Iga jade. A method for the treatment of iga-nephropathy. Berger's disease - pathogenetic mechanisms

Berger's disease, also known as IgA, is one of the most frequently reported forms of glomerulonephritis, - renal pathologies, where the lesion is the glomerular apparatus of the organ. The disease was first described in 1968 and has since been identified as a nosological unit. It is noteworthy that men are more likely to get sick (about two times), and the highest incidence rate is recorded in East Asian countries. The causes of the disease have not been identified for certain, there are only a few hypotheses. However, the mechanism of the development of pathology has been studied, methods for its diagnosis and therapy have been developed.

Berger's disease - pathogenetic mechanisms

The essence of the disease is the deposition of immune complexes based on immunoglobulin A in the mesangial (intervascular) tissue of the kidney parenchyma, which leads to dysfunction of the organ and the appearance of hematuria (blood excretion in the urine). Normally, immunoglobulin A provides local immunity mucous membranes of many organs and consists of heavy and light molecular chains. IgA nephropathy is morphologically characterized by the fact that immune complexes based on short protein chains of immunoglobulin A are deposited in the intervascular tissues of the kidneys.

The onset of pathological renal changes is associated with increased production of immune proteins by bone marrow tissues and some lymphoid cells, as a result of which the content of abnormal protein molecules in the blood serum rises sharply. Pathological immune complexes begin to filter through the vascular wall in the renal parenchyma and gradually fill the mesangial tissue, reacting with the bioactive substances contained here, which leads to the formation of growth factors and cytokines that stimulate the proliferation (division and growth) of the cells located here. This leads to the growth of the intervascular tissue of the kidneys, which compresses the vessels (blood circulation is disturbed) and partially renal glomeruli(glomeruli).

What becomes the trigger mechanism for pathological changes? Although the exact causes leading to the production of pathological protein complexes have not been established, based on the association of the onset of Berger's disease with certain diseases, several hypothetical versions have been developed:

contribute to the development of glomerulonephritis immune disorders occurring in the body with systemic connective tissue diseases (ankylosing spondylitis, SLE, Bechterew's disease, rheumatoid arthritis);
infectious factors - multiple formation of pathological immune complexes in response to some fungal, bacterial and viral infections (tuberculosis bacillus, some strains of streptococci, herpes and hepatitis viruses);
the influence of alimentary (food) causes is studied - milk proteins, substances contained in cereals (gluten);
considering the possibility genetic disorders(local chromosomal mutations).

Important! In favor genetic theory occurrence of Berger's disease IgAnephropathy), evidenced by the predominance of the incidence in representatives of one of the sexes (men) and the uneven racial distribution of the incidence of pathology.

Symptoms of the disease

The onset of Berger's disease usually occurs in childhood and early adolescence. A sign that becomes decisive for the suspicion of incipient glomerulonephritis is the appearance of blood (hematuria) in the excreted urine, which occurs simultaneously with inflammatory processes in the upper respiratory tract (pharyngitis, tonsillitis, laryngitis). Often we are talking about macrohematuria, when bloody inclusions in the urine are determined visually. Although in many cases the presence of erythrocytes in urine is determined only by microscopy of the sediment, then they speak of microhematuria.

The following external influences are capable of increasing the excretion of blood in the urine during this period:

UV irradiation ( long stay in the sun);
intestinal infections accompanied by inflammation of the intestinal wall;
vaccinations;
physical activity of considerable intensity.

During an exacerbation, they may manifest themselves pain (drawing pains in the lower back), there are transient increases in blood pressure. In most cases, the disease proceeds without pronounced symptoms (latent course). Hematuria is determined only when examining the urine sediment under a microscope (3-4 erythrocytes in the field of view), with functional tests, slight albuminuria is detected (up to 0.5 g of protein molecules per day). With an asymptomatic course from the side of the kidneys, some patients during the period of exacerbation note pain in the muscles and joints, slight hyperuricemia is determined in the laboratory, mild neurological disorders(polyneuropathy).

IgA nephropathy is characterized by the fact that kidney function is practically not affected. If acute renal failure is observed in some patients, then renal failure completely disappears after the end of the exacerbation. If the nephrotic syndrome develops, it is characterized by an increase in the content of lipids and protein in the urine (up to 3-4 g). Against the background of a significant decrease in the protein content in the blood serum and the loss of the required blood volume, edema develops, which first covers lower limbs, gradually going up.

