disease until kidney transplantation.

Figure 4.7. Membranoproliferative glomerulonephritis type I. (Microphotograph - A.V. Sukhanov, Moscow, 2004).

Girl M., 9 years old, nephrotic + nephritic syndrome.

A. Lobulated appearance of the glomeruli due to pronounced proliferation of mesangial cells, an increase in the mesangial matrix, stasis of mononuclear cells and neutrophils in the lumens of the capillary loops. Light microscopy, PAS x100.

B. On EM, five levels of the capillary wall can be distinguished, starting from the capillary lumen: 1) endothelial cell; 2) newly formed GBM; 3) cytoplasm of the mesangial cell; 4) initial GBM with subendothelial deposits; 5) podocytes. Stasis of mononuclear cells in the lumen of the capillary. Electron microscopy.

On light microscopy: 20 glomeruli, all increased in size, lobular (Figure 4.7A). Hypercellularity due to proliferation of mesangiocytes, endothelial cells and retention of leukocytes in glomerular loops. The wall of the capillary loops is significantly thickened. Diffuse degenerative changes in the tubules. Mild focal infiltration of the interstitium with mononuclear cells. Arteries and arterioles are not changed. Immunofluorescence microscopy reveals a pronounced (+++) glow of IgG and C3 along the capillary loops of granular glomeruli and in the mesangium. Electron microscopic examination revealed many mesangial, subendothelial and a few intramembranous deposits of the immune complex type. Many subendothelial deposits are in the process of resolution. In many areas of the capillary loops, new basement membrane formation and mesangial interposition are noted (Figure 4.7B). Significant increase in mesangial matrix and proliferation of mesangiocytes. There are many lymphocytes and segmented leukocytes in the capillary loops.

Morphological conclusion: Membranoproliferative glomerulonephritis type 1.

Clinical and morphological diagnosis: Steroid-resistant nephrotic syndrome with hematuria and arterial hypertension with membranoproliferative glomerulonephritis type 1.

The child was transferred to therapy with an alternating course of prednisolone with a reduction to 40 mg/m2/48 h in combination with an ACE inhibitor, against which for the first 3.5 years the girl’s GFR remained normal - 101 ml/min, despite persistent proteinuria 1-1 .5 g/s.

This clinical case demonstrates the effect on renal survival of long-term therapy with prednisolone in an alternating regimen in combination with ACE inhibitors in membranoproliferative GN type 1. Subsequently, during exacerbations of nephrotic syndrome, the girl received CsA, CP, MMF, but without a lasting effect. After 8 years from the onset of the disease, due to the development of the terminal stage of CKD, a preemptive (without dialysis) kidney transplantation was performed.

The term was first used in 1958 by Kark et al. and then included in the classifications of Fiaschi et al. (1959); Blainer et al. (1960), etc. However, from the very beginning this term suffered from uncertainty. Some believe that membranous-proliferative glomerulonephritis is a simple combination of proliferative and membranous changes (it was stated above that “true membranous glomerulonephritis” is not accompanied by cellular proliferation); the existence of focal and diffuse forms of membranous-proliferative glomerulonephritis is also allowed (Fiaschi et al., 1959; V.V. Serov, 1973, etc.). The difficulty lies in the fact that some researchers still attribute any thickening of the basement membranes of capillaries - focal or diffuse - to membranous glomerulonephritis (Schwartz et al., 1970). However, there is a form of glomerulonephritis for which the combination of diffuse thickening of the basement membranes of the capillaries with proliferation of glomerular cells is characteristic. In this case, lobulation is usually expressed in the glomeruli. Such changes were first described by Allen in 1951 as lobular glomerulonephritis (which, in particular, gave rise to a debate about the thickness of the basement membranes in lobular glomerulonephritis). Subsequently, it was shown that diffuse thickening of the basement membranes in combination with diffuse proliferation of mesangial and endothelial cells of the glomeruli can be used as a criterion for membranous proliferative glomerulonephritis, characterized by morphological features and a unique clinical picture (Burkholder et al., 1970; West and McAdams, 1970; B. N. Tsibel, 1972).

Rice. 14. Membranous proliferative glomerulonephritis (biopsy).

