Acute glomerulonephritis (GHG) is a diffuse inflammatory disease of the kidney with a primary glomerular lesion.
Etiology. The main etiological factor of OGN is streptococcus, mainly hemolytic type XII of group A, and diseases associated with streptococcal (usually focal) infection (tonsillitis, chronic tonsillitis, otitis media, sinusitis, scarlet fever, furunculosis, etc.).
In a number of cases, ANG may be a consequence of pneumonia, rheumatism, bacterial endocarditis, malaria, etc. The etiological significance of certain viruses has been established, in particular hepatitis B, herpes, rubella, infectious mononucleosis, adenoviruses. Among non-infectious factors, repeated administrations of serum and vaccines, exposure to a number of drugs due to individual intolerance to them, as well as some toxic substances such as alcohol, organic solvents, mercury, lithium, and others can be the cause of OGN. Cooling factor, especially exposure to wet cold, refers to allowing in persons sensitized with streptococcal or other infection.
Pathogenesis. Currently, it is widely recognized immuno-inflammatory concept of the genesis of this disease. Immune processes determine not only the occurrence, but also the progression of glomerulonephritis, the transition of its acute to chronic forms. Two variants of the immunopathogenesis of glomerulonephritis are possible. In one of them (autoimmune), immune complexes are formed as a result of the interaction of antibodies (autoantibodies) with antigens (autoantigens), which are protein particles of the renal tissue itself, mainly of the glomerular capillary basement membranes. These complexes are formed and located on the basement membranes, causing their damage. In another variant of immunopathogenesis, the formation of immune complexes occurs in the blood as a result of the interaction of antibodies with extrarenal antigens (including streptococcal ones). These immune complexes first circulate in the blood, then precipitate on the basement membranes of the glomeruli or in the mesangium and cause the development of the inflammatory process characteristic of glomerulonephritis. This is an immunocomplex variant of glomerulonephritis, which accounts for 60-80% of all cases of this disease. In the pathogenesis of glomerulonephritis, a role is also played by cellular immunity reactions involving T and B lymphocytes. Of the non-immune factors in the mechanism of development of this disease, impaired renal hemodynamics, microcirculation and rheological properties of blood are essential.
With recovery, all changes in the glomeruli and tubules undergo a reverse development, and the normal microstructure of the kidneys is restored. However, the data of puncture biopsies performed over time indicate that even with complete clinical recovery, histomorphological changes in the glomeruli can persist for several months and even up to two years, being the basis for the occurrence of chronic glomerulonephritis in the event of adverse conditions. This indicates the need for careful follow-up of patients who have had OGN for at least 2-3 years.
Clinical picture. The main, cardinal signs of OGN are edematous, hypertensive and urinary syndromes. In a typical (classical) variant of the onset and course of GHA, all signs of the disease are expressed.In the atypical (erased) variant, which occurs much more frequently than the typical, no extrarenal signs (edema, hypertension) are absent or mild, only moderate or minimal urinary syndrome is detected.
In typical cases, the OGN begins acutely, rapidly, and is clearly associated with a history of angina, an exacerbation of chronic tonsillitis, pharyngitis, or another focal streptococcal infection preceding the occurrence of dimensional signs of the disease in 1-3 weeks. Headaches, weakness, general malaise, loss of appetite, shortness of breath, palpitations, pain in the heart, lower back, in some cases, frequent and painful urination, a small amount and discoloration of urine, the appearance of edema. Pallor of integuments, puffiness of face is marked. In severe cases, patients take a forced sitting or semi-sitting position in bed due to acute (usually left ventricular) heart failure. Observed cyanosis of the lips, acrocyanosis, shortness of breath and deep, difficulty.
Often, the first manifestation of OGN is edema, characterized by rapid onset (sometimes within a few hours, days) and ubiquity of distribution (on the face, torso, limbs), in some cases they are accompanied by the development of ascites, hydrothorax, hydropericardium. There may be so-called hidden edema. The retention of body fluids in such patients can only be detected by systematically weighing them and controlling the amount of fluid they drink and the urine excreted during the day. In most cases, with a favorable course of the disease, the edema disappears by the 10-14th day. The complex of pathogenetic factors, including renal (reduction of glomerular filtration and increased tubular reabsorption of water and sodium) and extrarenal (increase in total vascular permeability, reduction of oncotic pressure in the blood, increased secretion of aldosterone and sodium retention in the body, increasing concentration in blood ADH and the associated increase in water reabsorption in the distal renal tubules, the hydrophilicity of the tissues themselves).
Hypertension is also among the most important and early signs of LUG. More often, blood pressure rises moderately: to 140-160 mm Hg. Art. systolic and up to 95-110 mm Hg. Art. diastolic, rarely reaches a high level - 220 / 115-230 / 130 mm Hg. Art. and higher. With a favorable course of the disease, the arterial pressure normalizes over a period of 2–3 weeks, with an unfavorable hypertension, it can also last longer. The pathogenesis of hypertensive syndrome is complex and not fully understood. An important role in its occurrence is given to an increase in the bcc and an increase in peripheral resistance, an increase in the activity of the renin-angiotensin-aldosterone system is of certain importance, especially with a prolonged and unfavorable course of Gna with a tendency to transition to CGN.
A common sign of OGN is bradycardia, which occurs in the first days of the disease and lasts 1-2 weeks. The combination of bradycardia, hypertension and edema is an important differential diagnostic criterion for distinguishing the edema caused by glomerulonephritis and heart disease, in which they are, as a rule, combined with tachycardia. Narrowing of the fundus arteries occurs in about 5-10% of cases. Sometimes in severe cases of the disease and high persistent hypertension, point hemorrhages are observed in the fundus.
In the first days of the disease, most patients have oliguria (up to 400-500 ml / day). A more significant decrease in daily diuresis is rarely observed and does not last long (1-3 days), then is replaced by polyuria. Severe oliguria or anuria, lasting more than 1-3 days, is dangerous in relation to the development of acute renal failure.
Proteinuria, with rare exceptions, is found in all patients with OGN.The degree of its manifestation is from 1 g / l and less to 16-30 g / l and more. Accordingly, daily proteinuria varies from a few hundred milligrams to 3-5-10 g and above. The highest proteinuria is observed at the beginning of the disease, then it gradually decreases and disappears completely in the range from 2-4 weeks to 1-3 months. In case of a prolonged course, 1-1.5 years may be maintained. In rare cases, in the presence of extrarenal signs of LUG, proteinuria may be absent.
Hematuria, or erythrocyturia, also appears at the onset of the disease, more often in the form of microhematuria (from 5-15 to 50-100 red blood cells in sight), less often in the form of gross hematuria, when urine becomes the color of meat slop. Arising in the first hours and days of the disease and disappearing later than other clinical and laboratory manifestations of LUG, proteinuria and hematuria most clearly reflect the dynamics of the disease, its activity, its course, the healing process. Sometimes persisting for a long time (up to 3-6 months) in the form of the so-called residual effects of acute nephritis, they indicate that the inflammatory process in the kidneys is not yet complete.
Changes in the peripheral blood during LUG are not specific and do not have a definite pattern. In the first phase of the disease, a small leukocytosis (9-12-109 / l) with lymphocytopenia can be observed. Often found eosinophilia. An increase in ESR up to 20-50 mm / h is to a certain extent an indicator of the activity of the pathological process, it decreases as the inflammation in the kidneys diminishes and returns to normal with recovery. Minor hyperazotemia occurs only in patients with oliguria, lasts only for a short time and usually disappears with an increase in diuresis. The level of total protein in the serum is maintained within the normal range and only in rare cases involving the nephrotic syndrome, decreases to 60 g / l and less. Dysproteinemia is expressed in a moderate decrease in the concentration of albumin and an increase in the content of globulins, mainly a, and a2-globulins, less often in u-globulins. Sometimes transient moderate hypercholesterolemia and hyperlipidemia are noted. With the rapid development of OGN, glomerular filtration decreases for a short time.
With an atypical, latent onset and course of OGN, extrarenal signs are absent or slightly pronounced. The only reliable diagnostic sign of the disease is only moderately or poorly pronounced urinary syndrome in the form of microproteinuria and microhematuria, which is detected only by targeted urine examination.
Complications. The course of acute respiratory failure in severe cases may be complicated by acute renal failure, acute heart failure and eclampsia.