In severe cases, edema becomes generalized (almost all organs swell), which manifests itself in the form of ascites (fluid in abdominal cavity) and anasarca (very edematous whole body). Such complications develop extremely rarely, mainly in patients suffering from other severe comorbidities.

Diagnostic methods for IgA nephropathy

Analysis is used in the diagnosis of Berger's disease clinical manifestations in combination with laboratory and instrumental studies. Main external symptom, leading to suspect this type of nephropathy is hematuria, which is detected visually or when laboratory research urine. Diagnostic value has a biochemical blood test, during which an increased content of immunoglobulin A and immune complexes formed on its basis are detected.

The diagnosis of IgA nephropathy is confirmed by biopsy. On histological analysis a fragment of the renal parenchyma is taken. The presence of this disease is proved by the growth (reproduction) of mesangial cells and interstitial substance detected by microscopy ( connective tissue). Histochemical analysis is also used, during which the accumulation (in the form of merged granules) of immune complexes is determined, where immunoglobulin A predominates.

Now, to determine the state of the renal tissues, modern radiation diagnostic techniques (ultrasound, magnetic resonance (MRI) and radiographic (RT) tomography) are additionally used. These studies help not only to formulate correct diagnosis, but also in the differentiation of Berger's disease from other urological conditions accompanied by similar symptoms, and above all - hematuria. These diseases include nephrolithiasis (the formation of kidney stones), kidney cancer, ureteral tuberculosis.

Treatment methods for nephropathy, diet for Berger's disease

In the treatment of Berger's disease, several methods can be applied. Medical tactics depends on the severity of the pathology, the presence / absence of renal failure, the age of the patient. If there is a connection between exacerbations of nephropathy with infectious diseases, sanitation of foci of bacterial lesions (removal of tonsils) is carried out or antibiotic therapy is prescribed (a course of antibiotics after determining the sensitivity of microflora to them).

Much attention is paid to maintaining normal (below 135/85) blood pressure figures. For this, drugs are used that inhibit the conversion of inactive angiotensin into an active form (Captopril, Kapoten), as well as drugs that block receptors that respond to the influence of this bioactive substance. If the course of the disease is not characterized by severe complications and progression of pathology, medical tactics limited to symptomatic treatment.

In cases of a progressive course of Berger's disease (proteinuria more than 1 gram, pronounced proliferative, especially necrotic processes in the glomeruli), preparations of hormones of the adrenal cortex are prescribed. Glucocorticoids have a pronounced immunosuppressive effect (suppress perverse immune processes) and a strong non-specific anti-inflammatory effect.

In a particularly severe course, especially in combination with concomitant systemic pathologies, cytostatic (antineoplastic) drugs (Cyclosporine, Cyclophosphamide) are prescribed. If the nephrotic syndrome is expressed, and the protein in the urine exceeds 3.5 g, a combination of glucocorticoid hormones and cytostatics is allowed.

In the treatment of Berger's disease, attention is paid to diet food patients. Although the diet is compiled individually, taking into account the characteristics of the body, there are several general recommendations. The use of broths (fish, meat), and salt (salty foods) is limited. With a decrease in kidney function, it is recommended to eat less protein foods (meat, cheese, legumes). With a tendency to obesity, animal refractory fats and easily digestible carbohydrates (bakery products, sugar, sweets, honey) are limited.

Berger's disease (IgA nephritis, IgA nephropathy, focal hematuric glomerulonephritis, synpharyngitis hematuria) is a relatively benign variant chronic glomerulonephritis, manifested by hematuria and accumulation of IgA-containing immune complexes in the mesangium. The proportion of IgA nephritis among other nephritis reaches 20-25%, in many countries (France, Australia, Japan) is the most frequent form bright jade.

Etiology and pathogenesis are little studied. The etiological role of a persistent viral infection is assumed based on the association of relapses of the disease with acute febrile illnesses (pharyngitis), data on the development of IgA nephropathy in a kidney transplant. Hyperproduction of an antigen (unidentified) on the mucous membranes induces the synthesis of antibodies (based on polymeric and monomeric IgA) with antimesangial activity, reacting with antigens of the gastrointestinal flora, food antigens with the formation of circulating immune complexes. Circulating IgA containing immune complexes, more often found during an exacerbation of the disease, damage the renal glomeruli. There are data on hereditary predisposition to IgA nephropathy.