Lobulation of the glomerulus, increased number of cells, thickened basement membranes of capillaries along the periphery of the lobules. Hematoxylin-eosin staining, UV. 300.
Rice. 15. Membranous proliferative glomerulonephritis (biopsy).

Diffuse thickening of the basement membranes of capillaries, most of which do not accept silver. The thickened mesangial skeleton is intensely silvered. Impregnation according to Jones-Mowry. Uv. 1300.

The glomeruli usually have a lobular structure (Fig. 14) and in this respect resemble lobular glomerulonephritis (Mandalenakis et al., 1971). The number of cells is increased by 2-2.5 times, most of them are located in the centers of the lobules. The basement membranes of the capillaries are thickened, look like homogeneous ribbons and are stained pink with hematoxylin-eosin, yellow with picrofuchsin, and red with the PAS reaction. When using some other stains, a significant change in the tinctorial properties of the basement membranes is detected, which is not found in any other lesions of the glomeruli. When stained with azocarmine, basement membranes, as a rule, do not perceive aniline blue and are stained red with azocarmine. However, the most clear change in the tinctorial properties of the basement membranes is found during silvering using the Jones method or its modifications. Basal membranes do not perceive silver and are stained with an additional dye (for example, orange G). At the same time, thickened and disintegrated mesangial fibers are silvered quite intensely (Fig. 15). This change in the tinctorial properties of the basement membranes can serve as a clear differential sign of membranous proliferative glomerulonephritis (Burkholder et al., 1970; West and McAdams, 1970).

For the first time, such changes in basement membranes in nephrotic syndrome were observed by Jones (1957) and attributed them to the evolution of membranous glomerulonephritis. However, as the observations of other authors and our own studies show, these changes are also found in cases with a clinical duration of the disease of several months, and the spiny projections characteristic of membranous glomerulonephritis do not occur for any duration of the disease. Mandalenakis et al indicate a predominant proliferation of mesangial cells and an increase in the mesangial matrix in this form of glomerulonephritis, due to which lobulation becomes distinct in the glomeruli. (1971); Michael et al. (1971); West and McAdams (1970); Burkholder et al. (1970). The essence of changes in basement membranes and the pathogenesis of membranous-proliferative glomerulonephritis are unclear. The disease occurs predominantly in adolescence and is characterized by nephrotic syndrome, a long, relatively benign course with spontaneous remissions, low levels of serum complement, and lack of effect from steroid and immunosuppressive therapy (West and McAdams, 1970). Burkholder et al. (1970) found deposits of IgG and IgM globulin in the basement membranes. On the contrary, Holland and Benett (1972) found predominantly βIC-globulin deposits in the basement membranes, and only a small amount of IgG. The authors doubt the immune nature of this form of glomerulonephritis and note the discrepancy between the constantly low level of complement and long-term remissions during the course of the disease. In this regard, the evolution of morphological changes in the glomeruli is of interest. Herdman et al. (1970) observed a decrease in the thickness of basement membranes during repeated biopsy in the case of membranous proliferative glomerulonephritis. During repeated biopsy with clinical remission, we established not only a decrease in the thickness of the basement membranes, but also the partial formation of new ones with the restoration of their tinctorial properties. The process occurred with the participation of podocytes and was accompanied by a decrease in the number of mesangial cells to normal (Fig. 16). These changes may correspond to clinical remission of the disease. Perhaps complement fixation causes the destruction of the capillary basement membranes' own glycoproteins and the infiltration of the membranes with plasma glycoproteins; The tinctorial properties of the deposited protein differ from membranes.

Rice. 16. Repeated biopsy of the same patient as in Fig. 15, taken after 2 years.

The capillary membranes are much thinner compared to the previous study, in some places they are indistinguishable from normal ones, some of them are silvered. The mesangial skeleton is also much thinner. Impregnation and increase are the same,
what is in fig. 15.

Restoring tinctorial properties is only possible with restoration of the membrane itself. The disease is characterized by a relatively long course, but gradually the glomeruli can hyalinize and renal failure develops (Jones, 1957; Mandalenakis et al., 1971). The tinctorial properties of the membrane, characteristic of this form of glomerulonephritis, are preserved in the remaining glomeruli and can be used for differential diagnosis and on sectional material. Changes in the tubules correspond to the phase of the disease - with nephrotic syndrome, protein and lipids can accumulate in the epithelium of the proximal convoluted tubules; with renal failure, tubular atrophy and nephron desolation are noted.

