Disease sexually transmitted:

Chancroid (soft chancre)

Chronic glomerulonephritis

  • What is Chronic glomerulonephritis
  • What triggers / Causes of Chronic glomerulonephritis
  • Pathogenesis (what is happening) during Chronic glomerulonephritis
  • The symptoms of Chronic glomerulonephritis
  • Diagnosis of Chronic glomerulonephritis
  • Treatment of Chronic glomerulonephritis
  • Prevention of Chronic glomerulonephritis

What is Chronic glomerulonephritis -

Chronic glomerulonephritis (CGN) is an inflammatory disease of the kidneys of immune origin with primary and primary lesion of the renal glomeruli, but also with involvement in the pathological process of other structural elements of the renal tissue has steadily progressive course and outcome in chronic renal failure (CRF)..

Compared with acute chronic glomerulonephritis occurs 2-4 times more frequently (L. A. perig, N. J. Melman, 1982). Patients with CGN is 1-2 all therapeutic patients (A. P. Peleschuk, 1974 - B. B. Bondarenko, 1980 - L. A. perig, 1983), and among the dead, he revealed in 1 all autopsies (E. M. Tareev, 1972). In epidemiological studies ,CGN detected in 0,22-0,25 cases (I. R. Lazo et al., 1977). The disease is slightly more common in men: 52,3 (S. I. Ryabov, 1980) to 57-64 (VI Bilko, 1980 - B. B. Bondarenko, 1980 - V. A. Kirsys, 1980), or in the ratio of 3 : 2 (E. M. Tareev, 1972 - Shulga, 1973). According to our data (S. A. Chizh, A. P. Lyashenko, 1982), based on the results of dispensary observation of 1052 patients with diffuse glomerulonephritis, men CGN was observed in 56.6 cases. There are significant differences in the frequency of this disease depending on age: age 20-50 years from 79,9 (VI Bilko, 1980) to 88.6 (S. I. Ryabov, 1980). According to our materials (A. S. Siskin, P. A. Lyashenko, 1982), 88 patients with CGN were aged 16-50 years. Among persons older than 60 years, the disease is met only 1.1 cases.

What triggers / Causes of Chronic glomerulonephritis:

Chronic glomerulonephritis is often a consequence of untreated or not promptly diagnosed acute glomerulonephritis, and therefore its causes in these cases are the same as when you FIRE. However, not all patients CGN in history there are indications of FIRE moved. So, even Yolhard (1936) noted the absence of the acute phase of the disease in 45 (278 cases), T. Addis - 46 (463 cases), N. A. Ratner (1974) - 55,9, Yaroshevsky A. J. et al. (1973) - 43,3 (244 cases) observed in their patients. Shulga (1973) found a history of acute glomerulonephritis only 1/3 of surveyed patients with CGN, and Ryabov S. I. (1980) 15 were under medical observation and have 26,3 during hospital examination and treatment. Cases when CGN arises and develops without acute phase and, therefore, in history there is no indication of a previous FIRE, currently denoted as primary chronic glomerulonephritis. To establish the cause of such an option CGN is not always possible (only 10-15 cases). Its origin is often attributed to the presence of long-existing focus of infection, prolonged exposure to chemical agents (particularly drugs) and some other factors.

Among the factors contributing to the transition of acute glomerulonephritis chronic, can have a value of the presence and especially the exacerbation of focal streptococcal and other infections, re-cooling, especially the action damp cold, unfavorable conditions of work and life, trauma, alcohol abuse (N. A. Mukhin, I. E. Timofeev, 1991) etc. the foci of infection are considered as sources of sensitization, supporting the inflammatory process in the kidneys.

Pathogenesis (what is happening) during Chronic glomerulonephritis:

It is generally accepted that the basis of development and progression of CG are immunopathological processes (V. V. Serov et al., 1992). So she, as well as in acute glomerulonephritis, there are two variants of immunological Genesis of chronic glomerulonephritis. Discussed possible involvement in the Genesis CGN and third, the cellular mechanism of immune T - and b-lymphocytes (see FIRE).

From non-immune factors in the pathogenesis of chronic glomerulonephritis great importance of hypercoagulability, increased intravascular coagulation, deposition of fibrin and its degradation products in the glomerular capillaries, and increase in the blood concentration of kinins, serotonin, histamine, renin, prostaglandins, etc. (S. A. Korzun, A. S. Siskin, 1980 - G. I. Alekseev et al., 1980, etc.). Violations in the system of hemostasis and fibrinolysis is an important pathogenetic links in the development and progression of glomerulonephritis.

Pathological changes in kidney chronic glomerulonephritis relate to all structural elements of the glomeruli, tubules, vessels, stremy and represent a great variety. Ultimately, these structural changes in all cases lead to the development of nephrocerus and secondary kidney scarring.

Macroscopically, when CGN kidneys gradually decrease in size and weight (less than 100g), is compacted tissue. In the early stages of the disease fibrous capsule usually well separated from the surface of the kidney, and in the later period it is thickened and hardly removed due to the formation of adhesions. The surface of the kidney more fine-grained, but sometimes remains smooth. The grit surface is explained by the fact that areas of sclerosis and atrophy (retraction) alternate with areas of hypertrophied nephrons (bulging). Reducing the size and weight of the kidney is due to the death of the parenchyma - renal nephrons. As a result, gradually, more or less quickly, the reduced mass of existing nephrons.

In terminalnog stage of chronic glomerulonephritis develops so-called secondary wrinkled Bud. Some authors (V. V. Serov, 1972 - A. P. Peleschuk, 1974) believe it is more correct to call it nephrotic wrinkled kidney. The term "secondary wrinkled Bud" they consider to be less successful, as scarring of the kidneys is always a secondary process, regardless of its Genesis.

Microscopically detected in the kidneys hyalinosis and zapustevanie glomerular atrophy respective tubules. In advanced stages of the disease remain only isolated hypertrophied nephrons. Meet glomerular the nephrons, like "headless", with the preserved structure of the tubular epithelium. In the interstitial tissue revealed massive lymphoid infiltrates of plasma.

When CGN there are also various by the nature and severity of the pathological changes of renal vessels. So, in small arteries and arterioles develops proliferative endarteritis with the outcome in the intimal sclerosis, narrowing or complete obliteration of the lumen of blood vessels. In hypertensive form of CGN found archaeologies and rarely arteriolosclerosis. Possible and hyperplasia of the intima of medium and large vessels of the kidney. As a result of these changes comes a growing progressive decrease in renal blood flow, and then again in the upcoming zapustevanie lymphatic vessels and impaired lymph circulation.

In the stroma of the kidney in CGN edema, cellular infiltration, sclerosis, which occur earlier and more pronounced in the medulla of the kidney. In the cortical substance in the place of the dead nephrons appear foci of sclerosis, the progression of the disease merge together and form extensive scarring of the field (V. V. Serov, 1972).

The introduction into clinical practice of lifetime needle kidney biopsy with histological examination of biopsy material by means of optical and electron microscopy allowed detailed study of histomorphological changes of all structural elements of the renal tissue at different stages of the pathological process from early phase to end. In addition to determining the morphological forms of chronic glomerulonephritis, histological examination of biopsy material allow to evaluate the course and prognosis of the disease, and to choose the most rational therapy. All this is of practical importance, and confirms the feasibility and necessity of a morphological classification of CGN.

In 1978 (London) experts who developed morphological classification of glomerulonephritis in which selected 10 main morphological forms. In our country widespread in clinical practice received a morphological classification of glomerulonephritis proposed in 1970 In V. Serov and added them in later years. Below is a brief description of the morphological types of glomerulonephritis in accordance with this classification (V. V. Serov, 1980 - V. V. Serov et al., 1992).

1. Minimal changes. The principal and characteristic feature of these changes is the destruction (and disappearance) of small spikes (pedikuly) podocytes in the background of focal swelling, loosening and thickening of the basal membrane and proliferation of the endothelium only in certain glomerular capillary loops. Clinically minimal changes in the glomeruli usually manifested nephrotic syndrome, and most often in the form of idiopathic nephrotic syndrome or lipoid nephrosis. The correct morphological diagnosis of this type of glomerulonephritis is possible only when electron-microscopic study.

2. Membranous glomerulonephritis. Histologically, are sharp diffuse thickening, swelling and splitting of the basal membrane of the glomerular capillaries, which can occur in several or all of the capillary loops of the glomerulus, therefore, distinguish between focal and diffuse membranous glomerulonephritis. Moreover, due to the depolymerization of polysaccharides (in particular, hyaluronic acid) that are part of the basal membrane, there is an increase in pore size, the diameter of which is several times higher than normal. Using electron microscopy on the basal membrane subepithelial identified deposits, "spines" consisting of immune complexes that contain (according to immunohistochemical research) immunoglobulin G and complement. I believe that the fixation of immune complexes on the basement membrane is the beginning of its damage and increasing the permeability of the glomerular filter of blood plasma proteins.

3. Proliferative intracapillary glomerulonephritis. Characterized by proliferation of endothelial cells and mezangiâ with relatively minor changes in the basal membrane of the glomeruli. This morphological type of glomerulonephritis can occur in different clinical forms of CGN.

4. Proliferative extracapillary glomerulonephritis. Characterized by the presence of observed resulting from proliferation of epithelial cells of the capsule (nephrothelium) of the glomerulus, which, filling the lumen of the capsule, form populonia compress the capillary loops of the glomerulus and break them in circulation. At the same time marked exudative JW-

tion and deposition of fibrin in the cavity of the capsule of the glomerulus. Further, the cells observed are subjected fibroplastic changes with the development of connective tissue and loss of glomerulus. Extracapillary nephritis is the morphological basis of malignant (subacute) glomerulonephritis.

5. Membranosa-proliferative glomerulonephritis. With this type of glomerulonephritis combined signs membranous and proliferative changes in the glomeruli, which are of a diffuse nature. Clinically, it is most often manifested latent glomerulonephritis.

6. Fibrosis (sclerosing) glomerulonephritis. Represents a generalized evolutionary form, which can be completed within membranous, proliferative, proliferative one-and membranous glomerulonephritis with minimal changes. Distinguish between diffuse and focal fibrosis glomerulonephritis.

The main features of diffuse fibroplastic glomerulonephritis are diffuse sclerosis mezangiâ, vascular loops of the glomeruli with the development of hyalinosis and sclerosis, formation of multiple adhesions between the loops of the glomerular capillaries and the sheets of the capsule of the glomerulus. In focal fibroplastic glomerulonephritis mentioned pathological changes were only detected in a small subset of glomeruli. Fibroplastic glomerulonephritis most often clinically consistent and hypertensive nephrotic current long form CGN, and, as a rule, it occurs in the so-called terminal nephritis.

In addition to these morphological types of glomerulonephritis presents Vladimir Serov classification stand out even mesangial glomerulonephritis in the form managemembers, mezangioproliferativnom and mesangiocapillary and focal segmental hyalinosis. Mesangial type of glomerulonephritis is characterized by the deposition of immune complexes in the subendothelial space of the basement membrane of the glomerular capillaries and in misangyi that leads to proliferation of endothelial and mesangial cells.

Mesangiocapillary segmental glomerulonephritis occurs extension mezangiâ, focal thickening and splitting of the basal membrane with the possible formation of deposits and mild proliferation of mesangial cells.

The main signs mezangioproliferativnom glomerulonephritis are diffuse or segmental confident or marked proliferation of endothelial cells and mezangiâ, as well as thickening and splitting of the basal membrane of capillaries in the segmental extension mezangiâ.

Misigieisi glomerulonephritis, which is characterized by the relatively rapid progression, characterized by diffuse thickening and splitting of the basal membrane of capillaries, diffuse proliferation of mesangial and endothelial cells, expansion mezangiâ, focal sclerosis of the vascular loops.

Lobular glomerulonephritis was considered as an option mesangiocapillary and is characterized by diffuse thickening and splitting of the basal membrane, sclerosis of the vascular loops and diffuse sclerosis mezangiâ, and the same signs that mesangiocapillary glomerulonephritis.

Examination of biopsy specimens of kidney tissue obtained using in vivo biopsy of the kidney, along with a primary lesion of the glomerular allows to detect violations of the structure of tubules, blood vessels, interstitial tissue. In the tubules found degenerative changes, which are mainly localized in the epithelium of the proximal and atrophic - dominated in the epithelium of distal tubules. However, there are various kinds of protein dystrophy (granular, gialinovo-tiny, vacuole). Atrophy of the epithelium of the tubules is more pronounced in the distal parts of the nephron in which the glomeruli are not functioning due to their hyalinosis and sclerosis. Along with the dead, roscovitine the nephrons occurs compensatory hypertrophy of neighboring nephrons. With the progression of CG is often the so-called glomerular nephrons with sclerotiorum glomeruli, atrophic processes in the tubules begin to dominate over the dystrophic - more and more nephrons are exposed to fibrous replacement, there is a destruction of renal parenchyma and eventually develops secondary wrinkled Bud.

In conclusion, it should be noted that as the author of the classification, and other researchers involved in histomorphology glomerulonephritis, emphasize that the morphological types are not stable. They reflect only certain phases of morphological abnormalities in renal tissue at CGN, and one type of glomerulonephritis can move on to another. So, the possible evolution of proliferative or proliferative one-in membranous proliferative one-fibrosis type with the progression of the disease. In addition, morphological diagnostics of glomerulonephritis is an approximation because it is based on histomorphological study only a small number of nephrons (5-10, but not more than 30 from 2-3 million).

Chronic glomerulonephritis

The symptoms of Chronic glomerulonephritis:

In the opinion of many clinicians-nephrologists, there are two types of chronic glomerulonephritis: primary and secondary chronic. To primary chronic glomerulonephritis are those cases that occur without preceding acute glomerulonephritis, i.e. from the beginning (primary) glomerulonephritis becomes chronic.

About secondary chronic glomerulonephritis say when in history there are indications of previous acute glomerulonephritis.

However, consensus about the appropriateness of allocating primary and secondary chronic glomerulonephritis, and the frequency of the two types of this disease in the literature does not exist.

The need for and appropriateness of the allocation of primary chronic glomerulonephritis in a number of prominent clinicians not only causes doubt (N. A. Ratner, 1971, 1974 - Yaroshevsky A. J., I. J. Askinazi, 1971 - Yu - Dmitry Shulga, 1973), but generally denied (M. I. Frankfurt, 1962 - O. Suk, 1967 - B. B. Bondarenko, 1980, etc.), as clinically CGN flows identical in patients without FIRE history and post it. In addition, according to biopsy of the kidney, there are no differences in the morphological picture of both types of CGN. With primary chronic glomerulonephritis cannot be ruled out a previous FIRE, since the latter could not be diagnosed in a timely manner due to the lack of extrarenal symptoms (edema, hypertension), and urine purposefully not been conducted. This assumption becomes more valid when you consider that at the present time FIRE has mostly latent within, manifesting only minor or moderate urinary syndrome.