The morphological basis of Berger's disease is mesangioproliferative (more often focal, less often diffuse) nephritis with deposition in the mesangium of immune complexes containing IgA, C3-complement fraction, less often IgG and fibrin. In severe cases, fibroepithelial crescents, necrosis of individual vascular loops of the glomeruli with focal fibroplastic transformation, and pronounced tubulointerstitial changes are found.

Berger disease clinic

Berger's disease develops mainly at the age of 15-30 years, much more often (3-4 times) occurs in men, characterized by bouts of macrohematuria, often occurring with dull pains in the lower back, myalgia, recurrent against the background of pharyngitis (at the height of fever, the so-called synpharyngitis hematuria). Sometimes these attacks are accompanied by transient acute renal failure. Proteinuria is usually minimal and highly selective. BP in most patients was within the normal range. A persistent increase in the level of IgA in blood serum (in 60% of patients) with an increase in the proportion of polymeric IgA in normal content other immunoglobulins and C3 complement fraction.

In a third of cases (more often in adults), atypical variants of the disease are observed, manifested by persistent microhematuria, significant proteinuria, recurrent acute nephritic syndrome with macrohematuria, nephrotic syndrome, malignant hypertension.

The course of the disease in typical more often persistent, benign. With massive proteinuria and other atypical variants the disease can often progress. Irreversible terminal renal failure develops on average 10 years after the onset of the disease in 10-20% of patients.

The severity of hematuria and hyperimmunoglobulinemia A does not affect the prognosis of the disease.

Diagnosis, differential diagnosis of Berger's disease

Criteria for diagnosing Berger's disease are:

recurrent hematuria that occurs during an acute respiratory illness (synpharyngitis);
young age and male sex;
increase in the serum level of IgA;
mesangio proliferative glomerulonephritis with immune complexes containing IgA and C complement fraction.

Often, differential diagnosis is difficult urological diseases(urolithiasis, tuberculosis, tumors urinary system, venous renal hypertension papillary necrosis). To exclude these diseases, cystoscopy, phase-contrast microscopy of urine erythrocytes and a set of instrumental methods are indicated to assess the state of the pyelocaliceal and vascular system kidneys.

Berger's disease is differentiated from acute glomerulonephritis, nephritis with systemic diseases connective tissue, alcoholism, lumbalgic-hematuric syndrome, Alport syndrome and other hereditary nephritis, as well as chronic interstitial nephritis.

In acute glomerulonephritis, in contrast to Berger's disease, hematuria is more delayed (appears 7–10 days after a sore throat or acute respiratory disease), hypertension, increased titers of antistreptococcal antibodies and a decrease in the level of C3-complement fraction of the blood are detected. In distinguishing IgA nephropathy from gouty interstitial nephritis, lumbalgic-hematuric syndrome and hereditary nephritis helps to determine the level of IgA and uric acid in the blood. Kidney biopsy data are critical.

Great difficulties may arise in the differential diagnosis of IgA nephropathy with nephritis in hemorrhagic vasculitis and alcoholic nephropathy due to the similarity of clinical manifestations, course, unidirectional immunological changes and the identity of morphological changes in the kidneys. At the same time, it is important to identify extrarenal lesions characteristic of hemorrhagic vasculitis (purpura, articular syndrome, abdominalgia) and chronic alcoholism ( alcoholic disease liver, indurative pancreatitis, cardiomyopathy, polyneuropathy).

When detecting hematuric mesangial nephritis in people older than 40 years, it is necessary first of all to exclude visceral alcoholism, as well as more rare causes hematuria - paraneoplastic nephropathy (with lung cancer, malignant lymphoma, mycosis fungoides) and subclinical forms of Crohn's disease, ankylosing spondylitis.

Treatment of Berger's disease

With a persistent course, symptomatic: sanitation of foci of infection, courses antibiotic therapy, long-term use 4-aminoquinoline drugs, non-steroidal anti-inflammatory drugs.

The appointment of immunosuppressants, drugs that selectively disrupt the synthesis of IgA (phenytoin, diphenin) is ineffective. With progressive forms of Berger's disease, the addition of nephrotic syndrome, an attempt to use glucocorticoids, anticoagulants and fibrinolytic agents, plasmapheresis is justified.