The diagnosis of LUG in typical cases is not difficult, especially if there is a clear connection with streptococcal infection. At the same time, the diagnosis of monosymptomatic, erased forms often causes great difficulties.
In the differential diagnosis of OGN, first of all, chronic glomerulonephritis in the acute phase, acute pyelonephritis or chronic exacerbation, renal amyloidosis, heart disease occurring with so-called congestive proteinuria, and less often - systemic connective tissue diseases with kidney damage, hemorrhagic capillary toxicosis, which can also occur with kidney damage and hematuria. The possibility of urolithiasis, tuberculosis and a tumor of the kidney or urinary tract should be considered.
Forecast. Mortality in patients with OGN does not exceed 0.1%, often associated with acute cardiac and acute renal failure. Approximately 50% of adults recover from FAT. With a favorable course, recovery occurs in the first 2-4 weeks or in the first 2-3 months, but can last 1-1.5 years. Preservation after this period, at least slightly pronounced urinary syndrome indicates the transition of CAP to CGN.This is facilitated by late diagnosis of OGN and hospitalization of the patient, late-initiated and inadequately administered therapy, features of the clinical variant and the morphological type of glomerulonephritis. Often, the disease acquires a chronic course in patients who have been discharged from the hospital with so-called residual effects of OGN (unstable microproteinuria, erythrocyturia). Possible repeated disease of OGN (2-3%) after full recovery.
Treatment. All patients with OGN should be hospitalized in the nephrology or therapeutic department. Bed rest is prescribed for a period of at least 2-4 weeks, a diet whose main principle is the restriction of table salt taking into account its content in food products (no more than 2-3 g / day at the onset of the disease), fluid (in severe cases up to 400-600 ml / day) with sufficient calories and the content of vitamins. Any non-sodium diet is advisable, for example, rice, fruit and rice, fruit and vegetable, potato, rich in calcium and potassium ions and poor in sodium. In the future, the salt content in food, and the amount of liquid are determined by the amount of diuresis, blood pressure level, the presence of edema, but a low-salt (6-8 g of salt per day) diet is recommended for a long time (2-3 months or more). Protein in the daily diet is appointed at the rate of 1 g / kg mass, in severe cases - 0.5-0.6 g / kg. A more severe restriction of the protein is shown only with hyperasotemia. Enough carbohydrates and fats are introduced to provide the required amount of calories from food by adding a significant amount of butter and (or) vegetable oil.
Symptomatic drug therapy is aimed at eliminating the main extrarenal manifestations of glomerulonephritis (edema, hypertension, heart failure). Rauwolfia (reserpine) preparations are indicated as antihypertensive drugs, especially in combination with saluretics (hypothiazide, furosemide, uregitis, veroshpiron). With a slight increase in blood pressure can be limited to antispasmodics (dibazol, papaverine, but-shpu, euphyllin), which are used orally or parenterally. Calcium antagonists are also used (nifedipine, corinfar, cordafen), which, in addition to the hypotensive effect, have the ability to increase the glomerular filtration rate and diuresis.
For the eradication of the edematous syndrome, diuretic (diuretic) remedies are recommended: hypothiazide, 50-100 mg each, furosemide, 40-80 mg, lasix orally or parenterally, 40-80-120 mg, uregit, 50-100 mg, aldactone, 200-300 mg / day, etc. If necessary, a combination of 2-3 drugs, for example, hypothiazide with furosemide, is prescribed to achieve a better diuretic effect. In the case of persistent nephrotic edema, intravenous infusion of blood plasma, albumin, osmouretik is shown - mannitol (20% solution of 200-300 ml drip for 3-5 days in a row), polyglucin solution (300-500 ml), large doses of lasix - up to 300-500 mg / day A good diuretic effect in such cases gives the appointment of heparin, which is used as one of the pathogenetic means of treating nephrotic syndrome, including due to acute glomerulonephritis. With long-term diuretic intake, potassium preparations (potassium orotate, panangin, asparkam, potassium chloride) or products rich in potassium ions (dried fruit, raisins, apricot, rice, unpeeled potatoes, etc.) are necessary.
The treatment of oliguria and acute renal failure in the case of OGN is not fundamentally different from the treatment of acute renal failure. At first, large doses of lasix are used (from 300 to 1000 mg IV per day), the administration of heparin (20-30 thousand U / day), antiplatelet agents, in the absence of effect, patients are transferred to hemodialysis.
Anti-histamine agents are used (diphenhydramine, pipolfen, suprastin, tavegil), ascorbic acid, rutin, calcium preparations.
At the onset of the disease, due to streptococcal etiology of OGN, antibiotics that do not have a nephrotoxic effect (penicillin, oxacillin, erythromycin, oleandomycin) are advisable in the optimal therapeutic dose for 10-14 days.
The prescription of sulfa drugs is contraindicated, nitrofuran preparations are not recommended.
Methods and means of pathogenetic medical therapy are used in connection with the immune genesis of OGN (glucocorticosteroids, immunosuppressants, anticoagulants, etc.). The use of glucocorticosteroid hormones (prednisolone, methylprednisolone) is most indicated and effective for nephrotic syndrome, as well as for a prolonged course of LUG and the absence of effect from symptomatic therapy. Under the influence of these drugs, diuresis increases, swelling disappears, urinary syndrome decreases or is completely eliminated, the serum protein composition improves, and hypercholesterolemia decreases. They are contraindicated in severe hypertensive syndrome, since they themselves have the ability to increase blood pressure.
The optimal daily dose of prednisone - 60-80 mg - is achieved within 4-6 days, starting with 10-20 mg, applied 3-4 weeks, then gradually decreases (2.5-5 mg every 2-3 days) and is canceled. The course of treatment is 4-6 weeks, if necessary, repeated after 3-6 months. The treatment is carried out against the background of antibiotics, potassium preparations, antacids, anabolic hormones, restrictions in the diet of salt, under careful control, taking into account contraindications and possible complications, after preliminary rehabilitation of the foci of infection.
Immunosuppressants (imuran (azathioprine), cyclophosphamide, leukeran) are used for steroid-resistant forms of OGN, contraindications for the administration of glucocorticoids and the development of severe side effects after taking the latter. Azathioprine (Imuran) is prescribed at 2-3 mg / kg of weight (150-200 mg / day), cyclophosphamide at 1.5-2 mg / kg of weight (100-150 mg / day), leukeran - at 0.2 mg / kg mass. Treatment is carried out in the hospital for 4-8-10 weeks, and then on an outpatient basis in a maintenance dose of 1 / 2-1 / 3 stationary, up to 8-12 months. Arterial hypertension is not a contraindication for prescribing these drugs. There is a need for strict control over the state of peripheral blood, since serious complications are possible: anemia, leukopenia, thrombocytopenia, agranulocytosis, pancytopenia.
For the treatment of glomerulonephritis are used and direct anticoagulants (heparin), less indirect (fenilin and others.) Action. Heparin is indicated primarily for patients with nephrotic syndrome, in the pathogenesis of which an increase in intravascular coagulation plays a major role with the deposition of fibrin in the glomeruli and impaired microcirculation in them. Heparin significantly increases diuresis, due to which in many cases it is possible to achieve the elimination of the edematous syndrome, which did not succumb to any other methods and means of treatment. Under the influence of heparin, proteinuria decreases or completely disappears, dysproteinemia and hypercholesterolemia decrease. The daily dose of heparin is from 20 to 40 thousand units. The course of treatment is from 3 to 10 weeks. Two methods of drug administration are possible: 1) in the morning 10-15 thousand IU intravenously and in the evening 10-15 thousand IU intramuscularly, 2) intramuscularly or subcutaneously (in the region of the anterior wall of the abdomen) 5-10 thousand IU every 4-6 hours. The treatment is carried out under the control of thrombin time, which should be doubled compared to baseline.
Combined therapy combined with cytostatics (Leukeran - 0.2 mg / kg or Imuran - 150 mg / day, etc.), prednisolone (30 mg / day), anticoagulant (heparin - 20-40 thousand U / day) is used only for nephrotic the form and severe course of the gna.
With a rapid increase in the symptoms of the disease and its severe course in the form of an acute-nephritic syndrome, pulse therapy with ultrahigh doses of prednisone is used.