Differential diagnosis in the early stages of the disease, when proliferation is less pronounced, it is carried out with membranous glomerulonephritis. The only reliable diagnostic sign is the loss of argyrophilia by the basement membranes with silvering according to Jones - Mowry in the case of membranous proliferative glomerulonephritis and the presence of silvering spines on a somewhat thinned membrane in membranous glomerulonephritis. In later stages of the disease, in the presence of a pronounced lobular structure of the glomeruli, proliferation and thickening of the membranes, differentiation is carried out with lobular glomerulonephritis. And in this case, a reliable sign is the ratio of basement membranes to silver. In lobular glomerulonephritis, argyrophilia of the basement membranes with silvering according to Jones - Mowry is always preserved or increases as the basement membranes thicken, while in membranous-proliferative glomerulonephritis, the affinity of the membranes for silver is completely or partially (in cases of membrane restoration) lost *.

* To obtain satisfactory results when silvering, the thickness of paraffin sections should not exceed 3 microns.

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Membranous-proliferative glomerulonephritis (mesangiocapillary glomerulonephritis)
Membranous proliferative glomerulonephritis (MPGN) is a chronic diffuse form of proliferative glomerulonephritis with specific histological and immunological changes and electron microscopic findings. changes in the kidneys can be caused by some unrelated systemic disorders (for example, lipodystrophy, a1-antitrypsin deficiency, congenital absence of the C2 component of the complement system), but usually MPGN acts as a primary disease. Its two types are well known: I and II. Clinically they are not distinguishable. Renal manifestations include nephrotic syndrome, acute nephritis, nephrosonephritis, asymptomatic proteinuria, rapidly progressive (crescentic) glomerulonephritis, chronic renal failure, or recurrent gross hematuria. Hypertension and azotemia are usually prominent. Despite the fact that the specific etiology is unknown, changes in the kidneys are caused by immunological mechanisms: type I is characterized by a typical pathway of activation of the complement system with the deposition of an immune complex, type II is characterized by an alternative pathway of activation with the nephrotic factor S3 detected in the serum. Girls get sick more often than boys, usually in adolescence or young adulthood. Both types are differentiated according to histological, immunological and electron microscopic examination. The histological picture in both types is significantly the same: the glomeruli increase in size, the mesangial cells proliferate quite uniformly, and the capillary walls thicken. There may be a marked increase in the amount of matrix with a tendency for the glomeruli to become lobulated. Epithelial crescentic formations often appear. In the initial stage, neutrophilic infiltration of the glomeruli is possible.
In type I, subendothelial accumulations and interposition of the mesangial matrix between the endothelium and the basement membrane lead to thickening of the capillary walls, giving the appearance of a double loop. In type II, thickening of the capillary walls occurs as a result of the deposition of dense refractive masses in the basement membrane itself, giving it a ribbon-like appearance. Electron microscopic examination reveals electron-dense masses in the middle part of the basement membrane, replacing and expanding the dense plate. The same masses are found in the mesangium, glomerular capsule and tubular basement membrane. Type II MPGN is sometimes called dense disease
deposits or with dense intramembrane deposits. Some authors distinguish type III of the disease with contiguous subepithelial and subendothelial deposits that destroy the basement membrane and cover the lamina densa.
The results of immunological studies indicate some differences in the manifestations of type I; The most common of these include granular deposits containing IgG, IgM, C3, Clq and C4 along peripheral loops with variable fluorescence of mesangial structures. In many patients, accumulations of properdin and S3 occur. In contrast, patients with type II MGPN show large accumulations of SZ in round, tuberous deposits within the mesangium and very little, if any, in intramembranous deposits; properdin is usually not found.
Serum complement in type I is represented by a reduced amount of Clq and C4 and a variable decrease in the amount of C3, on the basis of which the classical pathway of activation of the complement system is assumed, while in type II there is a constant decrease in the amount of this component, which is associated with an alternative activation pathway; Clq and C4 levels remain within normal limits. Nephritic factor S3 is detected more often than in type I.
Type I is 2-3 times more common than type II, which can develop in patients with lipodystrophy. Type II is more likely to recur in the transplanted kidney. Girls more often than boys suffer from the idiopathic form of the disease, which first appears in adolescence or early adolescence. Almost 1/3 of patients with MPGN have nephrotic syndrome, although this accounts for less than 10% of children suffering from it; In some patients, the picture of acute nephrosonephritis is expressed, and in the rest, massive hematuria, asymptomatic proteinuria and chronic progressive renal failure occasionally appear. Proteinuria is not selective. Hypertension and a decrease in GFR are noted in approximately 1/3 of patients, almost 10% develop renal failure within 2 years and the long-term prognosis should be approached with great caution, since in half of the cases the disease progresses and within 10 years can develop into chronic renal disease failure. There is no consensus regarding the treatment of patients.
Prednisone (an alternative high-dose regimen), dipyridamole, anticoagulants, and antimetabolic agents may be used. The results obtained by the authors of this section indicate that the rate of progression of the disease can be reduced and the patient’s condition will improve if he is treated early (in the acute stage) with azathioprine and prednisone every other day and treatment is continued for several years. For patients with end-stage renal failure, the most optimal solution is a kidney transplant; Although the disease may spread to the transplanted kidney, it may not be accompanied by significant clinical manifestations.