I.E. Tapeeva, S.O. Androcova, V.M. Epmolenko and others.

Is autoimmune kidney disease, which means that a person with weak immunity easy to get sick.IgA nephropathy is curable?Next, we will give you a detailed answer, and we hope you can benefit from the following articles.

There is a process to understand the prognosis of IgA nephropathy. It used to be considered that the prognosis of IgA nephropathy is good. But in recent years, with the gradual deepening of research on this disease, it has been proven that not all patients with IgA nephropathy have a good prognosis. common days There is only hematuria and no more than 1 g of protein in the urine within 24 hours. Yes, their prognosis is usually good. If there is always a lot of foam in the urine, within 24 hours there is more than one gram or more of protein in the urine. Moreover, patients with many proteinuria, their disease will usually worsen to chronic renal failure and the prognosis is poor. Even in some patients, kidney function is unexpected deteriorates. If we do renopuncture for them, we can find what is called《half moon》in the medical field. The crescent, which is composed of cells, exists in the place of the kidney glomerulus. After this kind of crescent, the prognosis is not very good. But the crescent is also divided into some genera. If cellular crescents are used shock therapy can improve the prognosis. If it has become fibrous crescent, I am afraid there is no point in treatment. In addition, it only needs 1~2 weeks from honeycomb crescent to fibrous crescent. Polohoy. Therefore, if you find that the condition of the disease worsens or there is a lot of foam in the urine or kidney function weakens, it is necessary to be treated in a timely manner. Don't delay! otherwise it will cause a lifetime of regret.

However, there is currently no effective treatment, which can cure this disease in Western countries. And in China, the disease can be managed without hormones and dialysis. What is the best treatment in China for IgA Nephropathy?

Traditional Chinese Medicine (TCM) is the spirit of China, and has already helped many patients to recover. For IgA nephropathy, TCM also has its function. In order to get the best and quick effect, we put forward new treatments: “four ‘one’”, i.e. Micro-Chinese Medicinal Osmotherapy, Mai-Kang Blend, Healing Herbs Chinese Medicine and Foot Bath. This “four ‘one’” treatment method is very safe and effective, based on TCM (All the medicines we have chosen differ from each other, and depend on the individual condition of the patients). This means that this therapy has no harm. And you don't need to suffer the pain caused by the treatment.

In summary, our “four ‘one’” method of treatment is best treatment in China for IgA Nephropathy. It will help you control the disease quickly and recover. Also, if your disease situation is severe, we can choose our seven TCM therapies as adjunct therapy. If you are suffering from IgA Nephropathy, it is highly recommended that you choose our treatment to help you live a happy life.

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- this is a form of glomerulonephritis of an infectious-autoimmune nature, characterized by mesangioproliferative inflammation with the deposition of immune complexes. Clinical course accompanied by periodic gross hematuria shortly after infectious diseases respiratory tract, organs of the gastrointestinal tract, occasionally possible permanent microhematuria, proteinuria, nephrotic syndrome with intermittent acute renal failure. Diagnosis is based on the results of laboratory tests of urine, blood immunograms, histological examination of a kidney biopsy. In the treatment of pathology, symptomatic therapy, immunosuppressive agents, antihypertensive drugs are used.

General information

Berger's disease (IgA nephropathy) is also known as focal proliferative glomerulonephritis, synpharyngitis hematuria, or idiopathic recurrent gross hematuria. Synonymous names reflect different features of the pathology - the proliferative nature of inflammation of the kidneys, the recurrent development of hematuria and its relationship with diseases of the upper respiratory tract (pharyngitis). It is considered the most common variant of glomerulonephritis in the world - the average incidence is 5 cases per 100 thousand of the population, in Asian countries it is recorded 5-6 times more often, ranging from 5 to 30% of all cases of kidney inflammation. Men suffer from Berger's syndrome several times more often than women, among the diseased persons aged 15 to 30 years predominate. There is some seasonality of exacerbations (an increase in the autumn-winter period), which is associated with a higher frequency colds during the cold season.