Chronic glomerulonephritis is characterized by a large variety of clinical manifestations. The presence and severity of symptoms depend on its clinical form, flow and renal function. However, in all cases of chronic glomerulonephritis is continually more or less rapid progression of the disease, leading ultimately to the development of chronic renal failure. Chronic glomerulonephritis has a fluctuating nature of the flow, when the periods of remission followed by periods of exacerbation. The duration of remission and severity of exacerbations can be one and the same patient different. During exacerbation of the disease in most cases, the clinical picture of chronic glomerulonephritis resembles or becomes similar to that in acute glomerulonephritis: edema, hypertension (if in remission they were absent), increases urinary syndrome. In other cases, the aggravation is only the increase in proteinuria, hematuria and cylindruria. May occur, especially in severe exacerbation, kidney function.

In the period of remission of clinical symptoms of chronic glomerulonephritis, and how its course, depend primarily on the clinical form of the disease. It is therefore appropriate to consider clinical features of this disease with consideration of the mentioned five clinical forms (or variants, syndromes) CGN.

Consequently, the lack of guidance in the earlier history of the transferred FIRE cannot serve as the basis for selection of primary chronic glomerulonephritis as a special type of CGN, and the feasibility of providing this type of glomerulonephritis with clinical positions is not justified, since the clinic, morphology and treatment of primary and secondary chronic glomerulonephritis is identical to (B. B. Bondarenko, 1980).

L. A. Pyrih (1983) in his proposed classification of chronic glomerulonephritis, in addition to the two types, highlights stage (anyparticular, hypertension and chronic renal failure), forms or variants (with urinary syndrome and nephrotic syndrome).

S. I. Ryabov (1980) developed a classification that combines the main pathogenetic, morphologic, and clinical principles. This classification takes into account almost all modern aspects of the development of glomerulonephritis. But, unfortunately, it cannot be used in practical activities of doctors in those clinics and hospitals where there is no opportunity to investigate the immunological and morphological features of glomerulonephritis.

Widespread clinical classification CGN proposed M. B. Tarieven. It identifies six main variants of chronic glomerulonephritis: 1) malignant (subacute, rapidly progressive, extracapillary)- 2) mixed - 3) nephrotic - 4) hypertension (vascular)- 5) latent - 6) terminal. Of them retained their value for CGN four options, because the first dedicated to independent nosological form of glomerulonephritis, and the latter is seen as a stage chronic kidney disease.

Classification E. M. Tareev test is simple and convenient for practitioner and can be used in hospitals where it is not possible to apply for diagnostic purposes hard-to-reach methods immunological and morphological studies.

Later N. A. Ratner (1965) also distinguished between four clinical forms of chronic glomerulonephritis: nephritic, hypertensive, mixed and latent, which are in essence similar to those in the classification of E. M. Tareev test.

Some authors (M. J. Ratner, 1971, 1980, etc.) there are still fifth - hematuric form of chronic glomerulonephritis, when the leading position in clinical and laboratory symptoms is hematuria. Eligibility the selection of this form of CGN is justified in cases of glomerulonephritis with no extrarenal signs of the disease, and in the urinary syndrome prevails hematuria with minor proteinuria.

About hypertensive form of CGN should speak only when hypertensive syndrome is the leading clinical and laboratory symptoms of the disease since its inception or in the coming years from its commencement (i.e. long before the development of ESRD) and steadfastly preserved throughout the disease.

In the classification M. J. Ratner (1980) highlighted the following clinical forms of chronic glomerulonephritis: 1) hematuric - hematuria of any degree of severity, daily urinary protein excretion 0.5 g - 2) proteinuric - moderate proteinuria (0.1 to 1.0 g per day) or severe (1,0-3,0 g / day) without hematuria - 3) proteinuric-hematuric-proteinuria (moderate or severe) in combination with hematuria (any severity) to 4) nephrotic - nephritic syndrome in the absence of hematuria and stable arterial hypertension - 5) nefroticeskih-hematuric - a combination of nephrotic syndrome with hematuria in the absence of stable hypertension - 6) nefroticeskih-hypertension - nephrotic syndrome in combination with stable arterial hypertension (without hematuria or hematuria). In this: classification discussed in detail and possible variants of the clinical course of glomerulonephritis, which in practical terms, the most important are three: reverse the development of symptoms (remission), i.e. the total or partial disappearance of existing symptoms is stable and for the course with exacerbations. There are also identified five types of functional state of the kidneys, including kidney failure (PN). The rapidity of the occurrence of renal failure glomerulonephritis is divided into three types: 1) rapidly - stage renal failure occurs no later than cseres 6-8 months of onset - 2) rapidly progressive causes of terminal renal failure in 2-5 years from onset of illness - 3) slowly progressive causes of terminal renal failure not earlier than 10 years from the onset of the disease.

The latent form (isolated urinary syndrome) is manifested only moderately or slightly pronounced urinary syndrome in the absence of extrarenal signs of disease. Daily proteinuria in most cases not more than 1.0 g, more rarely reaches 2.0 g (but not more than 3.0 g). In normal urine, it varies often within 0,033-1.0 g/l and rarely reaches 2.0-3.0 g/L. For this type of chronic glomerulonephritis characterized by minor erythrocyturia (5-10, at least 30-50 cells in field of view) and cylindruria.

Swelling absent or sometimes there is sponginess under the eyes, less frequently on the shins. Blood pressure long and steadfastly remains at a normal level, hence no clinical, radiological and electrocardiographic signs of hypertrophy of the left ventricle of the heart and changes in the vessels of the fundus. The appearance of edema, increased blood pressure and increase bladder syndrome is possible only in the period of exacerbation. In addition, the accession of hypertension observed in the period of development of chronic renal failure when the blood pressure level on progression of renal failure is becoming higher and more persistent, and edema, possibly due to the accession of heart failure. Kidney function when latent CGN for a long time (sometimes over a period of 20-30 years) remains normal, as evidenced by the high relative density of urine in a separate analysis, in a sample of General, normal values of GFR (80-120 ml/min), the content of urea and creatinine in the blood.

Of all clinical forms of CGN latent form in the most favourable prognostic regarding: compensation of renal function and disabled patients when preventive measures can be preserved for many years and even decades. At the same time, this is the most common form of CGN, therefore, early detection of such patients, the correct placement and clinical supervision of the them are of practical importance. Meanwhile, in the absence of edema and hypertension, as well as typical complaints of patients, early diagnosis of CGN with isolated urinary syndrome presents certain difficulties. Often the diagnosis of CGN is only in the stage of CKD. Only targeted (and sometimes random) urine test allows you to establish the correct diagnosis, of course, after exclusion of other possible causes for the appearance of proteinuria and hematuria.

Nephrotic form (nephrotic syndrome) occurs in patients with CGN less latent. The most characteristic signs are massive proteinuria of more than 3.0-3.5 g daily), Hypo - and dysproteinemia, hyperlipidemia (hypercholesterolemia) and swelling. Among these signs are the most significant clinical and diagnostic value has a high level of proteinuria, whereas, for example, swelling may be minor or absent, which is currently not very rarely observed in CGN patients with nephrotic syndrome treated with corticosteroids.

Proteinuria usually exceeds 3.0 g/l, often ranges from 3.3 to 33 g/l, reaching in some cases 90 g/l and more. The daily loss of protein in the urine is 5-10-15-30 However, the vast majority of it does not exceed 10-15 g of urine excretiruyutza not only albumin but also globulin, and sometimes macromolecular protein fractions. Consequently, proteinuria can be highly selective, accompanied by the excretion of only low molecular weight protein fractions (albumin, pre - and postalebumpin), srednesetevoj with the excretion of not only albumin but also such globulin fractions as a-1 and a-2-fast and R-globulin, and nizkointensivnoi (or nonselective), when the urine allocated almost all or almost all protein fractions contained in the serum, including such macromolecular as - and a-2-slow globulins, haptoglobin.

Hypoproteinemia, which is largely due to a great loss of protein in the urine (but not only these) may be of varying severity. The protein level in the serum in the majority of patients is 60 g/l and below, often reaching 50-40 g/l, and in some severe cases, 30 and even 25 g/l decrease in the concentration of total protein primarily associated with the decrease of blood albumin. Therefore, dysproteinemia is manifested by hypoalbuminemia, which ranges from 45 to 36 , and in patients with severe nephrotic syndrome, the concentration of albumin in the blood is reduced to 20 or even up to 18-12 . Along with hypoalbuminemia, hypogammaglobulinemia is often observed, sometimes very significant, with this attribute the decline in the body's defenses and weak resistance of these patients to endogenous and exogenous infections. There has also been progress in the direction of increase of level of a - and p-globulins. With. by reducing the content of albumin is to some extent associated with the presence of hypercholesterolemia (hyperlipidemia). This increases the content of other lipids, such as triglycerides. Due to severe hypercholesterolemia and hyperlipidemia serum becomes milky in color and resembles a liquid lymphatic duct.

The next important symptom of nephrotic form CGN - swelling. This feature was previously given a leading role in the clinic nephrotic syndrome. Currently, however, the value of its push into the background due to the fact that in some cases swelling may be mild severe or absent as indicated, for example, in patients undergoing treatment of glucocorticosteroid hormones. Yet in the majority of patients with CGN nephrotic syndrome swelling are severe, frequent, sometimes reach considerable extent with the development of ascites, hydrothorax, hydropericardium. In many cases they have more tenacity and resistance to even the most powerful diuretics - sometimes kept for months and years, periodically, then decreasing, then increasing. And only with the development of chronic renal failure gradually or quickly shrink and disappear, which is sometimes a false impression of coming improvement, also simultaneously reduced and proteinuria.

The face in patients with nephrotic form CGN puffy, on the extremities, especially the lower, lumbar region, abdomen, genital organs appear large swelling testovatoy consistency, after the finger pressure on the shins, lower back long remain depression (fossa). Pale skin, cold to the touch, dry, often flaky - with massive edema of the skin of the legs, feet and less in other places cracks through which constantly oozes edematous fluid causes maceration of the skin, and sometimes sores that serve as a gateway for infections. Patients are rather slow, sluggish, their movements are limited (sometimes dramatically) due to large swelling - complain of weakness, loss of appetite, chilliness. Characterized by oliguria, sometimes significantly.

Blood pressure is usually within normal limits, often reduced, but sometimes there is a transient increase it, which may be due to exacerbation of the disease. When the signs of CKD blood pressure increases significantly and hypertension remains permanently. Pulse rare. Muffled heart sounds. On ECG marked decrease in the voltage and signs of degeneration of the myocardium. There may be dyspepsia, nausea, unstable chair. From the peripheral blood of the observed increase in erythrocyte sedimentation rate (up to 30-60 mm/h), in some cases, some anemia. Blood levels of urea, residual nitrogen, creatinine, and glomerular filtration and concentration function of kidney in compensation period CGN are within normal limits. In the urine, in addition to protein, reveals a greater number of cylinders, especially hyaline that occur in early disease, and later appear granular and waxy cylinders. Erythrocyturia absent or insignificant (from single to 5-15 in the field of view).

In hypertensive form of CGN leading symptom of the disease is hypertension with minor severity of urinary symptoms and the absence of edema. Proteinuria usually does not exceed 1.0 g/L. Erythrocyturia is missing or varies from single to 3-5-10 cells in field of view. The hyaline cylinders, a single in the preparation or under review. For some patients, there may be a pasty eyelids, face and shins. During exacerbation of the disease, as with other clinical forms, these symptoms increase.

Typically, blood pressure increases at the very beginning or in the coming years from the beginning of chronic glomerulonephritis - with increasing duration of the disease pressure is becoming higher and more persistent. This hypertensive form differs from symptomatic hypertension that develops in the later stages of the disease in all clinical forms of glomerulonephritis when joining signs of CKD. Blood pressure often increases moderately (up to 160/100 mm Hg/calendar), rarely reaches 180/110 mm Hg. article, but in some cases, already in the early stages of the disease can greatly exceed this level, reaching 200/115-250/120 mmHg. article Patients complain of headaches, dizziness and sometimes blurred vision, pain in the heart, often of the type of angina. An objective study detected early clinical (percussion), x-ray and electrocardiographic signs of left ventricular hypertrophy. Heard the accent II tone of the aorta, often systolic murmur over the base of the heart and over the top. On the ECG, especially in patients with a long disease course, pomimo signs of left ventricular hypertrophy, found the phenomenon of myocardial ischemia, signs of overload left ventricular arrhythmias in the form of arrythmia, slowing intraventricular conduction.

From the side of the fundus, as in hypertension, revealed narrowing of retinal vessels, symptoms chiasm, "copper", "silver wire", sometimes bleeding, in severe cases, retinal detachment, neuroretinitis. Possible, though less common than hypertension, hypertensive krey, cerebrovascular accident, acute myocardial ischemia with foci of degeneration or necrosis, left ventricular failure by type of cardiac asthma in advanced stages - a total heart failure with an enlarged liver and swelling of the legs.

Is Considered (N. A. Ratner, 1974, etc.) that the predictive relation hypertensive form of CGN relatively favorable: these patients prior to the development of uremia live 10-30 years, if not die from other (cardiac, vascular) complications.

The mixed form is a combination and hypertensive nephrotic syndromes. In some cases, the development of one syndrome precedes the other, but more often they occur simultaneously, and the clinical picture of nephrotic syndrome is typically expressed brightly, and the level of arterial pressure increased significantly. Thus, for a mixed type of chronic glomerulonephritis characteristic features of nephrotic syndrome (massive proteinuria, Hypo - and dysproteinemia, hypercholesterolemia, and edema) and hypertension (high blood pressure, change from the retinal vessels, hypertrophy of the left ventricle of the heart, etc.). In prognostic terms, this form is the most unfavourable in comparison with other clinical forms of CGN. The life expectancy of patients is 3-5, with a maximum of 8 years. However, with careful and persistent treatment, proper placement of patients in some cases it is possible to achieve extended life.

amatoricesca CGN form is characterized by significant and persistent hematuria in the absence of edema, hypertension and low proteinuria. Dating this form is relatively rare in adults. Hematuria can sometimes reach considerable extent and becomes macroscopically distinguishable (gross hematuria). More often, however, she detected microscopically, when the number of cells in field of view is 100 or more, or when the red blood cells more or less densely cover the entire field of view. Daily excretion of red blood cells in the urine is 50-100 . 106/day, reaching 300-500 . 106/day or more. Proteinuria not exceed 1.0 g/l (or 1.0 g / day), ranging typically within 0,033-0,099 g/l, at least up to 0.99 g/L.

However, the diagnosis of hematuric CGN form is only considered in cases where excluded other diseases that can cause hematuria (for example, the fornical bleeding, tumors of the kidneys, bladder, polyps of the bladder, urolithiasis, etc.). Hematuric option CGN should be distinguished in particular from other independent nosological form of kidney disease - IgA nephropathy (Berger disease), which is more common in males are relatively young and pathogenetically due to deposition in the renal glomeruli of immune complexes with IgA - clinically it is characterized by hematuria with episodes of gross hematuria, benign course and rare outcome in ESRD. Hematuria can be combined with other clinical forms of CGN, but it does not reach usually pronounced degree and is a leading symptom of the disease.