Prophylaxis of OGN is based on modern ideas about its etiology and consists in carrying out activities aimed at preventing and thorough treatment of acute and exacerbation of chronic foci of streptococcal infection (tonsillitis, chronic tonsillitis, pharyngitis, etc.). It is necessary to avoid prolonged overcooling and especially the action of wet cold; take special care with regard to repeated injections of serums, drugs and vaccines to persons who have experienced allergic reactions to their administration, accompanied by pathological changes in the urine.
Patients who have had streptococcal or viral infection, or have been exposed to other factors threatening the development of OGN, are advised to perform 2-3 urine tests within a month at 10-14 days.
CHRONIC GLOMERULONEPHRITIS (CGN) is an inflammatory disease of the kidney of immune origin with primary and primary glomerular damage with subsequent involvement in the pathological process of the tubules and other structural elements of the renal tissue, has a steady progressive course with an outcome in CRF.
Etiology. CGN is often the result of uncured or not diagnosed in a timely manner OGN, therefore, the causes of its occurrence in these cases are the same as in OGN. Among the factors contributing to the transition of OGN to CGN, repeated cooling may be important, especially the action of humid cold, the presence and aggravation of focal streptococcal and other infections, unfavorable working and living conditions, injuries, alcohol abuse, etc. Primary chronic glomerulonephritis is not excluded, which occurs without a preceding LUG. It is not always possible to establish the etiology of this variant of CGN (in 10-15% of cases). It can be caused by bacterial, viral infections, exposure to many drugs (gold, D-penicillamine, captopril, antibiotics, etc.), repeated administration of vaccines and serums, insect bites, sensitization to pollen, chronic alcohol intoxication, etc.
Pathogenesis. The concept of the immune genesis of this disease is most substantiated, in favor, which is indicated, in particular, by the discovery in the blood of patients with anti-nephrotic autoantibodies, the effectiveness of glucocorticosteroid hormones and immunosuppressants, as well as the presence of deposits of immunoglobulins on the basement membranes of the glomerular capillaries. G and M, complement. The latter cause damage to the glomerular basement membrane and inflammatory reactions in the glomeruli. Of the non-immune factors, hypercoagulation, intravascular coagulation, loss of fibrin and its decay products in the glomerular capillaries, as well as an increase in blood levels of kinins, histamine, serotonin, renin and prostaglandins are important. Disorders in the system of hemostasis and fibrinolysis is one of the important pathogenetic links of the development and progression of CGN.
The clinical picture of CGN is characterized by great diversity. With the exacerbation of the disease in most cases, it resembles or is similar to that in GHA. During remission, the clinical manifestations of CGN, as well as its course, depend primarily on the clinical form of the disease.
There are five main clinical forms of this pathology.
The latent form (isolated urinary syndrome) is manifested only moderately or slightly pronounced urinary syndrome: proteinuria often does not exceed 1 g / l, less often reaches 2 g / l (but not more than 3 g / l), hematuria ranges from 5-10 to 30- 50 red blood cells in sight. This is the most common and most benign clinical course of CGN.
The nephrotic form (nephrotic syndrome) is much less common than isolated urinary syndrome.The most characteristic signs of it are: massive proteinuria (above 3-3.5 g / day), hypo- and dysproteinemia, hyperlipidemia (hypercholesterolemia) and edema.
Hypertensive form. The leading symptom of the disease is hypertension with a slight severity of urinary syndrome and the absence of edema. Blood pressure often rises at the very beginning of CGN, and as the duration of the disease increases, it becomes more and more stable. This hypertonic form differs from symptomatic hypertension, which develops in late periods in all clinical forms of glomerulonephritis, when signs of CRF are added. Blood pressure often increases moderately (up to 160/100 mm Hg. Art.), Rarely reaches 180/110 mm Hg. Art., but in some cases can reach 200 / 115-250 / 120 mm Hg. Art. Clinical, radiological and ECG signs of left ventricular hypertrophy, changes in the retinal vessels are detected, and in the later stages - the phenomena of neuroretinopathy.
Mixed form is a combination of nephrotic and hypertensive syndromes. In some cases, the development of one syndrome precedes another, but more often both syndromes occur simultaneously, and the clinical picture of the nephrotic syndrome is usually pronounced and blood pressure is elevated significantly. It is much less common in comparison with other clinical variants of CGN, but at the same time it manifests itself as a combination of the most characteristic symptoms of this disease (hypertension, edema, marked urinary syndrome).
The hematuric form is characterized by significant and persistent hematuria, insignificant proteinuria in the absence of edema and hypertension. Hematuria can reach a significant extent and can be determined macroscopically (gross hematuria). The diagnosis of the hematuric form of CGN is valid only in cases where all other diseases that may be the cause of hematuria (fornical bleeding, kidney, bladder tumors, bladder polyps, urolithiasis, etc.) are excluded.
Current and forecast. CGN has a long perennial course with periods of remission and exacerbations. The latent and hematuric forms of CGN differ in the most benign and slow course: the duration of the compensated stage is many years and even decades. The most severe and rapidly progressing course is the mixed form, in which the clinical and laboratory signs of CRF appear already after 5-7 years from the onset of the disease, and sometimes even earlier. The course of the nephrotic form of CGN is also less favorable than latent. In hypertensive form, the duration of the compensated stage ranges from 10 to 30 years. By the rate of progression stand out quickly progressive and slowly progressive CGN. At the first of them, the duration of the compensated stage is relatively small (from 2 to 3-5 years). At the second, these terms are noticeably increasing. Possible transformation of one clinical form of CGN to another.
Treatment. Specific methods of treatment of this disease does not yet exist, and the applied methods and means do not guarantee full recovery.
Patients with exacerbation of CGN should be hospitalized. They are assigned to bed rest, the duration of which depends on the severity of symptoms of exacerbation, the state of kidney function.
Diet therapy for CGN for a long time, therefore, when prescribing it, it is necessary to take into account the clinical form of the disease, its course (remission or exacerbation), stage (compensated or with symptoms of chronic renal failure). For latent and hematuric forms, dietary restrictions should be minimal. Nutrition corresponds to the physiological needs, the protein content in the daily diet should be an average of 1 g / kg of weight with a slight restriction of salt (up to 8-10 g / day) without significant limitation of fluid.For patients with the hypertensive form of CGN with the same protein content in the daily diet, a stricter limitation of salt and liquid is required. In the diet, it is necessary to include products of plant origin, rich in vitamins C, P (lemons, dogrose infusion, black currants, etc.), strengthening the walls of blood vessels and reducing their permeability. Large and persistent edema in patients with nephrotic syndrome requires a very strict and prolonged restriction of table salt (in severe cases up to 1-2 g / day, taking into account its content in food) and liquids, the amount of which, taking into account liquid meals, should not exceed 600-800 ml / day. Watermelons, pumpkins, melons, grapes, dried apricots, bananas have a diuretic effect. The amount of protein in the daily diet should be an average of 1.5 g / kg mass. In the mixed form of CGN, diet therapy is based on edema and hypertension.
The complex therapy uses methods and means of symptomatic and pathogenetic therapy.
In order to quickly eliminate the main extrarenal manifestations of glomerulonephritis, it is advisable to prescribe hypotensive, diuretic, cardiac and other drugs.
The most important link in the complex therapy of CGN is the use of methods and means of pathogenetic therapy - glucocorticosteroids, immunosuppressants, anti-inflammatory drugs, anticoagulants and antiplatelet agents. The method of conducting pathogenetic therapy is similar to that in OGN.
Glucocorticosteroid therapy is most effective in patients with nephrotic syndrome, with a latent form, it has no advantages over symptomatic agents, and with hypertonic and mixed forms, steroid hormones are not shown.
Immunosuppressants (cytostatics) are currently not used for the treatment of hematuric and latent forms of CGN. The feasibility of an isolated use of immunosuppressants in nephrotic, hypertensive and mixed forms of CGN is questionable due to their insufficient effect.
Anticoagulant and antiplatelet therapy, both independently and in combination with glucocorticoids and cytostatics, is prescribed for nephrotic and mixed forms of CGN, for exacerbation of the disease and the absence of effect from other therapies.