Causes

Berger's disease is a pathology with a complex and multifactorial etiology, which includes a number of infectious, immunological and genetic features of the body. The relationship of the disease with a number of bacterial and viral infections, some autoimmune pathological conditions and certain genetic mutations. The role of genetics in the pathogenesis of the condition is also indirectly proved by the features of the ethnic and racial spread of the disease. Thus, the following groups of etiological factors are distinguished:

infectious factors. These include a variety of bacterial and viral infections of the respiratory tract, gastrointestinal tract, and skin. Many patients often have a history of tonsillitis, gastritis, viral hepatitis, herpes virus infection. It is believed that defeat renal tissue in these infections due to an atypical immunological reaction to the antigens of the pathogen.
immunological factors. The pathogenetic substrate of the condition is the appearance of immune complexes that cannot be eliminated by the liver and kidneys. The reason for their formation is a violation of the synthesis different forms immunoglobulin A, an atypical reaction of immunity to exogenous (infectious, less often allergenic) and endogenous (tumor, cellular) antigens.
genetic factors. Ethnic features of the distribution of Berger's syndrome are due to genetic factors. In particular, atypical mutations on the 6th chromosome, changes in the genes that control the synthesis of chains of the major histocompatibility complex and hepatocyte receptors were found in patients. An increased incidence of pathology was revealed in persons with certain hereditary diseases - celiac disease, galactosemia and a number of others.

The Role of Influence external factors is the subject of discussion - perhaps they are the cause of the polymorphic clinical picture of the condition. The consumption of certain food products typical for the Asian region (unpeeled rice, seafood) can aggravate the course of nephropathy, which, along with genetic characteristics, causes more frequent registration of the disease in this territory. Role comorbidities(arterial hypertension, inflammation urinary tract) in the development of the disease has not yet been established.

Pathogenesis

Currently, several main pathogenetic scenarios for the development of IgA nephropathy are known. In case of disease, immune complexes appear in the blood, containing polymeric forms of immunoglobulin A, which are usually secreted on the mucous membranes and are found in an insignificant amount in the bloodstream. Isolation of increased amounts of polymeric varieties of IgA is due to anomalies in their synthesis in bone marrow and violations of elimination through the liver due to defects in hepatocyte receptors. Ultimately, the kidneys become the only route for excretion of immunoglobulins and their associated antigens, but the size of the molecules is too large, so they can be deposited in the glomeruli of nephrons.

Deposits of immune complexes in the tissues of the kidneys activate the leukocyte reaction and the complement system, which causes a flaccid diffuse inflammation with the ingress of red blood cells and small amounts of protein into the urine. The influence of factors activating the synthesis of immunoglobulins (inflammatory reactions, infectious diseases) leads to large quantities IgA into the excretory system and enhances immune responses. It is with this that exacerbations of IgA nephropathy are associated shortly after suffering tonsillitis, laryngitis, gastrointestinal diseases, and viral infections. The severity of inflammatory manifestations during an exacerbation can be high, can lead to transient acute acute renal failure. Latent and indolent forms may be asymptomatic long time, the development of CRF in most cases takes decades.

Classification

Berger's disease is divided into several clinical forms, which are characterized different severity manifestations, prognostic data and treatment approaches. The division is conditional - the varieties of the state can flow from one to another. This gives some researchers reason to consider them as stages in the development of a single pathological process, progressing under the influence of external and internal factors. Significant differences in the rate of progression lead to the appearance of existence various forms nephropathy. In urology and nephrology, there are three main forms of the disease:

Synpharyngitis form. It is considered the most common, manifested by periodic exacerbations that are associated with inflammatory diseases of the respiratory tract or gastrointestinal tract(intestinal infection). The peak of manifestations occurs 1-2 days after infectious pathology, their severity ranges from gross hematuria and back pain to transient acute renal failure. Between exacerbations, no clinical or laboratory symptoms nephropathy is not defined.
latent form. Registered in about a third of patients, characterized by less severe symptoms, but is considered to be more prognostic. Usually no subjective manifestations are detected, signs of Berger's syndrome are detected in a laboratory study of urine in the form of mild proteinuria and microhematuria. The amount of protein excreted in the urine gradually increases, the filtering ability of the kidneys decreases, which creates conditions for the development of chronic renal failure.
nephrotic form. It is diagnosed in a small percentage of patients with IgA nephropathy, accompanied by severe proteinuria, gross hematuria, oncotic edema, hypovolemia and hyperlipidemia. It rarely occurs primarily, usually becomes a complication of synpharyngitis and latent forms diseases.