For chronic glomerulonephritis characterized by long years course with periods of remissions and exacerbations. Duration of response and frequency of exacerbations in each case can be different and depend on the morphological type and clinical forms of glomerulonephritis.

Benign and slow within different latent and hematuric CGN form: the duration of the compensated stage is many years and even decades. In patients with latent form (with isolated urinary syndrome) while respecting the mode of work and rest, diet, in the absence of intercurrent diseases, with the exception of hypothermia, proper employment signs of chronic renal failure are absent for a period of 20-40 years (N. A. Ratner, 1974 - A. P. Peleschuk, 1974 - L. A. perig, 1982, etc.), and sometimes more. To a lesser extent this applies to patients with hematuric CGN.

Heavy and relatively rapid progression is characterized by a mixed form, in which clinical and laboratory signs of chronic renal failure are detected after 5-7 years of onset, and sometimes before. In prognostic terms, it was the worst form of CGN.

For type of chronic glomerulonephritis nephrotic less favourably than, for example, latent. These patients are susceptible to various intercurrent diseases (pneumonia, furunculosis, erysipelas, acute respiratory disease, etc.) that will not only contribute to the progression of nephrotic syndrome, but can also be the direct cause of adverse outcome. This is because the nephrotic syndrome in patients with severely reduced the body's resistance to various infections, which is associated with a significant decrease in the level of y-globulins. The latter plays an important role in the production of antibodies and maintain the immunological protective properties of the organism.

The severity of clinical manifestations of nephrotic syndrome and its flow is due to the fact that massive and persistent edema, in the majority of cases related to this syndrome, severely limit physical activity of the patient, and sometimes the possibility of movement. Disabled patients with this form of CGN is sharply reduced, and often they become disabled. Signs of kidney failure develops after 7-10 years of onset, sometimes faster.

However, it should be noted that for CGN with nephrotic syndrome and the prognosis for him was significantly improved thanks to the use in medical practice pathogenetic therapy (corticosteroids, immunosuppressants, anticoagulants and antiplatelet agents), a powerful diuretic and other means by which in some cases it is possible to achieve a stable and long-lasting clinical remission, and sometimes complete recovery. New treatments, preventive measures, active the clinical examination, anti-relapse treatment of this patients made more favorable prognosis not only in relation to their lives, but also in relation to disability.

In hypertensive form of CGN current and the speed of progression of the disease depends on severity of hypertension and its cerebral and cardiac complications. The duration of the compensated stage of the disease in this form CGN ranges from 10-30 years (N. A. Ratner, 1974), and according to Timofeev E. M. (1972) is 20-30 years. In patients with hypertensive form more often than in other forms of CGN, possible complications such as various arrhythmias, angina and myocardial infarction, left ventricular failure with symptoms of cardiac asthma and pulmonary edema (especially during hypertensive crisis), which may be the direct cause of death. In this group of patients is often disturbed vision, until the complete loss of his, which may be due to detachment of the retina, thrombosis of the Central retinal artery, hemorrhage into the retina, ischemia of the optic center, hypertensive neuroretinitis. For long-term persistent high hypertension develops chronic heart failure due to degenerative changes in the myocardium that occurs as under the influence of an overload of the latter, and due to the rapid development of coronary atherosclerosis and related disorders of the coronary circulation with symptoms of diffuse or focal myocardial hypoxia. Believe that chronic renal failure in patients with hypertensive CGN form appears later than when mixed and nephrotic, but earlier than when latent and hematuric forms of this disease.

These in vivo biopsy of the kidney with histological examination of punctate conducted in patients with CGN in the dynamics, indicate that the disease, rapidity of progression and the prognosis is largely dependent on the morphological type of glomerulonephritis. Most researchers believe that the course and prognosis is most favorable when CGN with "minimal changes" in the renal tissue. In these patients with the help of modern pathogenic agents, particularly corticosteroids, more often than in other morphological types, it is possible to achieve a long and stable clinical remission, slow down the progression of the disease, pushing for many years to the development of ESRD, and in some cases (usually in children) to achieve a complete and permanent cure.

Less favorable, but still relatively slow flow and the relatively long duration of the compensation period, renal function characterized by proliferative, membranous and proliferative one-types of membranous glomerulonephritis. The most unfavorable course and prognosis proliferative one-fibroplastic and especially fibroplastic types of glomerulonephritis.

Some authors on the rate of progression of isolated fast - and medlineplrectile chronic glomerulonephritis. When rapidly progressive CGN duration compensated stage, and hence of life of patients is relatively small (2 to 3-5 years). When medlineplrectile CGN those dates considerably increase.

Aggravation CGN is characterized in most cases the same symptoms as acute glomerulonephritis, i.e. along with the increase of urinary symptoms appear (if they were not) or become more severe extrarenal symptoms (edema, hypertension). When less marked exacerbation noted only moderate or slight increase of proteinuria, hematuria, cylindruria, without edema and hypertension.

In some cases, for CGN may be accompanied by very severe exacerbation with the development of so-called acute nephrotic syndrome, reflecting the very high activity of the inflammatory process in the kidneys. The combination of rapidly emerging and growing with symptoms reminiscent of the clinic version of the classic FIRE in its most severe manifestation - fast appearance or increase of oedema, severe General condition, severe oliguria, significant increase of proteinuria, hematuria, cylindruria, a sharp increase in blood pressure, especially diastolic. Against this background, in some cases, may develop typical complications of acute heart (mainly left ventricular) failure, ARF, eclampsia. The clinical manifestations and course of acute nephrotic syndrome resembles a rapidly progressive (sub-acute) glomerulonephritis, acquiring sometimes continuously recurrent in nature. His appearance as when FIRE and CGN significantly impairs the disease, complicates differential diagnosis and requires the inclusion in the complex therapy active treatment methods (in particular, "pulse therapy"), by which the syndrome is relatively fast (2-3 weeks) subjected to reverse development.

In some (rare) cases when CGN with isolated urinary syndrome, as well as with hematuric may experience intermittent course of the disease, when for some period of time (from several days, weeks to several months) completely disappears urinary syndrome. This creates a seemingly complete recovery of the patient. However, under the influence of precipitating factors (physical overload, hypothermia, intercurrent infection) again appear proteinuria, hematuria, cylindruria, which are stored for a long time, and then under the influence of treatment or without it, in favorable conditions of life and work again for a while disappear.

In patients with intermittent over CGN urinary syndrome expressed slightly or moderately: proteinuria varies from traces of protein - 0,033 g/l to 1.0 - 2.0 g/l, erythrocytes from 2-5 to 15-30 in sight. This option of course CGN often mistakenly regarded as a focal bead, since the appearance of urinary symptoms in most cases follows the aggravation of focal infection (tonsillitis, sinusitis, otitis, etc.) and disappears after her active treatment. However, even after radical readjustment of the focus of infection full recovery does not occur. The disease continues to progress, exacerbations occur under the influence of other causes, and often for no apparent reason. Over time, uric syndrome becomes persistent and does not disappear completely, despite ongoing active treatment.

Intermittent for CGN is rare, but it is possible, and this should be considered in the differential diagnosis with urinary syndrome with kidney diseases of other origin. The diagnosis must indicate that this is a CGN (latent or hematuric form) with intermittent flow.

Clinical observations indicate the possibility of transformation from one clinical form of glomerulonephritis in another. Thus, upon cooling, infection and other adverse factors on the background of the latent form of the disease occurs pronounced nephrotic syndrome (E. M. Tareev, 1972 - M. J. Ratner et al., 1980, etc.). According to L. A. Parigi and N. J. Melman (1982), this transformation of the isolated urinary nephrotic syndrome was observed in secondary-chronic glomerulonephritis 7,5 patients. At the same time, under the influence of therapy nephrotic syndrome in some cases can be transformed into a latent form of CGN. However, it must be emphasized that the transition nephrotic type of chronic glomerulonephritis in the isolated urinary syndrome can also be observed in the development of chronic renal failure or shortly before (signs of a false remission), but it is usually marked by the emergence and growth of hypertension.

Possible cases of complete clinical and laboratory remission of nephrotic syndrome in CGN as a result of pathogenetic therapy and spontaneously (B. M. Tareev, 1972). The duration of remission may last from several months up to 4-8 years of age and be repeated throughout the disease 2 to 4 times.

Regardless of the clinical form of the disease and its trends in some cases sooner, in others later, the disease enters its final stage - the stage of chronic renal failure with subsequent development ezotericheskoj uremia. The earliest sign of incipient chronic renal failure when CGN is a reduction in the glomerular filtration rate of 60 ml/min or less. Later decreases and the concentration function of the kidneys decreases relative density of urine in the sample of the General and even earlier in the sample with the dry food intake. In parallel or a bit later is a violation of nitrogen excretion function of the kidneys, resulting in increased blood levels of urea and creatinine. Of these indicators creatinine more fully reflects the state Azotowe dividing renal function, as increased level of urea in the blood may sometimes be due to extrarenal factors. It is therefore important to determine in the blood not only the content of urea and creatinine. It is advisable to examine the contents of these components of residual nitrogen in the daily quantity of urine, as in chronic renal failure excretion with the urine is reduced.

The early clinical signs of incipient chronic renal failure include increased blood pressure when the CGN where it was normal, and the increase in hypertension in those cases where it has already occurred. This is due to the decrease in renal blood flow, renal ischemia and activation of the renin-angiotensin-aldosterone system.

As a result of reduced renal concentration function daily diuresis increases to 2-3 l, which leads to the reduction or complete convergence of edema. Even nephrotic edema, stubbornly not yielded to diuretics, gradually decrease and often disappear completely without the use of diuretics. In connection with the death of active nephrons decreases and urinary syndrome, in particular proteinuria, including in patients with nephrotic syndrome. Increase diuresis, convergence of edema and the reduction of urinary symptoms create patient, and sometimes watching it at the doctor a false impression about the positive dynamics of the disease and the coming improvements. However, the fall in glomerular filtration and the relative density of urine, the appearance and increase in hypertension along with increasing concentration of nitrogenous waste in blood indicate the opposite, i.e. about a progressive unfavorable course of the disease, his transition into the last irreversible stage of chronic renal failure. According to B. B. Bondarenko (1980), the life expectancy of patients with CGN after the occurrence of chronic renal failure with hyperasotemia normally not exceed 4 years and only in rare cases up to 5-6 years.

For practitioner is of undoubted interest effect of pregnancy on the course of chronic glomerulonephritis. While on this question there is no single answer. Pregnant chronic glomerulonephritis is rare in 0,04-0,2 cases (M. M. Schechtman, 1980). In the literature there is evidence that pregnancy has an adverse impact on the CGN, and worsens the prognosis in female patients with CGN. Explain that during pregnancy, there is additional load on the diseased kidneys. The load due to the intensification of metabolic processes in the organism of the mother, and the necessity of excretion of products of metabolism of the fetus, and increased circulating blood volume and the impact of other adverse factors. At the same time, other authors believe that pregnancy has no adverse effects on the course of the disease. Even there is evidence of a favorable effect of pregnancy on the course of CGN. About

Chronic glomerulonephritis

Diagnosis of Chronic glomerulonephritis:

CGN is characterized by great diversity of clinical manifestations and morphological forms and can occur under the guise of other diseases of the kidneys, with which it is always necessary to differentiate. Insufficient knowledge of the characteristics of clinical and laboratory signs of these diseases, as well as a wrong interpretation of the detected changes in the urine, can cause still fairly frequent errors in establishing the diagnosis of CGN. Even despite the progress made in the diagnosis of renal disease, particularly glomerulonephritis, the number of such errors in General internal medicine departments reaches 12-25 and more, and in specialized Nephrology-7-10 (A. Y. Yaroshevsky, 1971 - L. A. perig, N. J. Melman, 1982).

Meanwhile, the timely diagnosis of CGN is of practical importance as it allows to take preventive measures aimed at preventing further progression of disease and development of renal failure.

In a typical clinical picture and clinical and laboratory manifestations, the presence of a history of acute glomerulonephritis diagnosis CGN to put easy. However, in many cases, especially when monosemeiotic or latent within it, and the absence in the history of FIRE, the changes in the urine can be regarded as a consequence of other primary or secondary kidney diseases, and diagnosis of CGN can be difficult. In such cases to confirm the diagnosis, it is necessary to use a full range of modern clinical laboratory, rentgenologicheski and other research methods, until in vivo biopsy of the kidney.

Chronic glomerulonephritis must be differentiated with the following diseases of the kidney, clinical signs and pathological changes in urine is similar or close to those in patients with chronic glomerulonephritis.

Aggravation CGN, with not only bladder syndrome, but extrarenal (especially severe) symptoms (edema and hypertension), as well as first discovered CGN with isolated urinary syndrome can be adopted primarily for acute glomerulonephritis. This is especially the case if the manifestations of the disease are found on the background or some time later after a streptococcal infection (exacerbation of chronic tonsillitis, colds and tonsillitis, etc.) or hypothermia, and the doctor with such patients meets for the first time. In such cases, crucial in the differential diagnosis of CGN and FIRE has a thorough history and analysis of the available medical documentation. If in history there are indications of past FIRE or nephropathy during pregnancy (in women) or in the records of the preserved urine tests from previous years, which showed even a slight proteinuria and hematuria, especially in combination with high blood pressure, it speaks in favor of chronic glomerulonephritis.

In the absence of anamnestic data and urine tests from previous years to make the correct diagnosis is to determine the condition of the kidney. In favor CGN showed a decrease in glomerular filtration, renal concentrating ability (relative density of urine in a separate analysis, and the samples in General and with the dry food intake), increase in blood levels of urea, creatinine. Patients FIRE also perhaps a slight and transient decrease in glomerular filtration with little hyperasotemia, but only in the rapid course of the disease with severe oliguria, hypertension and edema. However, the relative density of urine at the same time increased in connection with the production of small amounts of urine with a high concentration of osmotically active substances. When CGN with preserved renal function and the absence of an appropriate history is almost impossible to exclude FIRE, and only long-term monitoring of patients in the dynamics allows correct diagnosis.

Often hypertensive form of chronic glomerulonephritis incorrectly regarded as hypertensive heart disease because of the difficulty of differential diagnosis of these two different diseases, especially in their terminal stage and in the absence of data on long-term monitoring of patients and urinalysis. In such cases, very difficult, and often impossible, not only clinical, but also pathological differential diagnosis of these diseases: even histologically difficult to decide on the primary (due to hypertension) or secondary (due to CGN), the wrinkling of the kidney. Often such patients are observed and treated not about CGN, and hypertension.

Clinically about hypertension, you can think in those cases, when hypertension for many years preceded the development of urinary symptoms and edema, which such patients are usually the result of heart failure.

Chronic glomerulonephritis, conversely, proteinuria and hematuria, and edema usually precede the development of hypertension for many years or from the beginning combined with the increase in blood pressure. In addition, in patients with CGN urinary syndrome in most cases is more pronounced than for hypertension. The level of blood pressure in hypertensive patients compared with CGN higher, changes of the heart, blood vessels fundus of the eye and brain are more pronounced, hypertensive crises, coronary heart disease in the form of angina pectoris and myocardial infarction are more common. In hypertensive renal plasmatic decreases earlier than the magnitude of glomerular filtration, and in CGN, on the contrary, previously reduced clearance of endogenous creatinine.