In severe exacerbations of CGN, high inflammatory activity (acute-nephritic syndrome), persistent nephrotic syndrome, no effect from other methods and means of pathogenetic therapy, loading doses (pulse therapy) of glucocorticosteroids and cytostatics, as well as plasmapheresis and hemosorption are used. Pulse therapy with ultra-high doses of corticosteroids consists in intravenous drip (within 10-20 minutes) administration of 1000 mg of prednisolone or methylprednisolone in isotonic sodium chloride solution daily for 3 days.
Plasmapheresis, as one of the methods of extracorporal blood purification (including from immune complexes), is carried out according to the standard technique and consists in removing blood plasma (in one session up to 1.5-2 liters) and replacing it with fresh (fresh frozen) donor plasma or albumin. A total of 3-5 sessions of plasmapheresis are performed at intervals of 1-2 times per week.
In urology, chronic glomerulonephritis is understood as primary glomerulopathy, different in etiology and pathomorphology, accompanied by inflammatory and destructive changes and leading to nephrosclerosis and chronic renal failure. Among all the therapeutic pathology, chronic glomerulonephritis is about 1-2%, which suggests its relatively high prevalence. Chronic glomerulonephritis can be diagnosed at any age, but more often the first signs of nephritis develop in 20-40 years.Signs of a chronic process are prolonged (more than a year) progressive course of glomerulonephritis and bilateral diffuse kidney damage.
What is subacute glomerunephritis
This is a special form of glomerulonephritis, characterized by peculiar morphological changes in the kidneys, severe clinical manifestations, a rapidly progressing course, an early and rapidly increasing renal failure, ending in an unfavorable outcome for a short period of time - from 2-3 weeks to 6-12 months. For the first time the disease was described in 1914 by F. Folgard and T. Far, who considered it as a subacute form of glomerulonephritis and suggested the term "extracapillary nephritis" for it.
Previously, this disease was described by various authors as a special variant of acute or chronic glomerulonephritis. So, Ellis (1942) attributed it to one of the options for the course of acute glomerulonephritis. However, due to the characteristic features of the histomorphological picture and clinical manifestations, it is highlighted in a separate nosological form, which in clinical practice is most often referred to as subacute malignant glomerulonephritis. The term "extracapillary nephritis" reflects only its morphological essence. Other terms used in the literature to refer to this disease - “rapidly progressive”, “transient”, “super-sharp”, “anuric”, “violent”, “endo-extracapillary”, glomerulonephritis - to a lesser extent reflect its morphological and clinical essence, therefore they do not find a wide application in clinical practice. However, some authors (E. M. Tareev, 1983, B. I. Sulutko, 1983, N. A. Mukhin, I. E. Tareeva, 1992, and others) describe it as rapidly progressive glomerulonephritis.
Subacute (malignant) glomerulonephritis is a relatively rare kidney disease. Among all forms of glomerulonephritis, it accounts for 1–4% (G. Mazhdrakov, 1980, S. I. Ryabov, 1980, 1982, E. M. Tareev, 1983). Malignant glomerulonephritis with almost the same frequency occurs in persons of both sexes, mostly after 40 years. L. A. Pyrig (1982), on the basis of his own observations and generalizations of the literature, found that subacute malignant glomerulonephritis after the age of 40 years occurs 3-4 times more often than among younger people. According to the materials of S. I. Ryabov (1980), among the patients he observed with subacute malignant glomerulonephritis aged 13–83 years, 57.4% were over 40 years old. At the same time, according to other authors (A. Pukhlev, 1980), this disease is more common at the age of 15-30 years.
What provokes subacute glomerulitis
Since the disease in some cases occurs after streptococcal infection, an opinion is expressed about the possibility of an infectious etiology (E.M. Tareev, 1972, A.P. Peleshchuk, 1974). However, such a relationship of the onset of subacute malignant glomerulonephritis with a postponed streptococcal infection is relatively rare. In some cases, this disease may be due to hemorrhagic vasculitis, viral infections, bacterial endocarditis, SLE, nodular periarteritis, Goodpasture, Wegener syndromes, malignant neoplasms, abscesses of various localization, exposure to drugs, chemicals and other causes. Consequently, subacute (malignant) glomerulonephritis is a polyetiological disease, which has led some authors to refer to it as a syndrome. However, in many cases the cause cannot be established (idiopathic malignant nephritis).
Acute glomerulonephritis It begins 1-2 weeks after the infection or hypothermia and develops with edema, a rise in blood pressure.There are urination disorders, weakness, headache, eyesight deteriorates. When analyzing urine protein is detected (more than 3.5-4 g per day). The main symptoms of the disease persist for quite a long time (from 1-1.5 months to six months).
Treatment of glomerulonephritis
- Patients with acute glomerulonephritis and with exacerbation of chronic glomerulonephritis must be hospitalized.. The time of hospital stay, depending on the form of the disease and the severity of the patient's condition, is 1-2 months.
- Patients need bed rest for 2-3 weeks with high blood pressure, edema, changes in the urine.
- Patients are prescribed a diet in which they limit: intake of table salt, protein intake, intake of water.
Every day, it is necessary to check the volume of the released fluid and its compliance with the water load.
- To suppress infection, antibiotic therapy is carried out (only if the reason is established accurately).
- To suppress autoimmune reactions, glucocorticosteroids are prescribed.
- For marked edema, diuretics are prescribed (furosemide).
- While maintaining high blood pressure, antihypertensive therapy is prescribed.
With positive results of treatment and not earlier than six months from the onset of the disease, sanatorium-resort treatment is recommended for patients. With glomerulonephritis, the climatic conditions of Primorye and deserts are most suitable.
Today, glomerulonephritis affects from 10 to 15 adult patients per 10,000 people. In terms of the frequency of detection among all pathologies of the kidneys, this disease takes the 3rd place. Glomerulonephritis can be diagnosed among patients of any age group, but most often the disease occurs in people under 40 years of age.
Among the male population, this disease is detected 2 - 3 times more often. In children, among all acquired renal diseases, glomerulonephritis takes 2nd place. According to statistics, this pathology acts as the most common cause of disability, which develops due to chronic renal failure. Approximately 60 percent of patients with acute glomerulonephritis develop hypertension. In 80 percent of cases, children with an acute form of this disease provoke various cardiovascular disorders.
Recently, the frequency of diagnosing glomerulonephritis among residents of different countries is increasing. This is due to environmental degradation, as well as a general decrease in immunity among the population, which is a consequence of non-compliance with recommendations for a healthy lifestyle.
The mechanism of development of glomerulonephritis
Initially, an infection enters the body, which can be the cause of angina, bronchitis, pneumonia or other respiratory diseases. The pathogen, in this case beta-hemolytic streptococcus, is perceived by the body as a foreign body (scientifically - as an antigen). The consequence of this is the production of antibodies by your own body (specific proteins) against these antigens. The longer the infection is in the body, the more antibodies the body produces. Subsequently, antibodies bind to antigens, forming immune complexes. Initially, these complexes circulate in the bloodstream, but then gradually settle on the kidneys. The target for immune complexes is the nephron membrane.
Deposing on membranes, immune complexes activate the compliment system and trigger a cascade of immunological reactions. As a result of these reactions, various immunocompetent cells are deposited on the nephron membrane, which damage it. Thus, the main functions of the kidney are impaired - filtration, absorption and secretion.
Pathogenesis (education mechanisms) conditionally can be expressed in the following scheme - infection - the production of antibodies by the body - activation of the complement system - release of immunocompetent cells and their sedimentation on the basement membrane - formation
infiltration of neutrophils and other cells - the defeat of the basement membrane of the nephron - renal dysfunction.
The causes of glomerulonephritis are:
- sore throats and other streptococcal infections,
This cause of glomerulonephritis is the most frequent, therefore the term post-streptococcal glomerulonephritis is most often used. The causes of post-streptococcal glomerulonephritis are pathogenic strains of group A streptococcus. Among them, beta-hemolytic streptococcus deserves special attention. This is a gram-positive, immobile microorganism that is ubiquitous. In a certain concentration, it is located on the mucous membranes of a person. The main transmission path is aerogenic (airborne) and the food path. This microorganism produces many toxins, namely deoxyribonuclease, hemolysin, streptokinase A and B, streptolysin, hyaluronidase. He also has an extensive antigenic complex. Due to its antigenic structure and production of toxins, Streptococcus ranks second after staphylococcus on the medical significance.