Bilateral inflammation of the glomeruli of the kidneys is a serious infection called glomerulonephritis. Often this disease occurs after pharyngitis, tonsillitis, scarlet fever and other streptococcal infections. Proliferative glomerulonephritis is distinguished by the increased permeability of glomerular membranes.

What is the disease?

The kidneys contain glomeruli, they consist of blood capillaries. They filter the blood and participate in the removal of excess fluid. If the glomeruli are damaged, the kidneys function abnormally, which leads to the formation of renal failure. This condition can be life-threatening and requires urgent treatment.

There are different subtypes of this disease.

Diffuse proliferative glomerulonephritis characterized by alternating periods of exacerbation and remission. This disease is caused by damage to the blood vessels of the glomeruli.
Mesangial proliferative glomerulonephritis– this is weak or moderate diffusion. MPGN is characterized by a clear increase in capillaries in the glomeruli.
Membranous proliferative glomerulonephritis – noticeable thickening of the basement membrane.
Mesangial proliferative glomerulonephritis– morphological type of the disease, characterized by a moderate or weak diffuse increase in the capillary bed in the glomeruli

These are the most common types of glomerulonephritis, but other types of this disease are also classified in medicine.

Causes

The kidneys purify the blood that enters them, and then through the capillaries it enters the glomeruli. There, fluid passes through the glomerular membranes and primary urine is formed. If the membranes are highly permeable, then the disease develops. If you take a test, protein and red cells will be found in the collected urine. Doctors have not yet figured out the mechanism leading to such disorders.

There is a hypothesis that this is a response of the human immune system, because inflamed glomeruli are the cause of the appearance of antibodies. With the disease, different parts of the body swell, then the protein content in the urine decreases. The disease occurs in acute or chronic (sluggish) form. As the disease progresses, chronic kidney failure may occur.

Symptoms of the disease

Appetite decreases or disappears completely.
Urine has a brown tint due to the blood it contains.
24-hour fatigue and apathy.
Intense thirst.
Pain in the lumbar region.
Swelling on the face.
Cough, fluid accumulation in the lungs.
Night muscle cramps.
Brown coating on the tongue.
Smell of ammonia from the mouth.
The skin is yellow.

Types of diagnostics

If characteristic symptoms occur, laboratory tests are prescribed. The presence of respiratory tract infection is taken into account. To diagnose glomerulonephritis, clinical and laboratory data will be needed. Existing chronic infections, past experiences of acute glomerulonephritis and other systemic diseases are taken into account.

A general urinalysis is prescribed, red blood cells, protein, leukocytes are detected in it, and the specific gravity of the liquid changes.
To clarify the condition of the kidneys, Reberg, Zimnitsky, and Nicheporenko samples are taken.
Blood test for the presence of hepatitis virus.
Biochemistry of blood.
Determination of antibodies to streptococcus in the blood.
Immunogram.

From instrumental studies, the following tests are prescribed.

Ultrasound of the kidneys.
Kidney biopsy.
Excretory urography.
Electrocardiogram.