Symptoms of Berger's disease

Clinical manifestations depend on the form of this condition. The most common synpharyngitis hematuria is characterized by abrupt start 2-3 days after infectious disease- pharyngitis, laryngitis, intestinal infection. Sometimes the starting factor for Berger's disease can be vaccinations, heavy physical exertion, prolonged insolation (sun tanning, visiting a solarium). Patients complain of pain and discomfort in the lumbar region, urine becomes reddish (gross hematuria), its amount decreases. IN rare cases signs of acute renal failure are recorded - urinary retention followed by polyuria, disturbances in water-salt metabolism. In some patients, the attack is accompanied by an increase in blood pressure. Most often, in the synpharyngitis form of IgA nephropathy, renal function is fully restored after a few days or weeks.

The latent variety of the disease is characterized by a latent course with almost total absence symptoms of kidney damage. In the analysis of urine are determined pathological changes- protein release and small quantities blood. A number of patients have complaints of pain in the muscles, joints, periodic swelling. Over time, if untreated, this form of the disease leads to the development of chronic renal failure. The nephrotic form, on the contrary, is characterized by a pronounced clinical picture- nephrotic syndrome with severe edema of the body, the development of ascites, signs of dehydration due to loss of fluid in the urine.

Complications

The main and most common complication of IgA nephropathy is renal failure. Acute forms (ARF) can occur with an attack of synpharyngitis varieties and sometimes with a nephrotic type of disease. Chronic renal failure develops slowly, is recorded within 15 years in about half of the patients. Among other complications of nephropathy, there are risks of developing hypovolemic shock, nephrotic crisis, thrombosis at the height of an attack of the disease. Absence complex treatment many times increases the risk of kidney failure and other complications of nephropathy.

Diagnostics

In nephrology, the definition of Berger's pathology is made on the basis of the results of a general examination of the patient, anamnesis, laboratory data (general, biochemical and immunological parameters of blood and urine). In addition, in controversial cases, a histological examination of the kidneys, cystoscopy, radiographic diagnostic methods can be prescribed - mainly to exclude other diseases. Complicating the diagnosis of pathology are circumstances such as the recurrent course of synpharyngitis forms (during the period of remission, manifestations of nephropathy are practically not detected) and the absence of obvious symptoms in the presence of latent varieties. All diagnostic measures for nephropathy are divided into groups:

Physical examination and history taking. When questioning the patient, attention is paid to the frequency of allergic and infectious conditions in the past, trying to find their relationship with renal manifestations (hematuria, back pain). Nephrotic types of nephropathy are characterized by the presence of edema, an increase in the abdomen due to ascites, and symptoms of kidney failure.
Laboratory blood tests. Changes in the general blood test are insignificant - with acute attack possible increase in ESR, mildly pronounced leukocytosis, increased hematocrit. Biochemical indicators change more strongly - the level of blood globulins, creatinine increases (due to impaired filtration in the kidneys), with the development of nephrotic syndrome, hypoalbuminemia and hyperlipidemia occur. An immunological blood test indicates an increase in IgA levels and a slight decrease in complement fractions.
Laboratory studies of urine. With synpharyngitis type of pathology, macrohematuria, proteinuria up to the level of 1-2 g / l are noted in the urine, immunological study detects the presence of complexes based on IgA and a small amount of complement components (C3). The latent variant of Berger's disease is manifested by mild proteinuria (up to 0.3 g/l), the presence of leached erythrocytes in the urine.
Instrumental diagnostics. Ultrasound of the kidneys often does not reveal specific changes in the initial stages of the disease, only with a long course can a slight decrease in the size of the organ be detected. Basically, ultrasound and ultrasound of the kidneys are used to differential diagnosis. Excretory urography indicates a delay in contrast due to reduced filtration capacity.
Histological study. Kidney biopsy with histological examination of the material is the most exact method diagnosis of IgA nephropathy. Signs of inflammation are found in the mesangial space; histochemical methods reveal deposits of immune complexes in it.

Differential diagnosis of IgA nephropathy is carried out with other forms of nephropathy, urolithiasis, oncological lesions of urinary organs. excretory system. For this, patients are prescribed cystoscopy, radiological and ultrasound examinations, determine the level of urates in biochemical analysis blood. An auxiliary role in the diagnosis of nephropathy is played by the identification of diseases that can provoke kidney damage - inflammation of the tonsils, hepatitis, intestinal infections.