The most common disease that causes streptococcus is sore throat or tonsillofaringit. This is an acute infectious disease with lesions of the mucous membrane and lymphatic tissue (tonsils) throats. It begins suddenly with a sharp increase in body temperature to 38 - 39 degrees. The main symptoms are sore throat, general symptoms of intoxication, covering the tonsils with a purulent yellowish-white patina. In the blood, there is leukocytosis, increased ESR (erythrocyte sedimentation rate), the appearance of C-reactive protein. During the period of illness, positive bacteriological tests are recorded. By itself, a sore throat is rarely dangerous, most of all it is dangerous because of its complications. The main complications of streptococcal angina are post-streptococcal glomerulonephritis, toxic shock, rheumatic fever.
However, post-streptococcal glomerulonephritis is not enough single episode of angina. As a rule, multiple episodes of the disease or the so-called recurrent streptococcal tonsillitis are necessary. In this case, sensitization gradually occurs (hypersensitivity) Streptococcus antigens and antibody production. After each episode of the disease there is an increase in titers (concentrationa) anti-streptococcal antibodies. At the same time, the development of glomerulonephritis after a single episode of angina is extremely rare in children.
Diphtheria is an acute infectious disease that occurs with a primary lesion of the nasopharyngeal mucosa. Diphtheria is caused by a diphtheria bacillus or Leffler's bacillus. This microorganism has powerful pathogenic properties, and also produces exotoxin. Released into the bloodstream, exotoxin spreads with the blood flow throughout the body. It can affect the heart, nervous system, muscles. In diphtheria, the kidneys are also affected. However, it is not the glomeruli that are most often affected, but the kidney tubules. Thus, there is a picture of nephrosis, not glomerulonephritis. Acute glomerulonephritis occurs with hypertoxic (lightning fasta form of diphtheria. It is clinically manifested by edema, hematuria (blood in urine), a sharp decrease in daily diuresis (total urine flow).
Viral infection also plays an important role in the development of glomerulonephritis. Previously transmitted viral disease is the second most common (after streptococcal infectiona) cause of glomerulonephritis. Most often, the development of glomerulonephritis is provoked by viruses such as adenoviruses, ECHO, Coxsackie virus. The antigens are the complex structure of viruses. Also, glomerulonephritis in children may be due to chickenpox (windmills) or mumps (pigs).
Currently, drug kidney damage is becoming more common. So, some drugs have a nephrotoxic effect, which means their selectivity to the kidneys. Among such drugs, sulfonamides and penicillin preparations are of particular interest. The first category of drugs include sulfathiazole, sulgin, sulfacyl-sodium, and the second - D-penicillamine and its derivatives. Sulfanamide drugs can affect various structures of the kidneys with the further development of obstructive uropathy (diseases where urine flow is disturbed) or hemolytic kidney.
The fact that treatment with penicillins can provoke kidney damage has been known since the 50s of the last century. However, only recently was described a detailed morphological picture of the kidneys in penicillin glomerulonephritis. So, D-penicillamine has a special tropism (selectivity) to the glomeruli, that is, to the glomeruli. Affecting the functional units of the kidneys, drugs from this group lead to the development of membranous glomerulonephritis. At the same time along the membranes of the glomeruli is the deposition of immune complexes. Other types of glomerulonephritis, such as proliferative and exudative, can also cause penicillins.
Toxic kidney damage occurs in mercury poisoning, lead, arsenic. These and many other substances have nephrotoxic properties, affecting the glomeruli, tubules and other structures of the kidneys.
Symptoms of glomerulonephritis
In the clinic, glomerulonephritis secrete urinary and general (not urinarya) symptoms. The former include such as a decrease in daily urine output, blood and protein in the urine, the latter include increased blood pressure, edema. This is explained by the fact that the kidneys perform important functions in the body, as well as participate in the regulation of blood pressure and water-salt metabolism.
Pain in the lumbar region
Pain is one of the earliest symptoms of glomerulonephritis. Since in this pathology both kidneys are affected simultaneously (pathological process in glomerulonephritis bilateral), the pain is localized on both sides. Complaints to lower back pain on the left or on the right are not characteristic of glomerulonephritis.
The basis of the development of pain symptoms in glomerulonephritis are two points. The first is an increase in the size of the kidneys in the early stages. The kidneys themselves do not contain nerve endings. However, they are covered with a fibrous capsule, which is abundantly supplied with nerve endings. When the kidneys increase in size, the capsule that covers them is also stretched. It is the stretching of the fibrous capsule that provokes pain. The second mechanism of pain development is squeezing of the neuro-vascular endings, an increased tissue of the kidney.
The pain in glomerulonephritis is localized on both sides, is dull and permanent, and may increase with walking.
Dysuria and oliguria
Dysuric manifestations are various urinary disorders that are expressed in difficult and frequent urination. Dysuria is a symptom of glomerulonephritis only in its early stages. Very quickly, it goes into oliguria - a decrease in daily diuresis of less than 500 milliliters per day. The decrease in the volume of excreted urine develops due to impaired intrarenal hemodynamics. Due to the deposition of immune complexes on the basement membrane of the kidneys, filtration, absorption and secretion are disturbed.This leads to the formation of a smaller volume of urine, and most importantly - to the retention of fluid in the body.
The most severe and dangerous dysuric manifestation of glomerulonephritis is anuria - a complete cessation of urine excretion. Anuria is complicated by the most severe forms of glomerulonephritis. Together with the urine in the body lingers toxic metabolic products, such as creatinine, urea, ammonia. The delay of these substances leads to intoxication of the body, the development of uremia and encephalopathy.
A severe and difficult to treat symptom of glomerulonephritis is hypertension (high blood pressure). At the same time, the systolic pressure rises more than 120 millimeters of mercury, and the diastolic pressure rises more than 80 mm.development mechanisma) hypertension with glomerulonephritis is very complex and involves several mechanisms.
The mechanisms for the development of arterial hypertension are:
- delay in sodium, due to impaired kidney function,
- the delay in the body of water, resulting in increased volume of total circulating blood,
- an increase in renin synthesis due to a decrease in blood flow in the kidneys,
- decrease in prostaglandin synthesis E, A.
Another mechanism of arterial hypertension development is activation of the renin-angiotensin system. The activation of this system is due to hypoperfusion (reduced blood supplya) kidney. Due to insufficient blood supply, a cascade of reactions is activated, resulting in the release of renin. It is a hormonally active substance that, in turn, leads to the conversion of angiotensin I to angiotensin II. The latter leads to the secretion of the hormone aldosterone, which increases the reabsorption of sodium (reabsorption). Thus, a vicious circle is formed - the activation of various mechanisms, one way or another, leads to sodium and water retention. On the other hand, increased blood pressure is affected by a decrease in prostaglandin synthesis. Normally, these substances regulate vascular tone, preventing the narrowing of the vascular lumen. When prostaglandins are secreted insufficiently, the vessels narrow, which creates an additional burden on high blood pressure. Narrowed blood vessels and increased blood volume are the main cause of high blood pressure.
Edema, shortness of breath
The basis of the development of shortness of breath, as well as the basis of the development of arterial hypertension, is the retention of sodium and water. Water is retained in the tissues, thereby creating swelling. Until a certain time, the fluid is retained only in the tissues. However, it soon begins to move into the cavity and fill them. Thus, the excess body fluid accumulates in the pleural cavity, in the pericardial cavity, in the abdominal cavity, and so on. This, in turn, provokes other symptoms. For example, accumulating in the pericardial cavity, fluid compresses the heart, causing shortness of breath and bradycardia (slow heartbeat). Shortness of breath also provokes the accumulation of fluid in the lungs, which is the cause of venous stasis in the small circle of blood circulation. So, nephrogenic elements develop (kidney) pulmonary edema. Effusion of fluid into the abdominal cavity leads to the development of ascites, among the people - dropsy.
However, the first significant mechanism of edema is proteinuria.The loss of proteins by the body leads to the release of fluid from the bloodstream and the impregnation of tissue with this fluid (that is, to the formation of edema). Normal albumin (high molecular weight proteinsa) blood retains fluid in the vessels. But with glomerulonephritis, there is a massive loss of these proteins in the urine, as a result of which their concentration in the blood serum falls. The less albumin remains in the blood, the more fluid passes from the bloodstream to the tissues, and the more massive the swelling.