Consultations with other specialists are also required: ENT doctor, ophthalmologist, dentist - to detect infectious foci and diagnose the fundus of the eye, as well as hypertensive syndrome.

Types of treatment

The basic treatment regimen used is:

hospitalization in the nephrology department;
in the acute period - bed rest;
restrictions in the diet: water no more than a liter for adults, salt – 3, and protein – up to 80 g/day, reduce the consumption of fats and carbohydrates (stick to two weeks);
diuretic and antihypertensive therapy;
antiplatelet therapy (prescribed aspirin, dipyridamole);
anticoagulant therapy;
in the presence of a bacterial infection - antibacterial therapy (for this it is better to take a swab from the nasopharynx to study the type of bacteria and their sensitivity to the drug);
treatment of all concomitant diseases.

If membranous proliferative glomerulonephritis is treated with antibiotics, then calcium and other desensitizing agents, ascorbic acid and other vitamins are prescribed. In the mouth, foci of infection are sanitized daily with the help of medications, inhalations, and physiotherapy.

Diuretics are used to reduce swelling. The most effective are saluretics that have a beneficial effect on the heart. If there is arterial hypertension, then osmotic diuretics are indicated. Immunosuppressants are prescribed for nephrotic effect without signs of remission. During treatment, it is necessary to strictly monitor the level of leukocytes on the 10th and 14th days after pulse therapy. At some stages of treatment, increased fluid intake is recommended to stimulate frequent urination. For long-term acute forms of the disease with the presence of nephrotic syndrome, the use of medications that stimulate renal microstimulation is indicated.

If the disease is acute, the patient must be hospitalized - there is no other way of treatment. At first, the patient spends two weeks (and sometimes more) in bed, under a warm blanket - this ensures uniform warming of the body and normalizes kidney function. It is advisable for the patient to remain in this position until the swelling disappears (in severe cases, this may take a couple of months).

low-fat milk;
soft cheese;
orange juice;
egg;
cooked meat;
fish.

Fish soup, broths, jelly and other dishes containing extractive components are prohibited.

Some patients (not all) are recommended to do dry fasting for a couple of days. After the end of the hunger strike, you should adhere to the above-described diet for more than a year. Then you can remove all dietary restrictions, except for the amount of table salt. For three years after discharge, the patient is prohibited from heavy physical activity, hypothermia, and overheating.

Dispensary observation lasts three years after receiving the first normal test - the patient regularly visits the doctor and has his urine tested. This becomes especially relevant after suffering from acute respiratory viral infections, influenza, other colds and injuries. If a relapse is suspected, an in-depth examination is carried out. If there is deterioration, the patient is hospitalized. Before final deregistration, cholesterol levels and blood spectrum are checked.

Regarding treatment with folk remedies, the verdict of nephrologists is unequivocal - this method will not bring complete recovery. However, traditional methods are good as an additional factor in treatment, but not in the acute phase, but when the patient’s condition has returned to normal. Treatment with herbs during an exacerbation is fraught with a sad outcome, even death - urgent hospitalization and the use of potent medications are necessary. When the condition has stabilized, the doctor himself will prescribe diuretics based on birch leaves, strawberries, cornflower flowers, corn columns, etc.

Doctors do not advise women who have recovered from glomerulonephritis to become pregnant in the next three years. If it was not possible to avoid a relapse during pregnancy, then you need to follow the recommendations:

rest during the day in bed;
limit salt and liquid in the diet;
there is no need to limit protein (as is advised to other, non-pregnant patients);
use symptomatic therapy, exclude etiological treatment;
some types of physiotherapy (endonasal electrophoresis).

Ancoagulants that cause hemorrhagic syndrome and death in the fetus are contraindicated.

Disease prevention

To prevent the development of pathology, it is imperative to cure all foci of inflammation present in the body (sinusitis, tonsillitis, pneumonia, dental diseases). It should be taken into account that membranous proliferative glomerulonephritis and other kidney diseases are complications from other infectious diseases. Due attention should be paid to oral hygiene and the prevention of hypothermia. To develop immunity, you need to harden yourself and eat right, not smoke or abuse alcohol.

Membranous proliferative glomerulonephritis and certain kidney diseases are very dangerous pathologies. In this case, self-medication is especially dangerous - death is a real possibility. Even doctors prefer to treat such diseases in a hospital rather than at home.