Treatment of Berger's disease

Etiotropic specific treatment not developed, nephrologists use symptomatic, nephroprotective and supportive therapy. With the development of renal failure, the appointment of hemodialysis is indicated according to indications. Kidney transplantation, used in exceptional cases, is not effective method treatment - about every second patient develops similar changes in the transplanted organ. This indicates predominantly extrarenal causes of pathology. The following methods are most often used in the treatment of the disease:

nephroprotective therapy. The use of drugs that reduce arterial pressure(ACE inhibitors, angiotensin receptor blockers) and antiplatelet agents (dipyridamole). Apart from medicines to reduce the load on the excretory system, it is recommended to maintain an optimal water regime, limiting the consumption of table salt.
Antibacterial therapy. It is prescribed in cases where the relationship between nephropathy and the presence of a focus of bacterial infection (with synpharyngitis forms) has been accurately proven. The choice of antibiotic and the scheme of its administration depend on the nature of the pathogen, which is determined during additional diagnostics. Sometimes a method of removing the infectious focus (tonsillectomy) is used.
Anti-inflammatory therapy. For this purpose, glucocorticosteroid drugs (prednisolone and its analogues) are prescribed. They are used in all forms of this nephropathy, the dosage depends on the severity of proteinuria, which reflects the degree of damage to the kidneys.
immunosuppressive therapy. The use of cytostatics and other immunosuppressants is indicated in severe cases and severe immunological damage to the organs of the excretory system. They are included in complex therapy nephrotic forms of Berger's disease.

Depending on the presence of other symptoms of kidney damage and extrarenal manifestations, patients are also shown infusion therapy, statins (to reduce blood lipid levels), antihypertensive drugs. It is important to give up bad habits - smoking, drinking alcohol. To avoid provoking an attack of hematuria, avoid physical activity, prolonged exposure to the sun.

Forecast and prevention

The prognosis of Berger's disease is uncertain, depending on the indicators of a particular patient. According to statistics, within 16-20 years, approximately 30-50% of patients develop chronic renal failure, but its progression is extremely slow and benign. At proper observance doctor's prescriptions and maintenance therapy, the quality of life of patients is maintained at high level. Methods for the prevention of pathology have not been developed, some experts recommend timely full treatment chronic infections(inflammation of the tonsils and others), but there is no reliable evidence that these measures can avoid synpharyngitis nephropathy. Preventive actions(water regime, salt restriction, exclusion of bad habits) make it possible to significantly slow down the progression of kidney damage.

LgA nephropathy is a disease that is accompanied by lgA - immune complexes in the glomeruli. The disease is manifested by rather slow progressive hematuria, often renal failure and proteinuria. The basis for the diagnosis is a kidney biopsy and urinalysis. In general, the prognosis is favorable. As for treatment, it includes taking omega-3 fatty acids, glucocorticoids, and angiotensin-converting enzyme inhibitors.

LgA-nephropathy is a form of chronic GN, which is characterized by the accumulation of lgA-immune complexes in cubes. This is a fairly common form of GN throughout the world. The disease usually begins in adolescence and after 20 years. Women get sick about 2 to 6 times less than men. It is worth noting that this disease is mostly common among Asians and whites than among African Americans. In the US, the prevalence of the disease is 5%, in Australia and Southern Europe- from 10 to 20%, in Asia - from 30 to 40%.
The main reasons have not been identified. However, there is an assumption that lgA nephropathy arises from a variety of pathogenic mechanisms, among which abnormal glycosylation of gA-l and production of gA-l can be distinguished. This causes increased communication with mesangial cells. Also worth noting is reduced gAl clearance, excessive production of cytokines that stimulate mesangial cell proliferation, and defective mucosal immunity. There is also a familial nature. This suggests that the nature of the disease in some cases is still genetic.
Initially, renal function is preserved, but signs of kidney disease may occur. It is worth noting that in some patients the disease manifests itself with chronic or acute nephritic insufficiency, nephrotic syndrome and severe arterial hypertension.