Laboratory signs of glomerulonephritis
Glomerulonephritis is manifested not only by external signs, but also by deviations from the side of blood analysis and urine analysis. And if the patient cannot determine the changes in the blood, then some deviations in the urine analysis are visible to the naked eye.
Laboratory signs of glomerulonephritis
It is a mandatory symptom of acute glomerulonephritis. It can be of two types - macro and micro. Almost half of the patients have gross hematuria, in which blood in the urine is visible to the naked eye. In the remaining patients, microhematuria is noted, in which blood in the urine can be detected only by laboratory methods.
It is also a mandatory symptom of glomerulonephritis. The severity of this laboratory syndrome depends on the form of the disease. So, with glomerulonephritis with nephrotic syndrome, proteinuria is more than 3.5 grams per day and is carried out mainly at the expense of albumin. In nephritic syndrome, urine protein secretion is less than 3.5 grams.
This laboratory sign is noted in more than half of patients. Mainly manifested in the acute period of the disease.
Cylindruria (urine cylinder)
Cylinders are substances formed from blood cells. Most often leukocyte and erythrocyte cylinders are detected.
Nephritic syndrome is a symptom complex that occurs in diffuse proliferative and extracapillary glomerulonephritis. The onset of nephritic syndrome is always acute, which distinguishes it from other syndromes in glomerulonephritis.
Symptoms of nephritic syndrome are:
- blood in the urine (hematuria) - occurs suddenly and most often macroscopic, that is visible to the naked eye,
- protein in urine (proteinuria) - less than 3 grams per day,
- reduction of daily diuresis - up to oliguria (daily urine volume less than 500 milliliters) or even before anuria (less than 50 milliliters of urine per day),
- fluid retention in the body and the formation of edema - usually of moderate degree and not as pronounced as in nephrotic syndrome,
- a sharp decrease in renal filtration and the development of acute renal failure.
Nephrotic syndrome - a symptom complex, which is characterized by protein in the urine, a decrease in the concentration of protein in the blood and pronounced edema. The development of the nephrotic syndrome is usually gradual and not as violent as with the nephritic syndrome.
The most prominent and pronounced sign of nephrotic syndrome is proteinuria or protein in the urine. Daily loss of protein is more than 3.5 grams, which means a massive loss of proteins by the body. At the same time, proteinuria is realized mainly due to albumin, high molecular weight proteins. Thus, human serum contains two types of proteins (two fractions) - albumin and globulins. The first fraction is high-density proteins that most of all retain water in the bloodstream, that is, they maintain oncotic pressure.
The second fraction of proteins is involved in maintaining the immune response and does not have such an effect on oncotic pressure as the first. Thus, albumin holds water in the bloodstream.Therefore, when they are excreted in large quantities in the urine, water from the bloodstream goes into the tissues. This is the main mechanism for the formation of edema. The more albumin is lost, the more massive the swelling. That is why the nephrotic syndrome forms such edema.
The second sign of nephrotic syndrome is hypoalbuminemia and hyperlipidemia. The first sign indicates a reduced concentration of proteins in the blood, and the second increased concentration of lipids (fat) in blood.
Causes of Chronic Glomerulonephritis
Chronization and progression of the disease may be a consequence of untreated acute glomerulonephritis. However, there are often cases of development of primary chronic glomerulonephritis without a previous episode of an acute attack.
The cause of chronic glomerulonephritis can not find out in all cases. Leading importance is attached to the nephritogenic strains of streptococcus and the presence of foci of chronic infection in the body (pharyngitis, tonsillitis, sinusitis, cholecystitis, caries, periodontitis, adnexitis, etc.), persistent viruses (influenza, hepatitis B, herpes, variceal infection, fever, adnexitis, etc.), persistent viruses (influenza, hepatitis B, herpes, venous sinitis, fever, adnexitis, etc.), persistent viruses (influenza, hepatitis B, herpes, variceal infection, fever, adnexitis, etc.), persistent viruses (influenza, hepatitis B, herpes, variceal infection, fever, adnexitis, etc.), persistent viruses (influenza, hepatitis B, herpes, venous sinitis, fever, adnexitis, etc.) cytomegalovirus infection).
In some patients, chronic glomerulonephritis is caused by a hereditary predisposition (defects in the system of cellular immunity or complement) or congenital renal dysplasia. Also non-infectious factors of chronic glomerulonephritis include allergic reactions to vaccination, alcohol and drug intoxication. Other immune-inflammatory diseases such as hemorrhagic vasculitis, rheumatism, systemic lupus erythematosus, septic endocarditis, etc., can cause diffuse damage to nephrons. Cooling and weakening of the general body resistance contribute to the occurrence of chronic glomerulonephritis.
In the pathogenesis of chronic glomerulonephritis the leading role belongs to immune disorders. Exogenous and endogenous factors cause the formation of specific CICs consisting of antigens, antibodies, complement and its fractions (C3, C4), which are deposited on the basement membrane of the glomeruli and cause its damage. In chronic glomerulonephritis, glomerular lesion is intracapillary in nature, disrupting microcirculation processes with the subsequent development of reactive inflammation and dystrophic changes.
Chronic glomerulonephritis is accompanied by a progressive decrease in the weight and size of the kidneys, compaction of the renal tissue. Microscopically determined the fine-grained surface of the kidneys, hemorrhages in the tubules and glomeruli, loss of clarity of the brain and cortical layer.
Classification of chronic glomerulonephritis
In the etiopathogenetic relation, infectious-immune and non-infectious-immune variants of chronic glomerulonephritis are isolated. According to the pathological picture of the detected changes, minimal, proliferative, membranous, proliferative-membranous, mesangial-proliferative, sclerosing types of chronic glomerulonephritis and focal glomerulosclerosis are distinguished.
During chronic glomerulonephritis, a phase of remission and exacerbation is distinguished. The rate of development of the disease can be rapidly progressing (within 2-5 years) and slowly progressive (more than 10 years).
In accordance with the leading syndrome, there are several forms of chronic glomerulonephritis - latent (with urinary syndrome), hypertensive (with hypertensive syndrome), hematuric (with predominance of gross hematuria), nephrotic (with nephrotic syndrome), mixed (with nephrotic-hypertensive syndrome). Each of the forms proceeds with periods of compensation and decompensation of the nitrogenous function of the kidneys.
Symptoms of chronic glomerulonephritis
Symptoms of chronic glomerulonephritis due to the clinical form of the disease. The latent form of chronic glomerulonephritis occurs in 45% of patients, occurs with isolated urinary syndrome, without edema and arterial hypertension. It is characterized by moderate hematuria, proteinuria, leukocyturia. The flow is slowly progressive (up to 10-20 years), the development of uremia comes late. With the hematuric variant of chronic glomerulonephritis (5%) persistent hematuria, episodes of gross hematuria, anemia are noted. The course of this form is relatively favorable, uremia rarely occurs.
The hypertensive form of chronic glomerulonephritis develops in 20% of cases and occurs with arterial hypertension with mild urinary syndrome. Blood pressure rises to 180-200 / 100-120 mm Hg. Art., often subjected to significant daily fluctuations. Observed changes in the fundus of the eye (neuroretinitis), left ventricular hypertrophy, cardiac asthma, as a manifestation of left ventricular heart failure. The course of a hypertensive form of nephritis is long and steadily progressive with an outcome to renal failure.
Nephrotic variant of chronic glomerulonephritis, occurring in 25% of cases, occurs with massive proteinuria (more than 3 g / day), persistent diffuse edema, hypo- and dysproteinemia, hyperlipidemia, dropsy of serous cavities (ascites, hydropericardium, pleurisy) and associated with them , tachycardia, thirst. Nephrotic and hypertensive syndromes are the essence of the most severe, mixed form of chronic glomerulonephritis (7% of cases). It occurs with hematuria, severe proteinuria, edema, arterial hypertension. An adverse outcome is determined by the rapid development of renal failure.
Diagnosis of chronic glomerulonephritis
Clinical data are the leading criteria for the diagnosis of chronic glomerulonephritis. When collecting history takes into account the presence of chronic infections, acute acute glomerulonephritis, systemic diseases. Typical changes in the general analysis of urine is the appearance of red blood cells, leukocytes, cylinders, protein, change in the specific gravity of urine. To assess the function of the kidneys are carried out tests Zimnitsky and Reberg.