In some cases the correct diagnosis can be established only on the basis of data from in vivo biopsy of the kidney.

In the differential diagnosis of renovascular hypertension, hypertension in coarctation of the aorta, pheochromocytoma and aldosterone (horse syndrome), syndrome and disease Itsenko-Kushinga use aortography, angiography of the vessels of the kidneys and adrenal glands, ultrasound, x-ray methods, computed tomography, and determine in the blood and urine catecholamines and products of their metabolism (in pheochromocytoma).

In the latent stage of chronic pyelonephritis (especially primary), as well as chronic glomerulonephritis, can be manifested only minor urinary syndrome and less frequently arterial hypertension. In such cases, differential diagnosis between these diseases is difficult. In addition to a thorough history taking and clinical examination of the patient, sometimes you have to use the entire range of modern clinical laboratory, bacteriological, rentgenologicheski and radioisotope methods.

If in the history of the patient or medical records, there are indications cystitis, pyelitis, kidney stones, prostate adenoma, prostatitis, this allows more to think about chronic pyelonephritis. The diagnosis of this disease becomes more persuasive when observed or periodically appear dysuria, low-grade fever that cannot be explained by other causes, as well as at least a minor and non-persistent pyuria.

Important differential diagnostic importance of urine analysis for Chukovskomu-Addis and Nechyporenko (in pyelonephritis pyuria dominates erythrocyturia), the active cells or cells Shterngeymera-Malbina, which are often found in pyelonephritis and lacking in glomerulonephritis. The diagnosis of pyelonephritis becomes more convincing if the urine culture on the microflora bacteriuria more than 50-100 thousand microbial cells in 1 ml, i.e. notes of true bacteriuria.

In favor of pyelonephritis say these ultrasound and excretory urography: unequal size of the kidneys, anomaly of development (horseshoe or double kidney, hypoplasia or aplasia), uneven outlines, nephroptosis (especially if it's substantial), pyelectasis, deformation of cups, the kinks, atony, stricture of the ureter, double renal pelvis and ureter, the presence of stones, as well as uneven allocation of kidneys of contrast medium, indicating preferential loss of function of one kidney, what does not happen in glomerulonephritis. Radioisotope renography when unilateral pyelonephritis or in the case of a primary lesion one of the kidneys can detect the reduction (or a more pronounced decrease) function of one kidney compared with the other. With the same purpose can be used chromolithography, for which, as well as cystoscopy, now resorted to only when absolutely necessary, given the possibility of infection.

By means of the above methods is almost always possible to correctly diagnose. In those rare cases where it still remains unclear or questionable, it is shown a needle biopsy of the kidney, which allows you to confirm or exclude the diagnosis of glomerulonephritis or pyelonephritis. However, a negative biopsy results (no biopsy evidence of glomerulonephritis and pyelonephritis) still do not exclude the possibility of pyelonephritis. This is because morphologically pyelonephritis unlike glomerulonephritis is manifested polymorphism and the focality of the lesion of the renal tissue, when the areas of inflammatory infiltration interspersed with areas of healthy tissue and, therefore, the penetration of the needle is not damaged in the pathological process of the fabric makes it impossible to detect the inflammatory process.

Chronic glomerulonephritis clinical and laboratory signs has a lot to do with amyloidosis of the kidneys. Thus, the latent form of CGN are very similar or have similar manifestations with proteinuric, nephrotic - nephritic stage of amyloidosis.

For proteinuric stage of renal amyloidosis characterized by low, sometimes unstable (transient) proteinuria with very little sediment (isolated erythrocytes and hyaline cylinders, in the absence of edema and hypertension). Further proteinuria increases and it is accompanied by other signs of nephrotic syndrome, is no different from that of patients with chronic glomerulonephritis. Difficulties in the differential diagnosis increase if early clinical and laboratory signs of renal amyloidosis appear after moved streptococcal infection or other aggravating factors (intercurrent illness, hypothermia, trauma, etc.). Not it is less difficult and in the chronic renal failure.

In the differential diagnosis of these diseases should consider the following data. Secondary renal amyloidosis develops, as a rule, patients, long suffering from chronic inflammatory, especially meningitis, diseases (tuberculosis of various localization, congenital or acquired bronchiectasis, chronic lung abscess, osteomyelitis, etc.). Often it is the result of rheumatoid arthritis, Hodgkin's disease, myeloma and recurrent disease, ulcerative colitis, malignant tumors (in particular, hypernephroma), etc. Renal involvement in amyloidosis is often associated with amyloidosis of other organs - liver, spleen, intestine, heart, mucous membranes of the oral cavity, which is accompanied, for example, the increase in the size and density of the liver and spleen, unexplained diarrhea, abnormal heart rhythm, heart failure, etc.

Primary amyloidosis is now regarded as a disease is genetically determined, therefore, the diagnosis of its important presence in the history of hereditary predisposition.

Some differential diagnostic role can be played biopsy data submucosa straight or sigmoid colon, the mucosa of the lips, the performance of samples with kongoro, methylene blue, and samples of Evans. However, the diagnostic value of these studies have only in the presence of positive results that are reported more frequently in the later stages of amyloidosis. The negative results mentioned trials do not exclude the possibility of amyloidosis. In favor of amyloidosis shows and hypergammaglobulinemia, as well as hyperlife-2-waldenstrom detected using protein electrophoresis of serum in starch gel.

In amyloidosis of the kidneys may be enlarged and unlike CGN, even in the chronic renal failure is not reduced (remains within normal limits).

However, the considered differential diagnostic criteria do not always allow to convincingly exclude or confirm the diagnosis of amyloidosis of the kidneys, which is often misinterpreted as a glomerulonephritis. And only lifetime needle kidney biopsy with histological examination punctate enables virtually 100 cases, to confirm or exclude the diagnosis of renal amyloidosis.

As CGN, diabetic glomerulosclerosis is manifested urinary syndrome, hypertension and nephrotic syndrome often. The occurrence of these symptoms in patients, long suffering from diabetes, usually speaks in favor of diabetic glomerulosclerosis. The diagnosis becomes more convincing if you show signs of systemic microangiopathy, in particular retinopathy with microaneurysms and petechial hemorrhages in the fundus, and the symptoms of polyneuritis. Indirect confirmation of glomerulosclerosis is a gradual decrease of glycemia and glycosuria without increasing (or even decreasing) the dose of antidiabetic drugs. Finally and most convincingly, the diagnosis of CGN or diabetic glomerulosclerosis made on the basis of biopsy of the kidney.

Pregnant nephropathy usually develops in the second half of pregnancy and is either only moderately, severe urinary syndrome, or (more likely) in addition to urinary symptoms, edema and hypertension. If these pathological signs emerged for the first time and disappear after delivery or abortion, they should be regarded as a manifestation of nephropathy pregnant. In other cases, changes in urine (proteinuria, hematuria, cylindruria), and sometimes swelling and hypertension persist for many years after the end of pregnancy. This outcome allows us to think about the transformation of nephropathy in pregnant chronic glomerulonephritis, or, more usually, about already existing and not diagnosed promptly CGN, the aggravation of which occurred during pregnancy. In the absence of indications in the past signs of glomerulonephritis differential diagnosis of CGN with nephropathy pregnant can be difficult, especially that carried out a biopsy of the kidney pregnant undesirable. In addition, according to N. A. Ratner (1974), histomorphological pattern of the renal tissue nephropathy of pregnancy is virtually indistinguishable from that of patients with glomerulonephritis.

In favor of CGN may indicate a decrease in glomerular filtration and renal concentration function, severe hematuria, and maintaining bladder syndrome long-term (permanent) at the end of pregnancy. In cases where proteinuria, hematuria, cylindruria, and sometimes the extrarenal symptoms persist throughout the entire period of observation after birth or miscarriage and when it is known that pre-pregnancy pathological changes in the urine is not mentioned, you should think about the transition (transformation) nephropathy in pregnant chronic glomerulonephritis corresponding clinical forms (depending on the clinical manifestations of the disease).

Gouty nephropathy, or gouty kidney, develops in patients (usually men), long suffering from gout. As CGN, it is manifested moderate or mild proteinuria, hematuria and cylindruria, often with high blood pressure. However, unlike CGN urinary syndrome occurs in the characteristic lesions of the joints in the form of recurring arthritis very pronounced, most often the big toe, tophi on the ear. Attacks of gouty arthritis or arthritis may be accompanied by hypertension, oliguria, renal colic, as in the urinary tract are often found stones.

For gouty nephropathy characterized by an early decrease in renal concentration function (manifested by a fall in the relative density of urine in the sample of the General), alkaline reaction of urine and the development of anemia. Detected a high level of uric acid in the blood (hyperuricemia) in the period of exacerbation of the disease and in the urine in the period remarie. When histomorphological examination of biopsy material of renal tissue obtained by biopsy, there is a urate deposition in the lumen of the tubules and in the interstitial tissue as well as inflammatory response in the interstitial tissue.

Renal disease in diffuse connective tissue diseases (collagen diseases) are particularly common in patients with systemic lupus erythematosus and may be the first and the earliest manifestation (debut). Clinically they are characterized by either urinary syndrome, or a combination of the latter with arterial hypertension is often accompanied by the development of typical nephrotic syndrome.

The criteria for the differential diagnosis of CGN with kidney disease when these diseases are signs of damage, in addition to the kidneys, and other organs of the joints, nervous system, heart, blood vessels, digestive organs, etc., i.e. the consistency of the lesion. Important, particularly in SLE, have different allergies, intolerance to many medications, sun exposure, etc., of General symptoms like fever and weight loss, and increased erythrocyte sedimentation rate, leukocytosis or leukopenia (SLE), hypergammaglobulinemia, positive immunological tests, detection of blood LE-cells, etc.

Differential diagnosis is particularly challenging when moderately or slightly marked changes in the urine for a long time (sometimes several years) remain the only sign of SLE, systemic sclerosis, or other diffuse diseases of connective tissue. In such cases, the correct diagnosis can be established only with the help of the whole complex of clinical, laboratory, immunological and other studies. Crucial in the diagnosis data belongs needle kidney biopsy and histological examination punctate.

Systemic vasculitis, of which the greatest practical importance periarteritis nodosa and hemorrhagic vasculitis (disease Henoch-Schonlein purpura), often accompanied by kidney damage with severe hematuria (sometimes in the form of gross hematuria and mild or moderate proteinuria. Therefore, hemorrhagic vasculitis often have to be differentiated with hematuric CGN. Unlike CGN when the disease Henoch-Schonlein purpura along with urinary syndrome there are other manifestations of this disease is hemorrhagic skin rash, abdominal pain, sometimes tarry stools, bleeding in the fundus, arthralgia or arthritis, fever, leukocytosis, increased ESR, positive symptom harness, symptoms Nesterov, pinch, etc. it Should be noted that the complete disappearance of pathology of the kidney in patients with hemorrhagic vasculitis is rare. In many cases progress to chronic glomerulonephritis, sometimes with a rapidly progressive course.

For subacute bacterial endocarditis is characterized by proteinuria, hematuria, and cylindruria as a result of embolism of the renal vessels with the development of kidney infarction or alopecia glomerulitis. In some cases, the development of diffuse glomerulonephritis with all of the disease symptoms (sometimes with typical nephrotic syndrome). It often becomes chronic and persists even after recovery of the patient from bacterial endocarditis, which leads to the development of chronic renal failure.

When the atypical course, unexpressed clinical picture of subacute bacterial endocarditis signs of kidney damage in the form of microproteinuria and microhematuria may be the first and only symptoms of this disease that is often mistakenly regarded as an independent isolated kidney disease.

Differential diagnosis of CGN and kidney failure in bacterial endocarditis are as follows. The latter in most cases develops in patients with acquired or congenital heart disease, is accompanied by thermal reaction of varying severity, often chills and sweats, found enlargement of the spleen, less frequently the liver, signs of vasculitis (positive symptom .harness, pinch, Lukina-Libman-Etinger)- increased erythrocyte sedimentation rate, often leukocytosis (although possible and leukopenia), the positive formaula test, Wasserman - in 50-70 of cases, from the blood when sown on nutrient medium were plated microbe is the causative agent of this disease.

The diagnosis of subacute bacterial endocarditis is becoming more convincing if, in addition to these symptoms, embolism appear in different vascular areas.

Medication of kidney damage (nephropathy medication), as well as glomerulonephritis, characterized by proteinuria and hematuria. Unlike HRN pathological changes occur in the urine in patients receiving the drug and disappear after its abolition through different time intervals. However, if you are sensitive to one or another drug drug may develop this disease, which often takes a chronic course even after the removal of its cause and leads to the development of chronic renal failure. With medical renal disease are usually observed and other signs of drug intolerance (allergic skin rash, often in the form of urticaria, angioedema - changes in peripheral blood - leukopenia, eosinophilia, the phenomenon of agranulocytosis, etc.).

Polycystic kidney disease, in addition of proteinuria and hematuria (usually slightly expressed), clinically manifested hypertension, which can reach a high level. This congenital abnormality (abnormality) is often performed under the diagnosis of chronic glomerulonephritis. However, differential diagnosis of polycystic kidney disease and CGN, with careful examination of the patient not the problem. In favor of polycystic says determined by palpation and radiologically significant increase in the size of kidneys with bumpy uneven surface.

Currently, the most simple and at the same time reliable method of diagnosis is polycystic renal ultrasound. To retrograde (ascending) pielografii by which programme detected characteristic pattern: separated, elongated and deformed Cup on the background of a significant increase in the size of the kidneys (programme has the shape of a dragon), now seldom used. The important role played by data and scan of the kidneys. The scan indicated the areas that do not accumulate radioactive substances and which correspond to the cavities (cysts). In complex cases, used computed tomography.

Urolithiasis requires a differential diagnosis with hematuric CGN, especially in cases where in history there is no indication the attacks of renal colic. Sometimes along with microproteinuria and hematuria due to affiliate pyelonephritis pyuria is observed.

In the diagnosis of urolithiasis are important methods of ultrasound and radiographic examination (panoramic picture of the kidneys, excretory urography, retrograde pyelography), which allow to identify the stones, their localization and size. Widely used radioisotope renography that allows to detect the side of the lesion and degree of violations of urodynamics. However, this method makes it possible only indirectly judge the concrements in the urinary tract or to suspect their presence. The final diagnosis can be established by using rentgenologicheski methods of research. In typical cases, accompanied by attacks of renal colic with hematuria (often with gross hematuria) and microproteinuria, differential diagnosis of urolithiasis and CGN usually does not present great difficulties.

In patients with nephroptosis (one or two - sided, particularly pronounced in the urine, or more often occasionally found small amounts of protein (0,033-0,66 g/l) and erythrocytes (5-10, 15-30 in the field of view) that makes you think about CGN, with isolated urinary syndrome.

