Etiology, pathogenesis. The disease occurs most often after angina, tonsillitis, upper respiratory tract infections, scarlet fever, etc. Streptococcus group A plays an important role in the occurrence of gpomerulonephritis, especially type 12 beta-hemolytic streptococcus group A. In countries with hot climates, streptococcal lesions precede acute glomerulonephritis most often in countries with a hot climate. It can also develop after pneumonia (including staphylococcal), diphtheria, typhus and typhoid fever, brucellosis, malaria and some other infections. Possible occurrence of glomerulonephritis under the influence of viral infection, after the introduction of vaccines and serums (serum, vaccine nephritis). Among the ethnological factors is the cooling of the body in a humid environment ("trench" nephrite). Cooling causes reflex disorders of the blood supply to the kidneys and affects the course of immunological reactions. At present, it is generally accepted that acute gpo-merulonephritis is an immunocomplex pathology, symptoms of glomerulonephritis after an infection have been preceded by a long latent period during which the body's reactivity changes, antibodies to microbes or viruses are formed. The antigen-antibody complexes, interacting with the complement, are deposited on the surface of the basement membrane of the capillaries, predominantly the glomeruli. A generalized vasculitis develops, mainly involving the kidneys.
Symptoms of glomerulonephritis
Symptoms, course. Acute glomerulonephritis is characterized by three main symptoms - edematous, hypertensive and urinary. In the urine are mainly protein and red blood cells. The amount of protein in the urine usually ranges from 1 to 10 g / l, but often reaches 20 g / l and more. However, the high content of the beam in the urine is observed only in the first 7-10 days, therefore, in the later examination of urine, proteinuria is often low (less than 1 g / l). Small proteinuria in some cases may be from the very beginning of the disease, and in some periods it may even be absent. Small amounts of protein in the urine in patients undergoing acute nephritis are observed for a long time and disappear only after 3-6, and in some cases even 9-12 months from the onset of the disease.
Hematuria is an obligatory and constant sign of acute gpomerolonefritis, in 13-15% of cases there is gross hematuria, in other cases - microhematuria, sometimes the number of red blood cells may not exceed 10-15 in the field of view. Cilindruria is not a mandatory symptom of acute gpomerulonephritis. In 75% of cases, single hyaline and granular cylinders are found, sometimes epithelial cylinders are found. Leukocyturia, as a rule, is insignificant, but sometimes 20-30 white blood cells and more are in sight. At the same time, the quantitative predominance of erythrocytes over leukocytes is always noted, which is better detected when calculating the firm elements of urine sediment using the methods of Kakowski - Addis, De Almeida - Nechyporenko.
Oliguria (400-700 ml of urine per day) is one of the first symptoms of acute nephritis. In some cases, anuria (acute renal failure) is observed over several days. In many patients, slight or moderate azotemia occurs during the turning of the first few days of the disease. Often, in acute glomerulonephritis, the hemoglobin content and the number of red blood cells in peripheral blood are reduced. This is due to hydremia (increased water content in the blood), and may also be due to true anemia as a result of the influence of the infection that led to the development of glomeruponephritis (for example, with septic endocarditis).
Often, increased ESR is determined. The number of leukocytes in the blood, as well as the temperature reaction, is determined by the initial or concomitant infection (usually the temperature is normal and there is no leukocytosis).
Of great importance in the clinical picture of acute glomerulonephritis are edemas, which are an early sign of the disease in 80-90% of patients, they are located mainly on the face and together with the paleness of the skin create the characteristic "face nephritis". Often, fluid accumulates in the cavities (pleural, abdominal, pericardial cavity). The increase in body weight in a short time can reach 15-20 kg or more, but after 2-3 weeks the edema usually disappears. One of the cardinal symptoms of acute diffuse gpomerulonefrit is arterial hypertension, observed in 70-90% of patients. In most cases, blood pressure does not reach high levels (180/120 mmHg). In children and adolescents, increased blood pressure is less common than in adults. Acute arterial hypertension can lead to the development of acute heart failure, especially left ventricular failure. Later development of a hypertrophy of a left ventricle of heart is possible. The examination is determined by the expansion of the boundaries of cardiac dullness, which may be due to the accumulation of transudate in the pericardial cavity and myocardial hypertrophy. Often, functional systolic murmur at the apex, accent II of the aorta, and sometimes a gallop rhythm are heard: in the lungs there are dry and moist rales. On the ECG, there may be changes in the R and T teeth in standard leads, often a deep Q wave and a slightly reduced voltage of the ORS complex.