In the blood of chronic glomerulonephritis, hypoproteinemia and dysproteinemia, hypercholesterolemia are found, the titer of antibodies to streptococcus increases (ASL-O, antihyaluronidase, anti-streptokinase), the content of components of the complement decreases (C3 and C4), the level of IgM, IgG, IgA increases.
Ultrasound of the kidneys with progressive course of chronic glomerulonephritis reveals a decrease in the size of the organs due to hardening of the renal tissue. Excretory urography, pyelography, nephroscintigraphy help assess the state of the parenchyma, the degree of renal dysfunction. To detect changes from other systems, ECG and echocardiography, ultrasound of the pleural cavity, fundus examination are performed.
Depending on the clinical variant of chronic glomerulonephritis, a differential diagnosis with chronic pyelonephritis, nephrotic syndrome, polycystic kidney disease, kidney disease, kidney tuberculosis, kidney amyloidosis, and arterial hypertension is required. To establish the histological form of chronic glomerulonephritis and its activity, as well as the exclusion of pathology with similar manifestations, a biopsy of the kidney is performed with a morphological study of the obtained sample of renal tissue.
Treatment of chronic glomerulonephritis
Features of care and therapy for chronic glomerulonephritis are dictated by the clinical form of the disease, the rate of progression of disorders and the presence of complications. It is recommended to observe a gentle treatment with the exception of overwork, hypothermia, occupational hazards.During periods of remission of chronic glomerulonephritis, treatment of chronic infections supporting the process is required. A diet prescribed for chronic glomerulonephritis requires the restriction of salt, alcohol, spices, taking into account the fluid you drink, increasing the daily protein intake.
Drug treatment of chronic glomerulonephritis consists of immunosuppressive therapy with glucocorticosteroids, cytostatics, NSAIDs, the appointment of anticoagulants (heparin, phenindione) and antiplatelet agents (dipyridamole). Symptomatic therapy may include diuretic for edema, antihypertensive drugs for hypertension. In addition to complete inpatient courses of therapy during periods of exacerbation of chronic glomerulonephritis, they conduct supportive outpatient therapy during remission, treatment in climatic resorts.
Pathogenesis (what is happening?) During Subacute glomerulitis
According to modern concepts, the disease is an immune inflammatory genesis. There are two types of subacute glomerulonephritis. The first is regarded as a malignant variant of acute post-streptococcal glomerulonephritis, the second - as an autoimmune disease. The first type is based on the immune complex mechanism of development with the deposition of immune complexes (antigen - antibody) in the wall of the glomerular capillaries of the kidneys. In the second, autoimmune, antibodies are formed to the basement membrane of the glomerular capillaries (A. P. Peleschuk, 1983).
The pathomorphological picture of subacute malignant glomerulonephritis has been rather fully studied both from autopsy materials and from intravital puncture biopsy of the kidneys. Macroscopically, the kidneys of normal size or enlarged. The surface is smooth, the fibrous capsule is easily removed, the parenchyma is loose, yellowish-white or grayish-yellow. On the section, the cortex is broad with yellowish spots and stripes (due to lipid deposition). This usually enlarged kidney is called the "big white kidney." Sometimes on the background of the grayish-yellow surface of the cortical substance, numerous point and spotted hemorrhages in the form of red specks are seen. Such a kidney is called the "big variegated kidney."
For subacute malignant glomerulonephritis, the most characteristic are histological changes, such as the presence of hemilunus, which in typical cases of this disease are found in at least 80% of the glomeruli. They are formed due to pronounced proliferation of the epithelium of the parietal and visceral leaflets of the Sumliansky-Bowman capsule. Accumulating in the cavity of the capsule and filling the whole or almost all of its lumen, epithelium cells push the loops of the glomerular capillaries to the vascular pole and squeeze them. At the same time, the glomerular cavity takes the form of half moon, which is sometimes detected already a week after the onset of the disease.
Fibrin falls into the glomerular capsule cavity, resulting in fibroplastic and fibrous changes in the glomeruli. Due to the compression of the glomerular capillaries by the formed semi-lunar arises, their ischemia occurs, thrombosis and necrosis of the capillary wall occur. Along with the rapid proliferation of epithelial cells, there is a pronounced proliferation of the endothelium of the glomerular capillaries, which leads to obstruction of their lumen, contributes to glomerular ischemia, the development of thrombosis. As a result, the hyalinosis of the glomeruli rapidly develops, followed by their fibrosis and death. Deep changes are observed in the tubules. Already in the initial phase of the disease, pronounced dystrophic changes in the epithelium of convoluted tubules in the form of protein, granular, hyaline-droplet, vacuole and fatty degeneration, focal proliferation are detected. Subsequently, atrophic changes and necrosis of the epithelium occur rather quickly. Round cell infiltration and edema are noted in the interstitial tissue.
Symptoms of Subacute Glomerulitis
Most often, the disease develops 1-3 weeks after suffering a streptococcal infection or hypothermia. In some cases, the cause cannot be established. Mostly subacute malignant glomerulonephritis, like the classic version of acute glomerulonephritis, begins rapidly, with pronounced signs of edematous, hypertensive and urinary syndromes.
Along with edemas, which often reach a significant degree and are accompanied by the development of ascites, hydrothorax and hydropericardium, there is massive proteinuria exceeding 3.0-3.5 g per day, marked hypo- and dysproteinemia, hyperlipidemia, in particular hypercholesterolemia, i.e. there are all signs of nephrotic syndrome. In addition, hematuria, sometimes significant, is marked with cylindruria with the appearance of hyaline, granular and waxy cylinders in the urine, which indicates that the epithelium is severely damaged not only proximal, but also the distal tubules. Pathological changes in the urine are usually combined with a sharp decrease in diuresis, and in some cases oliguria gives way to anuria or the latter is observed from the very beginning of the disease, which makes one think about acute renal failure.
Arterial hypertension often reaches significant severity - up to 200-240 / 120-130 mm Hg. Art. Unlike acute or exacerbation of chronic glomerulonephritis with subacute malignant: glomerulonephritis clinical and laboratory signs of the disease do not tend to decrease, and even more to disappear. On the contrary, they staunchly persist or grow. About 1/3 of cases, hypertension acquires a malignant course (E.M. Tareev, 1972). As a consequence, it develops severe changes in the fundus with swelling of the nipple of the optic nerve, the phenomenon of retinopathy, often with hemorrhages in the retina and its detachment, thrombosis of the central artery of the retina, which leads to a sharp decrease or complete loss of vision. There may be dynamic disorders of cerebral circulation, strokes and thrombosis of cerebral vessels with relevant clinical signs. High and persistent hypertension is the cause of cardiac (predominantly left ventricular) failure, with symptoms of cardiac asthma and pulmonary edema. These complications of hypertension can serve as the immediate cause of death of the patient.
Severe and progressive violations of the structure of the glomerular and tubular apparatus of the nephrons lead to a rapid and significant reduction in renal function. As early as 1-3 weeks from the onset of the disease, clinical and laboratory signs of renal failure appear and grow rapidly. The glomerular filtration and the concentration ability of the tubules with the development of hypo- and isostenuria are significantly reduced. As a result, increasing hyperasotemia develops - the level of urea, creatinine, and residual nitrogen increases in the blood. As a manifestation of renal failure, anemia develops, in some cases significantly pronounced. ESR increases to 30-60 mm / h, moderate leukocytosis is often noted (10-15 thousand). Possible violations of the electrolyte balance of the body: hypernatraemia, hyperkalemia, etc. Metabolic acidosis develops.
The condition of patients progressively worsens. They complain of headache, shortness of breath, pain in the heart area, blurred vision, then nausea, vomiting, itching, loss of appetite, sleep disturbance, and general weakness. Frequent subjective symptoms of the disease are aching pain, sometimes quite pronounced, in the lumbar region. Patients are sluggish, inhibited, pale skin, puffy face, marked swelling of the whole body, limbs. In the terminal stage, hemorrhagic manifestations on the skin and the gastrointestinal tract are possible.Rapidly growing renal failure after a few weeks or months leads to death.
Subacute malignant glomerulonephritis is more severe in older individuals (after 50 years), which is associated with the possibility of previous diseases of the cardiovascular system.