The diagnosis of nephroptosis is established on the basis determined by palpation omitted the kidneys and is confirmed by ultrasonic and radiographic examination (panoramic picture of the kidneys or better excretory urography with the patient supine and standing). In the presence of nephroptosis may develop and glomerulonephritis (often pyelonephritis). The final question about the diagnosis in such cases is solved by a whole complex of clinical laboratory, biochemical, bacteriological and other methods of research, and if possible and necessary - with the help of biopsy of the kidney.

Kidney tumors (in particular, hypernephroma), accompanied, in addition to other signs of the disease, hematuria and proteinuria may not be regarded as CGN, moreover, often along with urinary syndrome accompanied by development of arterial hypertension. Hematuria in kidney tumors sometimes manifests itself in the form of clots.

In the differential diagnosis of these diseases must be considered, in addition to these, and such characteristic kidney tumor symptoms such as progressive weight loss, weakness, loss of appetite, low-grade fever, increased ESR, anemia, as well as age (usually after 50-60 years). Crucial in the differential diagnosis are methods and infusion excretory urography, renal angiography, and radionuclide scan of the kidneys (these scans can provide valuable information, especially in tumors of small size). Currently this is used for ultrasound - sonography and computed tomography of the kidneys.

Renal tuberculosis, diagnosis seems very difficult and often regarded as CGN. In this regard a long time, sometimes for several years, is not a rational therapy, which often contributes to the progression of the disease and the development of irreversible structural alterations in the renal tissue.

About renal tuberculosis may indicate the following data: a history of pulmonary tuberculosis or other localization, the presence of clinical and radiological signs of specific disease of the lungs and other organs, low-grade fever, weakness, sweating, positive Mantoux test, detection of tubercle bacilli in the urine by microscopic examination (flotation method), accession, in some cases, dysuric phenomena, lower back pain, leucocyturia. The diagnosis is confirmed if the urine culture on a nutrient medium grow tubercle bacilli or positive biological samples of Guinea pigs. Some importance ultrasound, rentgenologicheski and radioisotope research methods, in particular excretory urography and renal scan.

In establishing the diagnosis of chronic glomerulonephritis should be excluded and the possibility of so-called physiological (benign) of proteinuria, which includes in particular orthostatic (legationsrat) proteinuria, proteinuria voltage, or "marching", and congestive proteinuria.

In clinical practice, particularly important in the differential diagnosis given orthostatic proteinuria, occurring in adolescence in individuals of high growth with a pronounced forward deflection of the lumbar spine (lordosis). This type of proteinuria often have to be differentiated with latent form of chronic glomerulonephritis. For orthostatic proteinuria is characterized by the absence of protein in the morning urine (after sleep) and after the appearance of his stay on his feet (in vertical position).

To confirm or exclude orthostatic proteinuria in clinic orthostatic test is used. Its essence consists in the following. First take on the study of urine collected after sleep (no load), and then after finding investigated in a vertical position, or kneeling for at least 30 min with behind the head (on the neck) hands or by holding for a specified time hands the stick behind his back, in the lumbar. In this position, increased lordosis, and in the presence of orthostatic proteinuria in the urine collected after the end of the sample, the protein level sushestvenno higher than that in urine samples taken prior to the test, in which a protein may be absent. Chronic glomerulonephritis similar dynamics in protein concentration is usually observed.

"Marching" proteinuria occurs after severe and prolonged physical activity. She was transitory and disappears completely after a few hours or 1-2 days after completion of loading.

Congestive proteinuria detected in patients with heart failure IIB-III stages of different origin. Sometimes it can be significantly expressed (up to 3-10 g/l), RCT the presence of edema incorrectly regarded as chronic glomerulonephritis with nephrotic syndrome. However, when proteinuria congestive unlike nephrotic form of chronic glomerulonephritis edema are located mainly in sloping areas (legs, lower back) and are not on the face, not hypercholesterolemia, is not always marked hypoproteinemia. The crucial differential diagnostic importance is the fact that after the elimination of signs of circulatory failure, proteinuria disappears completely.

Justifying the diagnosis of chronic glomerulonephritis and conducting a differential diagnosis cannot be overlooked and kidney damage with the development of urinary symptoms in multiple myeloma (myeloma kidney), chronic myeloid leukemia, in patients with hepatorenal syndrome, syphilis, malaria, thrombosis of the renal veins and other diseases.

Timely and correct diagnosis of chronic glomerulonephritis is possible only with the exception of the above diseases. And this in turn is possible when the physician is well aware of the clinical picture and course of these diseases, as well as research methods that are most securely help solving the problem.

Chronic glomerulonephritis

Treatment of Chronic glomerulonephritis:

All patients FIRE and aggravation CGN must be hospitalized in specialized Nephrology, and in their absence - in the therapeutic Department. During this period, you must comply with bed rest, the duration of which in each case depends on the severity of symptoms of exacerbation, severity of the disease of the kidney function and possible complications, in particular cardio-vascular system, and ranges from 2-4 weeks to 2-3 months. This is one of the most significant and effective methods of treatment of glomerulonephritis. Stay in a horizontal position in a dry and warm bed in itself contributes to a more rapid disappearance or reduction of the main signs of the disease, especially heart failure, hypertension and edema. With a uniform warming of the entire body dilates the skin and subcutaneous arteries and arterioles, reflex-renal vessels. The result is lower total peripheral resistance to blood flow, blood pressure and, consequently, the load on the left ventricle, accompanied by a decrease and then complete disappearance of symptoms of heart failure. Improvement of renal blood flow helps increase GFR, increase diuresis, convergence of edema, reduction of hypovolemia and ultimately facilitates the work of the heart.

One of the most important elements of the complex therapy of acute and chronic glomerulonephritis diet therapy. It has been used since the time of Hippocrates to the present time remains the mainstay of treatment of glomerulonephritis. However, it should be noted that so far there is no consensus on some issues of clinical nutrition in glomerulonephritis.

The basic principle of diet therapy in acute glomerulonephritis is the restriction of salt (mainly sodium) and fluid with sufficient calorie and vitamin content. The provision on the need to limit sodium FIRE when it is recognized. In the presence of edema, especially in a period of growth, the content of salt in food is limited to 0.2-0.3 g per day, but no more than 2-3 g in the first period of the disease, taking into account its content in foods. The main is benatia diet, whereas total ban or severe restriction of fluid is of secondary importance. Therefore should not be administered medicinal preparations containing sodium ions (sodium bromide, sodium bicarbonate, etc.). Appropriate any benatia diet, such as rice, fruit rice, fruit and vegetable, potato, rich in calcium ions, potassium and poor in sodium. It is the ratio of potassium and sodium is approximately 20:1. Such a diet has a diuretic effect and hypotensive properties, promotes the convergence of swelling and elimination of heart failure, reduces the excitability of the Central nervous system, to a certain extent is desensitizing, as poor not only sodium, but also contains little protein, In severe cases the amount of fluid is limited to 500 ml per day. In the future, the salt content in food and the amount of liquid determined by the amount of urine output, blood pressure level, presence of edema and the condition of the hydrophilicity of tissue. However, the salted diet is recommended for 2-3 months or more.

During the expansion of diet apply potato-Apple-fat table (1,5-2 kg of potatoes of different cooking, 75 g butter, well washed in water, and 500 g of highly sugared apples) proposed M. I. Tumanova et al. (1963). This diet malamalama (25-30 grams protein), mainly carbohydrate and fat, contains up to 20 g of potassium and only 1 g of sodium chloride. Sometimes prescribed folk diuretic - a pumpkin. In this diet, there is a good diuresis (a day to 1.5 liters and more) and a rich selection of nitrogenous wastes.

Most clinicians-nephrologists believe it is necessary in the initial period of the disease be limited to inclusion in the daily diet of animal protein at the rate of 1 g per 1 kg of body weight of the patient, in severe cases of 0.5-0.6 g per 1 kg of body weight. Complete prohibition of animal protein, as had been the practice before, unnecessarily. Unreasonably well as the appointment of an excess amount of protein. The sharp restriction of protein is shown only when the giperazotemii that in acute glomerulonephritis is rare and does not last long.

To cover the required number of calories in the diet also includes carbohydrates and fats by adding cream and (or) vegetable oil. Existing opinion about sensitizing action of carbohydrates is not confirmed. In addition, food should be rich in vitamins.

Most nephrologists believe possible in acute glomerulonephritis apply in moderation flavorings or seasonings (onion, pepper, mustard, horseradish, parsley, etc.) in order to improve appetite and taste unsalted or salted food.

In the recovery period, after the disappearance of extrarenal signs of the disease and reduce bladder syndrome, it is recommended that a balanced diet, without limitation liquid, but with the restriction for a long period of time (one year) of salt (up to 6-8 g / day).

Chronic glomerulonephritis diet designed for the long term, that is why it is necessary to consider the clinical form of the disease, its course (remission or exacerbation), stage (compensated or with symptoms ESRD). In addition, the diet should spare the damaged kidney tissue and contribute to the elimination of the main symptoms of edema, hypertension, urinary syndrome. At the same time, prolonged use of this diet should not adversely affect the General nutrition of the patient, his health and efficiency. Therefore, in the daily diet of patients is necessary to provide sufficient calories, protein, fat, carbohydrates and foods rich in vitamins C, b, PP, P, etc. (fruit, vegetables, etc.).

Developed and proposed alternatives and modifications of diets with respect to clinical form, for the CGN and the status of renal function. These requirements diet therapy in glomerulonephritis is most consistent with diet No. 7 (7a, 7b). Regarding the content of protein in the daily diet of patients with chronic glomerulonephritis and acute, while there is no consensus. The most widespread opinion, according to which patients with chronic compensated (without renal dysfunction) glomerulonephritis must get enough protein (about 1 g per 1 kg of body weight), and nephrotic syndrome - 1.5 g per 1 kg of patient weight. In violation nitrogen excretion function of kidneys need to reduce the amount of protein, especially of animal origin, up to 40 g or less per day, until a sharp limit (up to 20-18 g / day) when expressed phenomena of ESRD.

In patients with latent glomerulonephritis (with isolated urinary syndrome) dietary restrictions should be minimal. Meals must meet the physiological needs of the body with the content in the daily diet of protein about 1 g per 1 kg of body weight with a slight restriction of salt (up to 6-8 g / day) and without significant restriction of the fluid. Similar should be the diet and hematuric CGN form. The diet should include foods of plant origin, rich in vitamins C, P (lemon, tincture of rose, black currant, etc.), strengthens the vascular wall and reduce its permeability. In patients with hypertensive CGN form with the same content of protein in the daily diet requires more stringent restriction of salt and fluid.

In all clinical forms of CGN, especially in hypertensive preferred lacto-vegetarian diet. In the case of persistent and resistant hypertension is recommended to periodically fasting days (fruit, rice, potato, vegetable, etc.). Such a diet poor in sodium chloride and rich in potassium, reduces blood pressure and increases the effectiveness of antihypertensive agents.

The most significant and at the same time the greatest difficulties in its implementation has dietary therapy for nephrotic and mixed forms of CGN. There must be a serious attitude and a deep understanding of the need to observe a strict diet restrictions not only (and not so much) doctor, how many sick people. The presence of large, sometimes massive and persistent edema in this group of patients requires a very strict and prolonged restriction of salt and fluid. And table salt in severe cases, limit to a minimum (for an adult 3-4 g / day) with regard to the content of her food, of which it is particularly rich bread (white bread - 0,6 , in black - 0.75 sodium chloride) and oil. For such patients bake a special "kidney bread", i.e. without added salt, and the oil is repeatedly washed or soaked in water. However, it should be borne in mind that prolonged and severe restriction of salt is fraught with the risk of developing such serious side effects as haripriya azotemia. Therefore, when persistent and persistent swelling, it is recommended to carry out so-called "zigzags", i.e., periodically it is possible to increase (reduce swelling), then again strictly limit the amount of salt in the diet.

Along with restriction of sodium chloride should be respected and fluid restriction. The number of her during the day, given liquid food, should not exceed 600-800 ml and depends on the daily urine volume and dynamics of edema syndrome. There is an opinion that the amount of alcohol consumed within a day of liquid must not exceed the daily urine of the previous day with the addition of 200-300 ml, taking into account the physiological loss through the respiratory system, gastrointestinal tract, and sweat glands (A. P. Peleschuk, 1974). The convergence or reduce swelling contribute to the discharge of Apple or Apple-potato days (1-2 times a week). Diuretic effect is watermelon, pumpkin, melon, grapes, bananas.

In the daily diet of patients with nephrotic syndrome should contain at least 1.5 g of protein per 1 kg of body weight. Some authors recommend the protein content increased to 2-3 g per 1 kg of body weight (M. N. Tumanova, 1963 G. Midrachov, 1980, etc.), given the high proteinuria in these patients and, hence, greater the loss of protein in the urine. However, enhanced protein diet care for the patient because of possible increase in blood levels of urea and an increase in proteinuria. According to Timofeev E. M. (1958, 1972, 1983), in patients with nephrotic syndrome is the most reasonable diet with a content of 1.5-2.5 g of protein per 1 kg of body weight when the total increased calorie.

In the mixed form of CGN (combination and hypertensive nephrotic syndrome) diet therapy should take into account limitations in each of these clinical forms separately, i.e. account must be taken of the presence and edema, and hypertension.

As with FIRE, allow the addition to be eaten in moderation flavouring agents or condiments (pepper, onion, mustard, parsley, horseradish, etc.), unless there is a contraindication on the part of the digestive system.

In the period of exacerbation of the disease, regardless of its clinical form requires a more severe restriction of salt and fluid, particularly in cases where increased blood pressure, appear and increase swelling. As with FIRE, the protein content in the daily diet is limited to 0.5-0.6 g per 1 kg of body weight mainly due to the proteins of animal origin.

Strict adherence to diet and with a favorable course of the disease even without medications might lead to low blood pressure, reduction of edema and heart failure events. However, in order to more rapid elimination of the major extrarenal signs of glomerulonephritis (edema, hypertension, heart failure), it is reasonable to prescribe anti-hypertensive, diuretic, heart and other symptomatic drugs. With the introduction into clinical practice of new diuretics (hydrochlorothiazide, furosemide, lasix, uregei, aldactone, etc.), as well as with the use of osmotic diuretics type manitol managed to achieve notable success in the struggle with edema, especially resistant nephrotic syndrome. The use of such a powerful antihypertensive agents (drugs rauwolfia, adrenomimetiki, ganglionic, b-blockers, etc.) have improved the prognosis of patients with hypertensive form of chronic glomerulonephritis.

In the treatment of hypertensive syndrome it is advisable to prescribe drugs rauwolfia (reserpine, rosedal, raunatin, serpasil, etc.), especially in combination with saluretikami (hydrochlorothiazide, furosemide, uregei, veroshpiron, etc.) in individual doses depending on severity of hypertension and effectiveness of the drug. With the same purpose, use b-blockers (propranolol, obsidian, etc.), methyldopa (dopegit, aldomet), and at high and resistant hypertension - drugs guanethidine number (ismelin, Isobaric), necessarily taking into account their possible side effects (orthostatic collapse) and carefully controlling the level of blood pressure. You can use and antihypertensive drugs such as gamiton, adelfan, depression, and angiotensin-converting enzyme inhibitor - captopril (capoten) in a dose of 25-100 mg/day.