Symptoms

The most common symptom of nephropathy is recurrent or persistent macroscopic hematuria, asymptomatic microhematuria that occurs with moderate proteinuria. Other symptoms of this disease usually do not occur.
In gA nephropathy, gross hematuria in most cases begins after fever associated with mucosal disease, on the first or second day, while simulating acute GN, in addition to the onset of hematuria, immediately following or coinciding with fever. The disease may be accompanied by pain in lumbar. At the time of diagnosis of nephropathy, arterial hypertension is not characteristic.

Diagnostics

The diagnosis is made by doctors on the basis of a urine test, and is confirmed only by a biopsy. It is worth noting that urinalysis reveals microhematuria, usually with erythrocyte casts and dysmorphic erythrocytes. Moderate proteinuria is typical and occurs with little or no hematuria. Approximately 20% of patients develop nephrotic syndrome.
Complement and plasma creatinine levels are usually normal. The plasma concentration of gA may well be increased. Circulating gA and fibronectin complexes may also be present. However, it is worth considering that the results may be of dubious value.

Renal biopsy shows granular inclusions of C3 and gA in extended mesangium on immunofluorescent staining with foci of segmental necrotic or proliferative changes. It is important that gA mesangial inclusions are not specific and are often found in other diseases, including various collagenoses, lung cancer, HIV infection, psoriasis, inflammatory diseases intestines, cirrhosis of the liver and in the disease of Schonlein-Genyuha purpura. Glomerular accumulation of gA is the main feature of Schonlein-Genuch purpura. These conditions may be indistinguishable on biopsy. Because of this, it has been suggested that purpura is a systemic form of nephropathy. However, this disease is clinically distinct from nephropathy and usually presents with abdominal pain, arthralgia, and rash.

Forecast

Usually nephropathy progresses slowly. Arterial hypertension, as well as renal failure, develops in 15-20% of patients over 10 years. Before terminal stage renal failure, the disease progresses in 25% of patients suffering from nephropathy for more than 20 years. If lgA-nephropathy was diagnosed in childhood, then the prognosis is favorable. However, persistent hematuria invariably leads to renal failure, proteinuria, and arterial hypertension. If the disease began at an older age, then the risk factors for the development of renal failure are such diseases as tubulointerstitial pathology, the transformation of GN into rapidly progressive, severe glomerular sclerosis, an increase in creatinine concentration, the absence of recurrent gross hematuria, persistently severe proteinuria and arterial hypertension.

Treatment

Normotensive patients with moderate proteinuria and intact renal failure usually do not require treatment unless renal function worsens or increases in proteinuria. Patients with more severe proteinuria and renal insufficiency are usually treated for nephropathy before the development of severe renal insufficiency.
With a premise, ACE inhibitors are used, as they can reduce proteinuria and blood pressure. However, data on the effectiveness of such treatment are rather contradictory. Patients who have the ACE DD genotype are at risk for disease progression and respond better to such therapy. Even with moderate renal insufficiency, patients with arterial hypertension are prescribed angiotensin receptor blockers or ACE inhibitors. If arterial hypertension is not controlled by monotherapy or if proteinuria does not decrease, then a combination of ACE inhibitors and angiotensin blockers. These are the ones that have their place here.

For many years, glucocorticoids have been used to treat nephropathy. However, their effectiveness is not dangerous. Often, methylprednisone is used intravenously once a day for three days at the beginning of the first, third and fifth months in combination with oral prednisone at 0.5 mg / kg every other day for six months. If patients have progression of the disease, as evidenced by worsening renal function or proteinuria, they are given glucocorticoids because of the risk of side effects. It may also be given to patients with significant renal insufficiency and severe proteinuria. Also used to treat a combination of azathioprine, cyclophosphamide and glucocorticoids. However, their safety and efficacy are questionable even when compared with glucocoticoids alone. The effectiveness of mycophenolate sofetil is also being studied. After transplantation, none of the listed drugs prevents relapse in patients.
Omega 3 are fatty polyunsaturated acids that are available in supplements based on fish oil. Typically, such a component was used to treat nephropathy. However, data on this drug are conflicting. The mechanism of action of such acids may include fusion with inflammatory cytokines. To reduce the inhibition of mesangial proliferation and gA synthesis, many experts offer other therapies. Meat, eggs, dairy products and gluten are excluded from the diet. As a result, the patient's immunoglobulin is normal, the production of gA theoretically decreased.

Because of the good survival and lack of recurrence, kidney transplantation is preferred. The disease recurs in only 15% of patients.