The onset of subacute glomerulonephritis can be manifested by acute renal failure. In some cases, it develops in patients with acute glomerulonephritis, which is transformed into malignant. This should be thought of if, after 2-3 weeks from the onset of acute glomerulonephritis, there is no improvement, the patient’s condition remains severe, edema, hypertension, proteinuria, hematuria, hypo- and dysproteinemia, hypercholesterinemia persist, and glomerular filtration and relative urine density decrease , urea and creatinine levels increase in blood.
In subacute (malignant) glomerulonephritis, the prognosis is always poor. Spontaneous or under the influence of treatment, recovery is extremely rare.
Treatment of Subtidar Glomernephritis
In patients with subacute (malignant) glomerulonephritis, treatment is still considered virtually unsuccessful. Only isolated, extremely rare cases of spontaneous recovery or under the influence of complex therapy, which often leads to short-term remission, are described. The use of immunosuppressants, glucocorticosteroids and anticoagulants in the treatment of this disease did not give encouraging results. True, some authors point to the possibility of a positive effect: to reduce or even eliminate edema, lower blood pressure, decrease urinary syndrome and improve kidney function, and in rare cases complete and lasting remission of the disease - under the influence of glucocorticosteroid hormones or when combined with immunosuppressants ( azathioprine, imuran, cyclophosphamide, etc.) and anticoagulants. So, N. A. Ratner (1974) describes the case of a complete and persistent (observation period of 9 years) clinical and laboratory remission in a patient with subacute malignant glomerulonephritis treated with prednisone. The majority of clinicians believe that treatment with corticosteroids and cytotoxic drugs, both separately and in combination, does not have a significant effect on the outcome of the disease and its prognosis.
The few clinical observations suggest that early commenced complex (four-component) therapy with glucocorticoids, anticoagulants (heparin), antiplatelet agents (curantil, dipyridamole), and cytostatics (azathioprine, cyclophosphamus, etc.) may slightly slow the progression of the disease and prolong the life of the disease. The effect of this therapy is somewhat enhanced if it is performed on the background of hemodialysis. The positive effect is noted from the use of "pulse therapy", plasmapheresis, hemosorption (N. A. Mukhin, I. E. Tareeva, 1992). In general, the effectiveness of various methods of treatment of malignant glomerulonephritis, including hemodialysis and kidney transplantation, is unsatisfactory. Therefore, mainly symptomatic therapy is used.
Patients are prescribed bed rest, a diet with limited salt and liquid, and with the appearance of renal failure - and protein. Food should be predominantly milky-vegetable. To improve the taste of light-salted food, it is allowed to add flavoring seasonings in moderate quantities (parsley, dill, vinegar, mustard, etc.).
Diuretics, antihypertensives, heart remedies, vitamins C, B, P, ascorutin, antihistamines, calcium gluconate, dicynone, etc. are commonly used (see treatment of acute glomerulonephritis).
In case of severe and prolonged oliguria or anuria, hyperasotemia, and hyperkalemia, the patient should be transferred to hemodialysis.
Causes of development
Streptococcus plays the main role in the development of the disease, although the bacteria themselves do not directly participate in kidney damage. By causing inflammatory processes in other organs, such as the tonsils, they stimulate the production of specific antibodies and immune complexes, which, passing through the blood through the kidneys, can fight the cells of their glomeruli, because they have something in common with streptococcal cells.
Thus, the main causes of the development of glomerulonephritis are various infectious diseases, and not always provoked by streptococci. Often, the occurrence of pathology is preceded not only by inflammation caused by bacteria of other species, but also by viral pathology. Therefore, in most cases, glomerulonephritis develops after transferring:
- sore throats
- scarlet fever
- hepatitis B,
- infectious mononucleosis, etc.
Important: As a rule, acute glomerulonephritis occurs 10–14 days after suffering another disease of bacterial or viral origin.
Often the disease is the result of suffering severe stress or hypothermia. However, it may also be the result of an allergic reaction to certain compounds, including plant pollen, drugs, including vaccines and serums, dust, etc. In other words, the inflammation of the glomeruli of the kidneys can occur due to an inadequate immune response, that is, to have an autoimmune nature.
Therefore, depending on the causes of the development of acute glomerulonephritis is:
- Primary - formed as a result of exposure to infectious agents, toxic substances or allergens.
- Secondary - occurs against the background of certain systemic diseases, such as systemic lupus erythematosus, etc.
All patients have different symptoms of acute glomerulonephritis and with different intensity. Classical signs of pathology are:
- swelling of the face and limbs
- arterial hypertension,
- the presence of blood in the urine, as a result of which it may acquire the color of "meat slop"
- reducing the amount of urine output to 500 ml or less (oliguria),
- pale skin
- discomfort in the lower back,
- nausea and vomiting,
- loss of appetite, etc.
But mostly in patients the symptoms of edematous, hypertensive or urinary syndrome are more pronounced.
Important: sometimes the swelling may be hidden, that is, the fluid is still retained in the body, but is distributed in such a way that it may not be visible from the outside. In order to establish this exercise constant control over the weight of the patient, with his steady growth indicate the presence of hidden edema.
It would seem that, at first glance, insignificant edema can develop into anasarca, ascites, hydropericardium, etc. over time. But it is considered to be more serious complications:
Thus, with promptly started proper treatment and full adherence to medical recommendations, acute glomerulonephritis can quickly and completely pass. But prolonged non-interference, failure to comply with the regimen or making your own adjustments to the doctor’s appointment can cause the disease to become chronic and cause life-threatening complications.
Prognosis and prevention of chronic glomerulonephritis
Effective treatment of chronic glomerulonephritis can eliminate the leading symptoms (hypertension, edema), delay the development of renal failure and prolong the life of the patient. All patients with chronic glomerulonephritis are in the dispensary at the urologist.
The most favorable prognosis has a latent form of chronic glomerulonephritis, a more serious - hypertensive and hematuric, unfavorable - nephrotic mixed form.Complications that worsen the prognosis include pleuropneumonia, pyelonephritis, thromboembolism, renal eclampsia.
Since the development or progression of irreversible changes in the kidneys are most often initiated by streptococcal and viral infections, and by wet hypothermia, their prevention becomes paramount. With concomitant chronic glomerulonephritis pathology, it is necessary to monitor related specialists - an otolaryngologist, a dentist, a gastroenterologist, a cardiologist, a gynecologist, a rheumatologist, etc.
Other forms of glomerulonephritis
There are some forms of glomerulonephritis, which differ in morphological features.
Forms of glomerulonephritis by morphological features are:
- rapidly progressive form of glomerulonephritis,
- mesangial-proliferative form of glomerulonephritis,
- membranous proliferative form of glomerulonephritis,
- membranous form of glomerulonephritis,
- glomerulonephritis with minimal changes.
Characterized by the formation and further deposition in the capsule of the nephron of the so-called hemi-moon. These semi-lunar consists of fibrin and blood cells (monocytes, lymphocytes). With their location they squeeze capillary loops and part of the loop of Henle (nephron structural element). As glomerulonephritis progresses, the amount of fibrin increases, which leads to complete obstruction (blockagea) membrane and the formation of necrosis.
Mesangial proliferative glomerulonephritis
This type of glomerulonephritis is characterized by proliferation (sprawla) mesangial cells in the parenchyma and vessels of the kidneys. Mesangial cells are cells that are located between the capillaries. The proliferation of these cells subsequently leads to impaired renal function and the development of nephrotic syndrome. The more proliferation occurs, the faster the clinical symptoms progress - blood pressure rises, renal function decreases. At the same time, cell proliferation can occur both segmented and diffuse.
Membranous and proliferative glomerulonephritis
This type of glomerulonephritis is characterized by the deposition of fibrin and immunocompetent cells in connective tissue structures located between the capillaries of the vascular glomeruli. This leads to a secondary change in the basement membrane.
The main characteristic of this form of glomerulonephritis is a change in the basement membrane, as well as the formation of deposits (sediments), which are located under the vascular endothelium. Subsequently, these deposits act as spines ("Teeth"), while thickening the membrane and causing sclerosis (deatha) glomeruli.
Glomerulonephritis with minimal changes
This type of glomerulonephritis is most common in children. This is the most benign form of the disease, since the changes from the glomeruli are insignificant.