Are also widely used calcium antagonists (nifedipine, corinfarum, kordafen), which, in addition to the hypotensive action, have the ability to increase glomerular filtration rate and diuresis.

When edema is prescribed a diuretic (diuretics) media: hydrochlorothiazide 50-100 mg, furosemide on 40-80 mg, lasix orally or parenterally by 40-80-120 mg, uregei 50-100 mg per day. If necessary to achieve a diuretic effect, combine two or three drugs, such as hydrochlorothiazide to furosemide. In the case of resistant nephrotic edema is shown an intravenous infusion of blood plasma, albumin, osmotic diuretics - mannitol (20 a solution of 300-400 ml per day intravenously 5-6 days in a row), solutions reopoliglyukina (300-400 ml), and sometimes large doses lasix - up to 300 to 500 and even 1000 mg per day (G. P. shultsev, 1972 - V. I. Shumakov, M. J. Ratner et al., 1980). A good diuretic effect in such cases is the use of heparin, which is used as one of the pathogenetic treatment of nephrotic syndrome, including those due to acute glomerulonephritis. Chronic administration of diuretics should be prescribed drugs potassium (potassium orotate, pananginum, potassium chloride) or foods rich in potassium ions (dried fruits, raisins, apricots, rice, unpeeled potatoes, etc.).

In heart failure, complicating FIRE, prescribed cardiac glycosides - strofantin, korglikon, and aminophylline or diaphyllin intravenously, diuretics (better lasix intramuscularly or intravenously), phlebotomy.

With the development of angiospastic encephalopathy (eclampsia) are recommended medicines hypotensive and sedative effect, as well as drugs that may affect brain edema (intravenous lasix, aminophylline, Dibazol, mannitol, magnesium sulfate, hexon or pentamin, chlorpromazine, a concentrated glucose solution), from enemas of chloral hydrate-0.5-1.0 g in 100 ml of water. In severe cases, shows a lumbar puncture, phlebotomy.

Treatment of oligoanuria and acute renal failure when FIRE is not fundamentally different from therapy ARF of other origin. When resistant anuria, uremia and hyperkalemia should be used for acute hemodialysis.

Taking into account of allergic origin of the FIRE is shown antihistamine preparations (Dimedrol, pipolfen, suprastin, diazolin, tavegil etc.). Recommended ascorbic acid, rutin, calcium supplements, although convincing data about their favorable influence on the course of the disease there.

Early in the disease it is advisable to prescribe antibiotics, given streptococcal etiology of FIRE and frequent detection in the throat and nasopharynx of patients with b-hemolytic Streptococcus, even in the absence of tonsillitis. Recommended antibiotics, does not have a significant nephrotoxic effect (penicillin, oxacillin, erythromycin) in the optimal therapeutic dose for 10-14 days, and if necessary (presence of foci of infection, intercurrent infection, fever) and longer. Contraindicated in the presence of sulfa drugs, are not recommended the nitrofurans, methenamine.

Chronic glomerulonephritis are the same as diuretics and antihypertensives, and in acute, however, to assign them more durable. As with hypertension, antihypertensive drug in maintenance doses taken for many months and years. In the absence of their effect necessary to change or be used in other combinations.

It should be borne in mind that long-term use saluretikov can disrupt electrolyte balance, in particular to develop hypokalemia due to excessive excretion of potassium through the urine. In such cases, you must assign either a diet rich in potassium ions (rice, apricots, unpeeled potato, etc.), or potassium (potassium chloride, pananginum, potassium orotate), or to combine saluretics with potassium-sparing diuretics (aldosterone antagonists - aldactone, verospiron).

In the absence of effect from saluretikov that not very rarely observed in patients with nephrotic edema, in order to increase oncotic pressure of blood administered intravenously 3-4 days in a row reopoligljukin, neocompensan or gemodez 200-500 ml daily for 4-5 days - mannitol by 200-400 ml, more than 20 solution intravenously (administered over 15-20 min) 4-6 days in a row. With regard to intravenous injection of 100-200 ml of a 10 solution of albumin, the diuretic effect is insignificant and of short duration. Diuretic effect of diuretics is enhanced by the glucocorticosteroid therapy and heparin.

Patients with hematuric CGN administered ascorbic acid, rutin, ascorutinum, with severe hematuria - menadione, dicynone, aminocaproic acid. If necessary, recommend antihistamines (diphenhydramine, suprastin, pipolfen, tavegil etc.), sedatives, cardiac glycosides.

In the presence of foci of active streptococcal infection shows the inclusion in the complex therapy of antibiotics, non-nephrotoxic action (penicillin, oxacillin, ampicillin, oleandomitsin, etc.) in optimal doses for up to 10-14 days.

The most important link in the complex therapy of diffuse glomerulonephritis is the use of methods and means of the so-called pathogenetic therapy - corticosteroids, immunosuppressants, antiinflammatory agents, anticoagulants, and antiplatelet agents. Observed by most researchers relatively high efficiency of the mentioned pathogenetic drug therapy of diffuse glomerulonephritis associated with autoimmune Genesis of the latter.

Corticosteroids have anti-inflammatory, desensitizing and immunosuppressive properties. Under the influence of corticosteroid therapy increases the urine output, swelling, reduced or in some cases disappears completely urinary syndrome, especially proteinuria and cylindruria, improved protein composition of blood serum, reduced hypercholesterolemia. According to clinical observations, corticosteroid hormones most shows and effective in nephrotic syndrome, especially in children with so-called pure lipoid nephrosis, when it is possible to achieve not only long-term remission, but full recovery. Whether the use of corticosteroid therapy in nephrotic syndrome acute and especially chronic glomerulonephritis almost no one in doubt.

This method of therapy to some extent effective in hematuric and latent forms of glomerulonephritis. However, the appropriateness of its purpose has been questioned, since these forms of the disease occur, as you know, most favorably, and the use of large doses of glucocorticoids may be associated with the risk of severe complications that often accompany massive corticosteroid therapy.

There are different opinions about the appointment of glucocorticosteroid hormones in acute glomerulonephritis. Most clinicians-nephrologists believe that they should be prescribed only when protracted course of acute nephritis, when disappear or are greatly reduced hypertension, edema, phenomena of heart failure. According to A. P. peleschuk (19,74), almost 50 patients FIRE with protracted course and a propensity to transition into a chronic using corticosteroids can be achieved either complete cure or transfer heavy nephrotic form in easier and prognostically more favorable latent. There is another point of view according to which PHYSICAL therapy steroid hormones generally impractical, except in nephrotic syndrome (N. Popov, 1973).

The success of corticosteroid therapy is largely dependent on histomorphological pattern of renal disease, i.e. the morphological type of glomerulonephritis. The most effective use of steroid hormones with "minimal changes" in the glomeruli and in membranous glomerulonephritis, the less effective during the proliferative one-membranous and inefficient or almost no effect in patients with proliferative one-fibroplastic glomerulonephritis. Recent morphological type clinically corresponds most often a combination of nephrotic syndrome with hypertension, i.e. in the most predictive of adverse mixed form of glomerulonephritis that are difficult and other methods of treatment. In this regard, to take a decision on the evidence and the advisability of the appointment of corticosteroid therapy should (subject to availability) based on the results of biopsy of the kidney (N. A. Mukhin, I. E. Timofeev, 1983).

The effectiveness of steroid therapy decreases with increasing stages of the disease - it is believed that when the duration of CGN for more than five years the use of steroid hormones in most cases does not lead to success. It is not recommended to prescribe these drugs in renal failure (urea content in blood serum of more than 10 mmol/l). There are the cases when prolonged use of large doses of hormones led to the development of nephrosclerosis with impaired renal function. Contraindicated for patients with severe hypertensive syndrome that accompanies the jade because corticosteroids have the ability to raise blood pressure.

In the appointment of corticosteroid therapy, it is advisable to take into account the selectivity of protein in egory: improved outcomes in highly selective and decreases with nizkointensivnoi or nonselective proteinuria.

The basic principle of corticosteroid therapy is the prescription of large doses of drugs for a long time. Daily dose of prednisone is 60 to 80 mg, the course of treatment usually lasts for 4-6-8 weeks, 3-6 months (M. J. Ratner, Biryukova L. S., 1992). The optimal daily dose of reach by a uniform increase within 4-6 days, starting with 10-20 mg this dose treatment lasts 3-4 weeks, after which the drug is gradually reduced by reducing the dose rate of 1/2 - 1 tablet (2.5-5 mg) every 2-3 days. The course of treatment if necessary, repeat after 3-6-12 months. A second course of treatment is usually more effective than the previous one. It should be borne in mind that the dose of prednisolone is less than 50 mg/day is ineffective or do not give effect.

In addition to the above, the proposed and other schemes of treatment with steroids. For example, to avoid the development of severe side effects during long-term treatment with high doses, the following scheme is used prolonged intermittent treatment, in which the end of the regular course continues the long-term (over several months) the treatment dose of hormonal drugs for 3 days a week, either continuously (M. J. Ratner, Biryukova L. S., 1992).

Corticosteroid therapy should be carried out on the background of antibiotics, potassium supplements, antacids, restriction of salt, and taking into account the contraindications and possible complications. Previously careful sanitation of foci of infection in order to improve treatment, prevention of relapse and generalization of focal infection. Because corticosteroids reduce the synthesis of protein and have a catabolic effect, it is recommended to appoint and anabolic hormones (nerobolum, nerobol, retabolil, etc.) in conventional doses for 2-3 weeks. Therapist of thequarter effect of corticosteroids is typically 3-4 weeks after the appointment of the maximum doses of the drug either during the lowering the dose and within 1-3 months after the end of treatment.

In addition to glucocorticoids in the therapy of glomerulonephritis are used and immunosuppressants, mainly cytotoxic agents. These include antimetabolites (imuran, azathioprine, mercaptopurine) and alkylating agents (chlorambucil, cyclophosphamide, chlorambucil, leukeran) is the therapeutic effect of these medications based on their immunosuppressive, anti-inflammatory and inhibitory proliferative processes. Their use is indicated for steroidantibiotic forms of glomerulonephritis, the presence of contraindications to the administration of glucocorticoids and the development of severe side effects last.

Azathioprine (imuran) and mercaptopurine 2-3 mg per 1 kg body weight of the patient (150-200 mg / day), cyclophosphamide - 1.5-2 mg per 1 kg of body weight (100-150 mg / day), leukeran - 0.2 mg per 1 kg of body weight within 4-8-10 weeks. Further, it is recommended supportive therapy at a daily dose equal to 1/2 or 1/3 is optimal for 6-12 months or more.

Clinical observations show that the only effective long-term therapy with cytostatics. In some cases, may be recommended and intermittent treatment of ultra-high doses ("pulse therapy") of cyclophosphamide or imuranom.

Cytostatics used in nephrotic syndrome. Hypertension is not a contraindication for these drugs, but their effectiveness in the treatment of hypertension decreases as significant when fibroplastic changes in the kidneys. Described cases of successful application of imuranom in subacute (malignant) the jade - with his help managed to get a remission of this previously incurable diseases (N. A. Ratner, 1971).

However, it should be noted that in therapy immunosuppressive medications possible serious complications: anemia, leukopenia, thrombocytopenia, agranulocytosis and pancytopenia. Cyclophosphamide can cause azoospermia, persistent and painful hemorrhagic cystitis, and alopecia. So assign it, especially the long-term, undesirable, should be preferred to chlorambucil or azathioprine (imuranom) (E. M. Tareev, 1983 - J. M. Ratner et al., 1978, 1980). In the treatment with these drugs requires great caution and care, strict monitoring of peripheral blood.

To reduce the side effects of cytostatics is recommended to be administered in combination with steroid hormones (prednisone 20-30 mg / day) and with other agents that enhance the blood (leucogen, pentoksil etc.) (L. A. perig, A. D. Tatarenko, 1978). The combined use of moderate doses of prednisolone with cytostatics on the effectiveness of similarly massive corticosteroid therapy - fewer complications, relapses of the disease. Recommended doses of these drugs (M. J. Ratner et al., 1978, 1980): 30 mg prednisolone 0.15-0.2 mg/kg of body weight of chlorambucil or 30 mg of prednisone 1.0 to 2.5 mg of azathioprine, or 30 mg of prednisone 1.5-2.5 mg/kg body weight of cyclophosphamide. This type of therapy and massive doses of corticosteroids are equally effective for the same clinical forms of CGN. According to the observations of M. J. Ratner et al. (1980, 1981), remission more resistant relapses occur less often. In addition, compared with glucocorticosteroid therapy this method of treatment gives slightly better results in the immediate outcomes of CGN.

The treatment of glomerulonephritis and apply drugs 4-aminohinolinovogo number (reskin, delagil, chloroquine, plaquenil), a similar mechanism of its action is to the immunosuppressants. They have anti-inflammatory effects, stabilize lysosomal membranes and reduce output from cells lysosomal enzymes, inhibit the synthesis of prostaglandins, reduce platelet aggregation and have a mild immunosuppressive effect. In the hospital these drugs are administered in a dose of 0.5-0.75 g per day for 3-6 weeks, and then maintenance doses (0.25 g) for several months or even years on an outpatient basis. About 1/NC of patients showed improvement in the course of the disease (P. A. Peleschuk, 1974). However, with prolonged use possible side effects: increased hematuria, dyspepsia, dermatitis, blurred vision, hair depigmentation, suppression of hematopoiesis. Given this, and the relatively low efficiency, their use is becoming more limited.

More shows and effective use of these drugs in combination with indomethacin (metindol).

ri treatment of glomerulonephritis and use of nonsteroidal anti-inflammatory drugs (indomethacin, indomethacin, voltaren, ibuprofen, etc.), anti-inflammatory effect which is associated with the suppression of the synthesis of prostaglandins (S. I. Ryabov, 1980 I. M. Kutyrina et al., 1981). In addition, assume that it inhibits platelet aggregation and deposition of fibrin in the glomerular capillaries, reduces the permeability of the basal membrane. However, under the influence of this drug reduced glomerular filtration, renal plasmatic, decreases the excretion of sodium in the urine and increased blood pressure (M. J. Ratner et al., 1978 - S. I. Ryabov, 1980).

Indomethacin is used with moderate exacerbation of glomerulonephritis in patients with latent and hematuric forms, less is indicated for the nephrotic syndrome and the mixed form of CGN. The optimal therapeutic dose of indomethacin (metindol, voltaren) 25 mg 4-6 times a day for 4-8 weeks, maintenance doses (50-75 mg) it can be continuously applied on an outpatient basis. Possible side effects are headaches, dyspepsia, epigastric pain, development of hypertension, in rare cases, cataracts, glaucoma, the formation of gastrointestinal ulcers.