Hypertension in acute glomerulonephritis may be accompanied by the development of eclampsia, but there is no uremia. Eclampsia is more correct to assume. Acute encephalopathy, as it is caused by arterial hypertension and edema (hypervolemic swelling of the brain). Despite the severe clinical picture of eclamptic seizures, they rarely end in death and pass for the most part without a trace.
There are two most characteristic forms of acute glomerulonephritis. Cyclic form begins violently. There are swelling, shortness of breath, headache, pain in the lumbar region, the amount of urine decreases. In urine tests - high numbers of proteinuria and hematuria. Blood pressure rises. Edema lasts 2-3 weeks. Then, during the course of the disease, a fracture occurs: polyuria develops and blood pressure decreases. The recovery period may be accompanied by hypostenuria. However, often with good well-being of patients and almost complete restoration of working capacity, there can be a long-term, for months, a slight proteinuria (0.03-0.1 g / l) and residual hematuria can be observed. The latent form is not uncommon, and its diagnosis is of great importance, since often in this form the disease becomes chronic. This form of glomerulonephritis is characterized by a gradual onset without any pronounced subjective symptoms and is manifested only by shortness of breath or swelling in the legs. In such cases, glomerulonephritis can only be diagnosed by systematic examination of the urine. The duration of the relatively active period in the latent form of the disease may be significant (2-6 months or more).
Acute glomerulonephritis may be accompanied by nephrotic syndrome. Any acute glomerulonephritis that has not completely disappeared within a year should be considered to have passed into chronic. It should be remembered that in some cases, acutely beginning diffuse glomerulonephritis may assume the character of subacute malignant extracapillary glomerulonephritis with rapidly progressive course.
The diagnosis of acute diffuse glomerulonephritis does not present great difficulties in the severe clinical picture, especially of young streets. It is important that the symptoms of heart failure (shortness of breath, edema, cardiac asthma, etc.) are often leading in the picture of the disease. To establish the diagnosis in these cases, an essential role is played by the fact that the acute development of the disease occurs in patients without prior cardiac pathology and that this reveals a pronounced urinary syndrome, especially hematuria, as well as a tendency to bradycardia.
Difficult differential diagnosis between acute glomerulonephritis and exacerbation of chronic glomerulonephritis. It is important to clarify the period from the beginning of the infectious disease to the acute manifestations of nephritis. With acute glomerulonephritis, this period is 1-3 weeks, and with exacerbation of the chronic process - only a few days (1-2 days). Urinary syndrome may be the same in severity, but a persistent decrease in the relative density of urine below 1.015 and a decrease in the filtration function of the kidneys is more characteristic of an exacerbation of the chronic process. It is difficult to diagnose the latent form of acute gpomeuronefrita. The predominance of red blood cells in the urine sediment over leukocytes, the absence of active and pale leukocytes (when stained according to Sternheimer-Malbin), the absence of dysuric events in the anamnesis help to distinguish it from chronic, latent pyelonephritis. These X-ray studies can be important for the differential diagnosis of pyelonephritis, kidney stones, kidney tuberculosis, and other diseases with low urinary syndrome.
Treatment of glomerulonephritis
Treatment. Bed rest and diet are prescribed. Sharp limitation of salt in food (not more than 1.5-2 g / day) in itself can already lead to increased water excretion and the elimination of edematous and hypertensive syndromes. At first, sugar days are prescribed (400-500 g of sugar per day with 500-600 ml of tea or fruit juices). In the future, give watermelons, pumpkins, oranges, potatoes, which provide almost completely non-sodium food.
Prolonged restriction of protein intake in acute glomerulonephritis is not sufficiently substantiated, since, as a rule, there is no delay in nitrogenous slags, and the expected increase in blood pressure under the influence of protein nutrition is not proven. From protein products it is better to use cottage cheese, as well as egg white. Fats are allowed in the amount of 50-80 g / day. To ensure daily calories add carbohydrates. Liquids can be consumed up to 600-1000 ml / day. Antibacterial therapy is indicated when there is a clear connection between glomerine nephritis and an existing infection, for example, with prolonged septic endocarditis and chronic tonsillitis. In chronic tonsillitis, tonsildectomy is indicated 2-3 months after subsidence of the acute phenomena of glomerulonephritis.