Therefore, the presence of hypertension, especially severe, is a contraindication for indomethacin and other drugs of this group. Given this, and the relatively low efficiency, currently these drugs are used less frequently, mostly in outpatient practice. Contraindicated and they when kidney function, because they can reduce it.

In recent years for the treatment of glomerulonephritis, mainly nephrotic syndrome due to the disease began to use direct anticoagulants (heparin) and less indirect (fenilin etc.) actions.

The mechanism of therapeutic action of heparin is still not clear. However, I believe that the effectiveness of this drug is associated with effects on immune link in the pathogenesis of nephritis, thanks to its anticomplementary properties, with suppression of the activity of hyaluronidase and decrease the permeability of the glomerular capillaries. He has antilipemics action. A beneficial effect of heparin in glomerulonephritis associated with termination or a reduction in deposition of fibrin in the glomerular capillaries, reduction of platelet aggregation in them, which leads to the improvement of microcirculation in the glomeruli and retards the progression of morphological damage of the renal tissue (E. M. Tareev, 1983). It is established that, in addition to the anticoagulant, heparin has anti-hypertensive, diuretic and natriuretic effect (V. V. Serov et al., 1992), associated primarily with inhibition of aldosterone.

Practically it is important that the heparin has been shown to increase urine output, so that in some cases it is possible to achieve reduction or complete elimination of edema syndrome, not previously yielded to any other methods and means of treatment. Under the influence of heparin significantly reduced the protein Riya, dysproteinemia and hypercholesterolemia.

Heparin is shown primarily in patients suffering from acute and chronic glomerulonephritis with nephrotic syndrome, in photomorphogenesis which plays an important role intravascular coagulation with the deposition of fibrin in the glomeruli.

Daily dose of heparin varies from 20 to 40 thousand UNITS. The course of treatment for 3-10 weeks. Possible two methods of drug administration: 1) in the morning 10-15 thousand UNITS intravenously 10-15 thousand and evening IU intramuscularly 2) intramuscularly (or subcutaneously in the anterior abdominal wall) 5-10 thousand UNITS every 4-6 h (N. A. Mukhin, I. E. Timofeev, 1983, 1985, 1992). The treatment is performed under the control clotting time of blood, which must be doubled compared to the original.

Upon completion of the course of treatment with heparin to continue anticoagulant therapy may be prescribed anticoagulants of indirect action (fenilin, omifin, plantan, etc.) at a dose sufficient to maintain the prothrombin index level 45-60 , for a long time-up to 1-2 months or more. When using anticoagulant therapy should be aware of the contraindications to their purpose and possible serious side effects.

For the treatment of chronic glomerulonephritis is widely used antiplatelet agents - drugs that can decrease platelet aggregation (dipyridamole, glockenspiel, persantin), to lower intravascular GE-malagarazi.

Revealed hypotensive effect of chimes as a consequence of increased synthesis of prostoglandin E and also the increase in effective renal blood flow and glomerular filtration rate. Therefore, it is appropriate to use in hypertensive form of CGN. Appoint a glockenspiel in a daily dose of 200-400 mg, often in combination with anticoagulants (heparin) or with indomethacin, at least - on their own. The treatment optimum daily dose of 6-8 weeks, and then maintenance doses (50-75 mg) duration 6-12 months or more.

Combination therapy. In severe forms of CGN - membranous, proliferative one-membranous, and when extracapillary nephritis recommended the so-called quadruple therapy consisting of a combination of cytostatic agent, an anticoagulant, a antiagreganta and prednisolone in the above-mentioned doses. Treatment is continued at optimal doses, 6-8 weeks or more. This complex of pathogenic agents is particularly effective in nefroticeskih-hypertensive CGN form: positive therapeutic effect was observed in about half of patients (J. M. Ratner et al., 1978). The treatment becomes more successful when you turn on high doses of prednisone (60 to 100 mg/day) for 6-8 weeks followed by a gradual decrease and cancel it. Early administration of this therapy can, in some cases extracapillary nephritis to achieve partial remission, a significant increase of kidney function and elimination of renal failure.

In severe exacerbation of CGN, high activity of the inflammatory process (acute nephrotic syndrome), resistant nephrotic syndrome, the absence of effect of other methods and means of pathogenetic therapy is used a loading dose ("pulse therapy") of corticosteroids and cytotoxic agents, and plasmapheresis and hemosorption. "Pulse therapy" ultra-high doses of corticosteroids is intravenous drip (within 10-20 min) 1000-1500 mg of prednisolone or a corresponding dose of methylprednisolone in isotonic sodium chloride solution daily for 3 days. At the same time using the oral prednisolone in a dose of 60-90 mg (M. J. Ratner, Biryukova L. S., 1992). Similarly entered and cytostatics (imuran or cyclophosphamide) g 800-1000 mg for 2-3 days.

Plasmapheresis as a method of extracorporeal blood purification (including immune complexes) is carried out using a standard procedure and involves the removal of blood plasma (for one session up to 1.5-2.0 l) and replacing it with fresh.

Need removal of foci of infection (removal of tonsils, dental health, etc.). Prolonged dietary restrictions (salts and proteins) do not prevent the transition of acute glomerulonephritis in chronic. Patients with chronic nephritis should avoid cooling, especially exposure to damp cold. They recommended the dry and warm climate. Under satisfactory General condition and absence of complications shown Spa treatment in Central Asia (Bairam-Ali) or on the southern coast of Crimea (Yalta). Bed rest is required only at the time when significant edema or heart failure, and uremia.

For the treatment of patients with chronic glomerulonephritis essential diet, which is prescribed depending on the form and stage of disease. Nephrotic and mixed forms (swelling) intake of sodium chloride with food should not exceed 1.5 to 2.5 g/day, which cease to salt food. With adequate renal function (no swelling) food should contain a sufficient amount (1-1. 5 g/kg) of animal protein, rich phosphorus-containing amino acids. It normalizes nitrogen balance and compensate for the protein loss. In hypertensive form moderately recommended to limit the intake of sodium chloride up to 3-4 g/day, with normal content in the diet of proteins and carbohydrates. The latent form of the disease significant restrictions in the diet of patients do not require, it must be a full, varied and rich in vitamins. Vitamins (C, complex B, A) should be included in the diet with other forms of chronic glomerulonephritis. It should be borne in mind that long-term protein-free and salt-free diet prevents the progression of nephritis and reflects badly on the General condition of patients.

It is particularly important to corticosteroid therapy, which is the basis of pathogenetic therapy in this disease. The course of treatment used 1500-2000 mg of prednisolone (prednisone) or 1200-1500 mg of triamcinolone. Start treatment usually with 10-20 mg of prednisone and adjusted the dose to 60 - 80 mg/day (dose triamcinolone increase from 8 to 48 - 64 mg), and then gradually reduce it. It is recommended to conduct repeated courses of treatment (acute exacerbations) or supportive of small courses.

In patients receiving corticosteroids may exacerbate latent foci of infection. In this regard, treatment with corticosteroids is best done by assigning antibiotics simultaneously, or after the removal of foci of infection (e.g., tonsillectomy).

Contraindication to the prescription of corticosteroids in patients with chronic glomerulonephritis is a progressive azotemia. At moderate hypertension (BP 180/110 mm Hg. article ) treatment corticosteroids can be performed simultaneously using antihypertensives. High hypertension requires prior reduction of blood pressure. With contraindications to corticosteroid therapy or at its inefficiency, it is recommended to use non-hormonal immunosuppressants: aaathioprine (imuran), 6-mercaptopurine, cyclophosphamide. These drugs are more effective, and their treatment is better tolerated by patients while receiving prednisolone at moderate doses (10-30 mg/day), which prevents the toxic effects of immunosuppressive drugs on the blood. In the later stages - when glomerular sclerosis and atrophy with the presence of hypertension high - immunosuppressants and corticosteroids are contraindicated because of immunological activity in the kidney is already there, and the continuation of such treatment only aggravates hypertension.

Immunosuppressive properties are also drugs 4-aminohinolinovogo series - hingamin (delagil, resochin, chloroquine), hydroxychloroquine (plaquenil). Resochin (or chloroquine) used 0.25 g 1-2 to 3 times a day for 2-3 - 8 months. Resochin can cause side effects - vomiting, optic nerve damage, so you need the supervision of an ophthalmologist.

Indometacin (indomethacin, indocid) - indole derivative, is a nonsteroidal anti-inflammatory drug. Assume that, in addition to providing analgesic and antipyretic action, indomethacin affects mediators of immunological damage. Under the influence of indomethacin reduces proteinuria. Assign it inside of 25 mg 2-3 times a day, then depending on tolerability, increase the dose to 100-150 mg/day. ru/" target="_blank">Treatment is a long time, for several months. The simultaneous use of steroid hormones and indomethacin significantly reduce the dose of corticosteroids with gradual complete their abolition.

Deposition of fibrin in the glomeruli and arterioles, the presence of fibrin in the formation of the capsule "observed", mild increase in plasma fibrinogen serve as a pathogenetic rationale for holding anticoagulant therapy of chronic glomerulonephritis. Enhancing fibrinolysis by neutralizing the complement, heparin affects many allergic and inflammatory manifestations and as a result reduces proteinuria, reduce the dysproteinemia, improves the filtration function of the kidneys. Assigned n/a 20,000 IU per day for 2-3 weeks followed by a gradual reduction of the dose during the week or in/in the drip (1000 U per hour) heparin can be used in combination with corticosteroids and cytotoxic drugs.

A mixed form of chronic glomerulonephritis (swollen and pronounced hypertensive syndromes) shows the use of natriuretic, as they have a pronounced diuretic and hypotensive action. Hydrochlorothiazide is prescribed at 50-100 mg 2 times a day, lasix 40 - 120 mg/day, ethacrynic acid (uregei) 150-200 mg/day. Saluretics it is useful to combine and competitive antagonist of aldosterone aldactone (veroshpiron)-50 MG4 times a day, increasing excretion of sodium and reduces the excretion of potassium. Diuretic effect of hydrochlorothiazide (and other saluretikov) is accompanied by the excretion of potassium, which can lead to hypokalemia with the development of its characteristic General weakness, weakness and disturbances of contractility of the heart. Therefore, you should appoint a solution of potassium chloride. When persistent edema in the background hypoproteinemia is possible to recommend the use of middle fractions of polymer of glucose - polyglucin (dextran) in the form of intravenous drip of 500 ml 6 solution, which increases the colloid osmotic pressure of plasma of blood, promotes the movement of fluid from the tissues into the blood and causes diuresis. works better on the background of treatment with prednisone or diuretics. Mercurial diuretics in renal edema should not be used because of their diuretic effect due to toxic effect on tubular epithelium and glomeruli of the kidneys, which leads along with increased diuresis to decrease the filtration of the kidney. In the treatment of renal edema purine derivatives - theophylline, aminophylline, etc. - are ineffective.

In the treatment of hypertensive form of chronic glomerulonephritis can be assigned antihypertensives used in the treatment of hypertension: reserpine, reserpine with hydrochlorothiazide, adelfan, terazid, kristeen, dopegit. However, avoid sudden fluctuations in blood pressure and orthostatic downs, which could affect renal blood flow and filtration function of the kidneys. In preeclampsia period and in the treatment of eclampsia, which can occur during exacerbation of chronic glomerulonephritis, patients can be assigned to magnesium sulfate - for intravenous and intramuscular introduction of it in the form of a 25 solution can reduce the pressure and improve kidney function with its diuretic effect, and also helps reduce inflammation of the brain.

Outcome of chronic glomerulonephritis is kidney scarring with the development of chronic renal failure - chronic uremia. Immunosuppressive therapy significantly changed the course of the disease. There are cases of complete remission with disappearance of both General and urinary symptoms.

Prevention of Chronic glomerulonephritis:

One of the important problems of modern Nephrology is a science-based organisation and proper conduct of prevention of kidney disease.

As with other diseases, in diseases of the kidneys should be allocated to primary prevention, aimed at the primary prevention of kidney disease in healthy people, and a secondary, or relapse, aimed at preventing the transition of acute disease into a chronic, and prevention of relapses (exacerbations) existing chronic kidney disease.

The reasons leading to the development of acute glomerulonephritis, diverse, and therefore its prevention in each case should be individualized. However, you can specify a number of General measures aimed at the prevention of acute glomerulonephritis. This is primarily the strengthening, hardening of the body, improving its ability to fight infection. Physical exercise, hydrotherapy increases the body's resistance to adverse environmental conditions, in particular to cooling and exposure to damp cold, to colds. It should be kept from contact with patients with streptococcal infections. In diseases of angina, exacerbation of chronic tonsillitis, pharyngitis and other focal streptococcal infections required bed rest and off work for 7-10 days, the purpose of this period of sulfonamides or antibiotics. During and after 10-30 days after the disease had to take on a urine analysis so as not to miss the possible of renal disease, including acute glomerulonephritis.

The main objective of the clinical examination of patients with glomerulonephritis is to achieve rapid and complete recovery in acute glomerulonephritis to prevent relapse and further progression of chronic glomerulonephritis, restore and preserve for a long time, their ability to work. The task of the clinical examination included an early and proactive identification, registration, thorough examination, timely and effective treatment of patients with acute and chronic glomerulonephritis, regular monitoring, preventive and anti-relapse treatment is timely and correct placement of this cohort of patients in order to create the most favorable conditions for the stable and long-term preservation of their disability - selection and direction in Nephrology specialized sanatoria profile.

Dispensary service of this group of patients is carried out by local therapists or therapists Guild, and the organization, management and control of the clinical examination is therapeutic heads of departments clinics and health posts.

In clinics with specially trained nephrologists, clinical examination of patients with this profile must be fully executed. In large cities, who have one of the Nephrology hospitals office (center) with specially trained, qualified physicians-Nephrology, management and monitoring of the renal clinical examination of patients is carried out by doctors of the specified Cabinet (center).

Patients with acute glomerulonephritis, check out of the hospital in a state of full recovery without extrarenal symptoms and without bladder syndrome, should be under medical supervision for 3 years. At discharge from hospital with residual symptoms of glomerulonephritis in the form of microhematuria or with the protracted course of the disease clinical supervision is carried out within 3 years after full normalization of urine. If within 1-1,5 years pathological changes in the urine does not disappear and remain extrarenal symptoms, it should be assumed that acute glomerulonephritis took a chronic course - such patients in the future should be conducted both with chronic glomerulonephritis.

Patients with chronic glomerulonephritis require constant long-term medical supervision. Only in case of persistent and complete clinical and clinical-laboratory remission, coming under the influence of pathogenetic therapy of persistent and continuing for 5 years, patients can be removed from the dispensary. However, they must comply with prevention and control urine during and after suffering intercurrent diseases.

In addition, examination of patients with glomerulonephritis includes adherence to the timing of the survey and perform the necessary laboratory and instrumental studies. So, in acute diffuse glomerulonephritis after discharge from the hospital clinical examination of patients, the General analysis of urine and blood should be conducted in the first two months once in 10-14 days, and then once every 1-2 months during the year. A year after the complete disappearance of the renal and extrarenal signs of acute nephritis clinical examination, urinalysis and blood can be done once every 3-6 months (for 3 years). However, in the event of intercurrent illness, trauma, hypothermia urine and blood, and a medical examination should be carried out during and after this illness, after injuries etc.