It is advisable to use steroid hormones - prednisolone (prednisone), triamcinolone, dexamethasone. Treatment with prednisone is prescribed not earlier than in 3-4 weeks from the onset of the disease, when the general symptoms (in particular, arterial hypertension) are less pronounced. Corticosteroid hormones are especially indicated in the nephrotic form or in the protracted course of acute glomerulonephritis, as well as in the so-called residual urinary syndrome, including hematuria. Prednisolone is used, starting with a dose of 10-20 mg / day, quickly (within 7-10 days) bring the daily dose to 60 mg. This dose continues to be given for 2-3 weeks, then it is gradually reduced. The course of treatment lasts 5-6 weeks. The total amount of prednisolone per course of 1500-2000 mg. If during this time a sufficient therapeutic effect is not achieved, it is possible to continue the treatment with maintenance doses and prednisone (10-15 mg / day) for a long time under medical supervision. Corticosteroid therapy affects both edematous and urinary syndrome. It can promote healing and prevent the transition of acute glomerulonephritis to chronic. Moderate arterial hypertension is not a contraindication to the use of corticosteroids. With a tendency to increase blood pressure and increasing edema, treatment with corticosteroid hormones should be combined with antihypertensive and diuretic agents. If the body has foci of infection, then at the same time as corticosteroid hormones, it is necessary to prescribe antibiotics.
In the presence of hypertension and particularly when there eclampsia is a complex antihypertensive therapy peripheral vasodilators (verapamil, hydralazine, sodium nitroprusside, diazoxide) or sympatholytic (reserpine, clonidine), in combination with saluretikami (furosemide, ethacrynic acid) and anxiolytics (diazepam and others). . Ganglioblockers and (3-blockers can be used. Osmotic diuretics (40% glucose solution, mannitol) are used to reduce cerebral edema. They give ether-oxygen anesthesia during spasms (at 1 stage). Bleeding is carried out with incessant cramps.
Prognosis for glomerulonephritis
Forecast. There may be a full recovery. Fatal outcome in the acute period of the disease is rare. The transition of acute glomerulonephritis to a chronic disease occurs in approximately 1/3 of cases. In connection with the use of corticosteroid hormones, the prognosis is now significantly improved. In the acute period, patients are disabled and must be in the hospital. With a typical course, after 2-3 months, a full recovery may occur: those who have undergone the disease may return to work even in the presence of moderate urinary syndrome or residual albuminuria. Persons who have experienced acute glomerulonephritis are subject to follow-up, since clinical recovery can often be apparent. In order to avoid recurrence of the disease, special attention should be paid to the fight against focal infection. It is necessary to avoid work related to cooling in a humid environment for a year.
Prevention basically comes down to the prevention and early intensive treatment of acute infectious diseases, the elimination of focal infection, especially in the tonsils. Preventive importance has the warning and sharp cooling of the body. Persons suffering from allergic diseases (urticaria, bronchial asthma, hay fever), prophylactic vaccinations are contraindicated.
Subacute diffuse glomerulophritis has a malignant course and, as a rule, ends in the death of patients 0.5-2 years from the onset of the disease. Crucial to the occurrence of malignant course of subacute glomerulonephritis, apparently, is the activity of immunological reactions.
Symptoms, course. The disease usually begins as acute glomerulonephritis (often violently), but may occur latent at first. Characterized by large persistent edema, severe albuminuria (up to 10-30 g / l), as well as pronounced hypoproteinemia (45-35 g / l) and hypercholesterolemia (up to 6-10 g / l), i.e. signs of lipoid-nephrotic syndrome At the same time, pronounced hematuria with oliguria is observed. With the latter, the relative density of urine is high only at the beginning, and then it becomes low. Progressively reduced filtration function of the kidneys. Already from the first weeks of the disease, azotemia can increase, leading to the development of uremia. Arterial hypertension in this form of jade is very high and is accompanied by severe changes in the fundus (retinal hemorrhage, edema of the optic nerve discs, the formation of exudative white retinal spots).
The diagnosis is made, given the rapid development of renal failure, persistent severe arterial hypertension, often recurrent in malignant type. Due to the fact that the syndrome of malignant hypertension can be observed in hypertension and in a number of kidney diseases - occlusive lesions of the renal arteries (especially often), chronic pyelonephritis, as well as in extrarenal diseases (for example, in pheochromocytoma), subacute gomperuponephritis has to be differentiated with them. A great manifestation of edematous-inflammatory and lipoid-nephrotic syndromes indicates subacute glomerulonephritis.