Once in 6 months, we recommend careful examination of the patient involving an ophthalmologist, otolaryngologist, urologist, gynecologist, studied urine on Nechiporenko (or Chukovskomu - Addis), in General, glomerular filtration, blood on the content of urea, creatinine, total protein and protein fractions, potassium, sodium, calcium, sodium chloride.

Chronic glomerulonephritis terms volume and perform the necessary investigations depend on the clinical form of the disease and its course. In patients with latent and hematuric form of medical inspection is carried out 2 times a year. The measure blood pressure, examine the fundus of the eye, perform ECG, urinalysis General, daily proteinuria, Nechiporenko or Chukovskomu-Addis, General, General blood test and cholesterol, total protein and protein fractions, urea, creatinine, potassium, sodium, calcium, sodium chloride, determine the glomerular filtration clearance of endogenous creatinine. However, in the amplification of hematuria is necessary to carry out the General analysis of urine and blood every 2 to 4 weeks, and the appearance of gross hematuria is more often shown to consult a urologist or hospitalization in urological or nephrological Department to clarify the causes of hematuria.

In hypertensive form of CGN is the same amount of research, and when latent and hematuric forms of glomerulonephritis. However, due to the need to monitor the level of blood pressure and the action of hypotensive drugs clinical examination of patients in this group is held once every 1-3 months (depending on the severity of the hypertensive syndrome).

Clinical examination of patients with nephrotic form of CGN is made monthly or once in 2 months, but not less than once per quarter. Particular attention is drawn to the severity of edema syndrome, daily urine volume, the level of daily proteinuria, hypercholesterolemia, Hypo - and dysproteinemia. Sometimes patients with nephrotic syndrome long take diuretics, therefore, careful monitoring of electrolyte composition of the blood, primarily the concentration of potassium.

In the mixed form of CGN terms of the dispensary survey and scope of research are the same as in nephrotic syndrome. Special attention is drawn to the blood pressure, the condition of the fundus, the severity of edema and proteinuria, as well as on the state of nitrogen excretion function of the kidneys, ori because this form of chronic glomerulonephritis it is broken faster than the other. It is necessary at least once in 3-6 months to investigate glomerular filtration and blood levels of urea and creatinine.

In case of exacerbation of chronic glomerulonephritis or occurrence of intercurrent diseases, if patients for any reason cannot be admitted to a hospital, a medical examination and the necessary clinical and laboratory investigations are performed more frequently according to individual characteristics of the current main and intercurrent diseases.

The task of dispensary service to patients includes the selection and direction of the Spa treatment in specialized renal sanatorium.

Minimum research under the direction of patients in sanatorium renal profile should include a General clinical examination of organs and systems, measurement of blood pressure and temperature, x-ray chest, ECG, examination of the fundus, the General analysis of blood and urine, a sample of General, analysis of blood for urea and creatinine.

Indications for referral of patients for treatment in the sanatorium deserts (Bairam-Ali, Sitorai-Mahi-hasa) - residual effects and the prolonged period (more than 6 months) of acute glomerulonephritis, chronic glomerulonephritis with latent, hematuric (no gross hematuria), hypertension (blood pressure above 180/110 mm Hg. calendar), and nephrotic (without the expressed phenomena. These same indications should be guided by and at the direction of patients on the seaside (South coast of Crimea) climatic health resorts and spas with thermal baths (Yangan-Tau).

Contraindicated to send in sanatorium patients with chronic glomerulonephritis with renal failure, high hypertension (above 180/110 mm Hg. century), with severe edema and hypoproteinemia in nephrotic form, with gross hematuria.

The identification and selection of patients with acute and chronic glomerulonephritis, and patients with other kidney diseases that are subject to dispensary accounting and monitoring, carried out primarily physicians and urologists, as well as doctors from other departments in hospitals, clinics, dispensaries, health units and medical centres of industrial enterprises and institutions.

In order to timely identify patients in the early stage of the disease is necessary in order for any treatment of the patient in the clinic, health center mandatory along with measurement of blood pressure, examination of the organs, the blood test was also conducted urine analysis. If detected in the urine pathology, it is necessary to conduct a more thorough examination of the patient available in this health care setting methods, and if necessary to send him to the hospital (preferably dedicated) to clarify the causes of pathological changes in the urine and diagnosis.

In the primary prevention of FIRE should also be borne in mind the tendency of some people to have allergic reactions in response to the introduction of serums, vaccines, individual hypersensitivity to the drugs. Therefore, special caution should be observed with repeated injections of serums, vaccines for people at their introduction previously experienced an allergic reaction, accompanied by pathological changes in the urine. With the same caution applies to the prescription of antibiotics with nephrotoxic effects, as well as other medications to persons with hypersensitivity to them.

Primary prevention of chronic glomerulonephritis is closely linked to prevention and successful treatment of acute glomerulonephritis, as in most cases of chronic glomerulonephritis is the result of untreated or not promptly diagnosed with acute glomerulonephritis. Prevention CGN primarily consists in a thorough and timely treatment of patients with acute glomerulonephritis with subsequent long-term medical observation for them. In some cases, both acute and chronic glomerulonephritis begins and asymptomatic (latent form), and only urinalysis reveals proteinuria and hematuria. So with all the complaints of patients in the clinic, and also, upon receipt of persons, the direction to the resort, after a sore throat and other streptococcal diseases, it is necessary to carry out urine tests, to detect glomerulonephritis with atypical early.

Secondary prevention of glomerulonephritis. It should be aimed at preventing the recurrence of FIRE and CGN, as well as on the prevention of recurrence and, consequently, the preservation for a long period of time of compensation of renal function and disability of patients with chronic glomerulonephritis.

Secondary prevention should include the following set of events: the correct placement of patients, compliance with the required mode of work and rest, the appointment of a diet in accordance with the nosological form of the disease, its clinical variant and the condition of the kidney, sanitation foci of infection, prevention and treatment of intercurrent diseases, restorative and desensitizing therapy. If necessary, continue with maintenance doses initiated in hospital pathogenetic therapy. To this end, patients with acute glomerulonephritis after discharge from the hospital without extrarenal symptoms and with normal urine are released from work for up to two weeks in the presence of residual effects (microproteinuria, microhematuria) the duration of temporary disability is increased to 1-1. 5 months, and prolonged for up to 2-3 months.

The total time of disability with regard to a two-month stay in hospital is between 2-8 (with a favorable course of the disease) to 4-6 months with prolonged period, especially in patients with nephrotic syndrome and in patients treated with glucocorticosteroid hormones or immunodepressantnoe drugs. This group must be employed in job not related to hypothermia, especially by the action of the damp cold, and overheating (hot shops), without heavy physical activity and a prolonged stay on their feet - they must be exempted from travel on business trips, especially long-term. They should recommend in the first 3-6 months (if possible daily) for 1-2 hours to comply with bed rest, i.e. in a horizontal position. Within 6-12 months not recommended prolonged walking, sports, swimming.

Appointed a diet with restriction of salt (up to 6-8 g / day) and fluid (up to 1-1,5 l). These limits should be more stringent for susceptibility to hypertension and edema (up to 5-6 g of salt and not more than 1 l of fluid per day based liquid foods). Food should contain enough vitamins, especially b, C and e, protein (average of 1 g per 1 kg of body weight), carbohydrates. Recommended juices, canned vegetables, fruits and berries that contain a lot of vitamins. In moderate doses in food are allowed to add flavoring seasonings (pepper, mustard, horseradish, etc.), as well as onions, garlic. Not allowed to drink alcoholic beverages.

In case of angina, exacerbation of chronic tonsillitis, flu and other diseases needed bed rest, the patient was dismissed from work for the entire period of the disease, but not less than 7-10 days for active treatment with antibiotics, are appointed by antihistamines, calcium chloride, ascorutinum, is careful monitoring of the blood pressure, urine and blood samples.

In addition, careful conservative, but with no effect - radical (surgical) debridement of the lesions strep infection. With surgical removal of foci of infection (e.g., tonsillectomy) is recommended no earlier than 3-6 months after the elimination of acute events with subsequent stay in hospital for 2-3 weeks because of possible relapse of acute nephritis.

Patients treated in the hospital on massive doses of corticosteroids, in the case of accession of intercurrent illness or after injury, surgery along with antibiotics and other treatments should be assigned to prednisolone in doses of 15-30 mg per day.

It requires great caution in the administration of vaccines, serums, during vaccination, as possible disease recurrence, particularly in patients with increased allergic adjustment of an organism.

If patients need to continue with maintenance doses initiated in hospital treatment metindol on an outpatient basis, in doses of 50-75 mg / day) in combination with the glockenspiel (75-100 mg daily) for 3-12 months, this requires careful monitoring of their condition, the level of blood pressure, urine and blood samples. Tighter control is required if patients with acute glomerulonephritis with protracted for the recommended long-term therapy outpatient immunosuppressive drugs or glucocorticosteroid hormones. Dose maintenance therapy and its duration indicated in the medical history of the disease in the care of the patient from hospital.

Treatment of acute glomerulonephritis in an outpatient setting, with steroids and immunosuppressive drugs should be undertaken with great caution, under careful supervision and in exceptional cases (in particular, with the protracted period of acute glomerulonephritis with nephrotic syndrome) in connection with the possible development of severe side effects.

Patients with chronic (compensated) glomerulonephritis with latent (isolated urinary syndrome), characterized by the most favorable course, can do the job in their profession, if it is not connected with the possibility of hypothermia and great physical activity, with night shifts. Food should be varied and full as in the content of proteins, fats and carbohydrates, and vitamins. Significant restrictions in the use of salt is not required, but food should be salted. Allowed to use in moderate doses onion, garlic, parsley and other flavoring seasonings (pepper, horseradish, mustard, etc.). Periodically, especially in the spring, it is recommended that courses vitamin therapy vitamins C, B6, BI, B12, askorutin, nicotinic acid.

In hypertensive form of CGN, except for the right of employment, more patients are encouraged to strictly follow a diet with restriction of salt (6-8 g / day) and fluids, with the exception of or significant restriction of extractive and stimulating substances (thick soups, spicy food, coffee, strong tea, etc.). Prohibited Smoking and drinking alcoholic beverages. Taste seasonings are permitted, but in more limited quantities than when latent nephritis. Under the control of blood pressure treatment is supportive, individually tailored doses of antihypertensive agents (reserpine, dopegit, hamiton, clonidine, etc.) or other drugs with hypotensive action (Pinegin, kristeen, adelfan, obsidan, kordafen, corinfarum, etc.). If necessary, combine them with saluretikami (hydrochlorothiazide, furosemide or lasix, veroshpiron, etc.). which promotes more rapid reduction of blood pressure and is particularly indicated if, in addition to hypertension, there are swelling or tendency to their education. Not recommended to appoint ganglionic because of the possibility of serious side effects (orthostatic collapse) and reduced renal blood flow. At high and steady level of blood pressure is possible under strict control to assign capoten (captopril), adrenomimetiki (ismelin, Isobaric) in individually selected optimalniho given the risk of orthostatic collapse. Helps reduce blood pressure and improve the efficiency of antihypertensive drugs diet with a high content of potassium and poor in sodium (e.g., rice).

In patients with hematuric CGN employment and diet are similar to those in CGN with isolated urinary syndrome, however, are recommended foods that contain high amounts of vitamins C and e (lemons, onions, rosehip infusion, etc.). In the amplification of hematuria, you must assign ascorbic acid, or vitamin C, calcium chloride or calcium gluconate orally for 10-14 days, rutin or ascorutinum, diphenhydramine or pipolfen. With a significant increase in hematuria appoint Epsilon-aminocaproic acid 1.0 g 3-4 times a day for 5-7 days, 10 solution of calcium chloride intravenously, menadione orally or intramuscularly within 3-5 days, dicynone.

Patients with nephrotic form CGN require especially careful monitoring of their condition and the control diet. They are symptomatic and, if necessary, and supporting a pathogenetic therapy immunosuppressive drugs, corticosteroids, anticoagulants, drugs 4-aminohinolinovogo series metindol. The capacity of these patients in most cases significantly reduced, and sometimes in connection with edema syndrome and generally lost. Such patients require in the direction of MEDC to establish the degree of disability. They must avoid the slightest cooling, colds and various infections, which is very likely due to reduction of the protective properties of the organism and which in some cases can cause death.

Special attention should be paid to diet. Food should be high-calorie, contain a sufficient amount of protein (at least 1-1. 5 g per 1 kg of body weight), fat, carbs, well vitaminsyou. Require significant restriction of salt (up to 2-4 grams a day and sometimes less) and liquid (600-800 ml, a maximum of 1 liter per day based liquid dishes, compotes, etc.). Recommended watermelons, melons, pumpkins, grapes, apricots, bananas, possessing diuretic.

Depending on the presence and severity of edema syndrome shown diuretics in individual doses (furosemide, lasix, veroshpiron, uregei, aldactone, hydrochlorothiazide, etc.) or a combination of saluretics (lasix, hydrochlorothiazide) with potassium-sparing (verospiron, aldactone) medicine.

With prolonged use of diuretics, it is recommended to appoint preparations of potassium (Panangin, asparkam, potassium orotate, potassium chloride), and to consume foods rich in potassium (Fig, dried fruits, raisins, unpeeled potatoes, dried apricots, dried apricots, etc.) are resolved and flavor seasonings (onions, peppers, horseradish, mustard, etc.).

In the mixed form, the most severe with the flow, it is necessary to observe the principle of secondary prophylaxis is recommended for patients with hypertension and nephrotic form of chronic glomerulonephritis. This group of patients requires the most serious and careful attention to him, needs constant observation and symptomatic treatment (use of antihypertensive and diuretics, potassium supplements), in a significant restriction of salt and fluid.

The objective of secondary prevention of patients with chronic glomerulonephritis also include outpatient maintenance therapy with different drugs. The recommended dosage and duration of the course of such therapy should be indicated in the medical history of the disease. Outpatient treatment metindol is held in a daily dose of 50 to 75 mg (on 25 mg 2-3 times a day) for 3-12 months. Imuran also be prescribed in doses of 50-75 mg per day for 3-6-12 months (and sometimes more) under the strict control of the state of the peripheral blood due to the possibility of the development of leukopenia, thrombocytopenia and anemia.

Patients whom are discharged from the hospital after a course of massive glucocorticosteroid therapy, the occurrence of focal infection and other intercurrent diseases, injuries, colds along with antibiotics is necessary to prescribe prednisone (15-30 g / day) or its analogues (metipred, triamcinolone, dexamethasone) for the period of illness, injury or surgery.

Prevention of chronic glomerulonephritis is aimed at preventing recurrence of the disease (limitation of physical activity, elimination of stress conditions, cooling, protection from intercurrent diseases, sanitation foci of chronic infection, vaccination on an individual plan). Patients shows clinical supervision with monitoring of renal function.

Which doctors should be consulted if You have Chronic glomerulonephritis:

 

Nephrologist
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