Treatment with steroid hormones of this form of glomerulonephritis is less effective, and in some cases is not indicated due to high and progressive arterial hypertension (blood pressure above 200/140 mm Hg). Recently, it is recommended to use anti-metabolites and immunosuppressants (6-mercaptopurine, azathioprine, and also cyclophosphamide) with careful monitoring of the morphological composition of the blood. Treatment with immunosuppressants is more effective in combination with corticosteroid hormones, which are prescribed in smaller doses (25-30 mg / day). This combination not only contributes to the effectiveness of treatment, but also reduces the risk of complications from both corticosteroids and immunosuppressants (in particular, severe leukopenia).
Hypothiazide is used to combat edema and arterial hypertension (50-100 mg / day). It is also shown the appointment of other antihypertensive drugs: dopegita, reserpine, clonidine. At the same time, a sharp decrease in blood pressure should be avoided, since this can lead to a deterioration of the filtration function of the kidneys. With an increase in renal failure and an increased content of nitrogenous slags in the blood, it is necessary to reduce protein intake from food and introduce large amounts of concentrated glucose (80-100 ml of 20% solution w / w), as well as 5% glucose solution of 300-500 ml w / w drip. In the absence of edema, 100-200 ml of 5% sodium bicarbonate solution should be added dropwise. If signs of heart failure appear, digitalis preparations and diuretics are prescribed. Применение диализа (перитонеального или искусственной почки) менее эффективно, чем при хроническом гломерулонефрите, из-за высокой активности и быстроты прогрессирования основного почечного процесса. Пересадка почки не показана.
Прогноз подострого гломерулонефрита плохой. This disease usually ends lethal after 6 months, but not later than 2 years. Death occurs from chronic renal failure and uremia, less often from cerebral hemorrhage.
Chronic diffuse glomerulonephritis - long-lasting (at least a year) proceeding immunological bilateral kidney disease. This disease ends (sometimes many years later) with shrinking of the kidneys and death of patients from chronic renal failure. Chronic glomerulonephritis can be either the outcome of acute glomerulonephritis or primary chronic, without a prior acute attack.
Etiology and pathogenesis, see Acute glomerulonephritis.
Symptoms, the course is the same as in acute glomerulonephritis: edema, hypertension, urinary syndrome and impaired renal function.
During chronic glomerulonephritis, two stages are distinguished: a) renal compensation, i.e. sufficient nitrogenous kidney function (this stage may be accompanied by pronounced urinary syndrome, but sometimes it takes a long time latently, manifested only by small albuminuria or hematuria), b) renal decompensation characterized by inadequate nitrogenous kidney function (urinary symptoms may be less significant, as a rule, there is high arterial hypertension, edema more often moderate, in this stage of expression gipoizostenuriya us and polyuria, which terminate development azotemicheskoy uremia).
The following clinical forms of chronic glomerulonephritis are distinguished. 1. The nephrotic form (see Hvfrotichesky syndrome) is the most common form of primary nephrotic syndrome. In contrast to pure lipoid nephrosis, this form is characterized by a combination of nephrotic syndrome with signs of inflammatory kidney damage. The clinical picture of the disease can be determined for a long time by nephrotic syndrome, and only later does the progression of glomerulonephritis itself occur, with impaired nitrogenous kidney function and arterial hypertension. 2. Hypertensive form. For a long time, arterial hypertension predominates among the symptoms, while urinary syndrome is not very pronounced. Occasionally chronic glomerulonephritis develops in the hypertensive type after the first violent attack of glomerulonephritis, but more often it is the result of the latent form of acute glomerulonephritis. Blood pressure reaches 180 / 100-200 / 120 mm Hg. Art. and may be subject to large fluctuations during the day under the influence of various factors. The hypertrophy of the left ventricle of the heart is broken, the accent of II tone over the aorta is heard. As a rule, hypertension still does not acquire a malignant character, BP, especially diastolic, does not reach high levels. Observed changes in the fundus in the form of neuroretinitis. 3. Mixed form. In this form, there are both nephrotic and hypertensive syndromes. 4. Latent form. This is a fairly frequent form, usually only manifested by a weak urinary syndrome of arterial hypertension and edema. It can have a very long course (10–20 years or more), later it still leads to the development of uremia.
It should also highlight the hematuric form, as in some cases, chronic glomerulonephritis can manifest hematuria without significant proteinuria and common symptoms (hypertension, edema).
All forms of chronic glomerulonephritis "can periodically give relapses, very reminiscent or completely repeating the picture of the first acute attack of diffuse glomerulorrhephritis. Especially often exacerbations are observed in autumn and spring and occur 1-2 days after exposure to an irritant, most often streptococcal infection. For any course of chronic Diffuse glomerulonephritis enters its final stage - the secondary wrinkled kidney. For the secondary wrinkled kidney, a picture of chronic azotemic uremia is characteristic (see Chro nical renal failure).
Diagnosis. With a history of acute glomerulonephritis and severe clinical picture, the diagnosis does not present much difficulty. However, in the latent form, as well as in hypertensive and hematuric forms of the disease, its recognition is sometimes very difficult. If there is no definite indication in the history of acute acute glomerulonephritis, then for moderately severe urinary syndrome, differential diagnosis has to be performed with one of many single or bilateral kidney diseases. It should also be remembered about the possibility of orthostatic albuminuria.
When differentiating hypertensive and mixed forms of chronic glomerulonephritis from hypertension, it is important to determine the time of appearance of the urinary syndrome in relation to the occurrence of arterial hypertension. In chronic glomerulonephritis, urinary syndrome may well precede arterial hypertension or occur simultaneously with it. Chronic glomerulonephritis is also characterized by lower severity of cardiac hypertrophy, less tendency to hypertensive crises (except for exacerbations occurring with eclampsia) and more rare or less intensive development of atherosclerosis, including coronary arteries.
The prevalence of erythrocytes over leukocytes in the urine sediment, the absence of active and pale (when stained by Sternheimer-Mapbin) leukocytes, as well as the same size and shape of two kidneys and the normal structure of the pelvis and cups and in the case of differential glomerulonephritis in differential diagnosis with chronic pyelonephritis detected by x-ray examination. The nephrotic form of chronic glomerulonephritis should be distinguished from lipoid nephrosis, amyloidosis, and diabetic glomerulosclerosis. In the differential diagnosis of renal amyloidosis, the presence in the body of foci of chronic infection and amyloid degeneration of another site is important.
The so-called stagnant kidney sometimes gives rise to incorrect diagnosis, because it can occur with significant proteinuria with moderate hematuria and high relative density of urine. A stagnant kidney is often manifested by edema, sometimes arterial hypertension. The presence of independent primary heart disease, enlarged liver, the location of edema mainly on the lower limbs, less pronounced hypercholesterolemia and urinary syndrome, as well as its disappearance with a decrease in cardiac decompensation indicate stagnant kidney.
Treatment. It is necessary to eliminate the foci of infection (removal of the tonsils, sanitation of the oral cavity, etc.). Long-term dietary restrictions (salt and protein) do not prevent the transition of acute glomerulonephritis to chronic. Patients with chronic nephritis should avoid cooling, especially exposure to wet cold. They are recommended dry and warm climate. With a satisfactory general condition and the absence of complications, sanatorium-resort treatment is shown in Central Asia (Bayram-Ali) or on the Southern Coast of Crimea (Yalta). Bed rest is necessary only in the period of the appearance of significant edema or the development of heart failure, as well as with uremia.
For the treatment of patients with chronic glomerulonephritis, diet is essential, which is prescribed depending on the form and stage of the disease. In case of nephrotic and mixed forms (edemas), the intake of sodium chloride with food should not exceed 1.5-2.5 g / day, for which they stop salting food. With sufficient excretory function of the kidneys (no edema), the food should contain a sufficient amount (1-1.5 g / kg) of animal protein, rich in high-grade phosphorus-containing amino acids. This normalizes the nitrogen balance and compensates for protein loss. In hypertensive form, it is recommended to moderately limit sodium chloride intake to 3–4 g / day with a normal content of proteins and carbohydrates in the diet. The latent form of the disease does not require significant nutritional limitations for patients; it must be complete, diverse 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 a long protein-free and salt-free diet does not prevent the progression of nephritis and has a bad effect on the general condition of patients.
Especially important is corticosteroid therapy, which is the basis of pathogenetic therapy for this disease. 1500-2000 mg of prednisolone (prednisone) or 1200-1500 mg of triamcinolone are used for the course of treatment. Treatment is usually started with 10-20 mg of prednisolone and the dose is adjusted to 60–80 mg / day (the dose of triamcinolone is increased from 8 to 48–64 mg), and then it is gradually reduced. It is recommended to carry out repeated full courses of treatment (for exacerbations) or supporting small courses.
While taking corticosteroid hormones, exacerbation of hidden foci of infection is possible. In this regard, treatment with corticosteroids is best done by prescribing antibiotics at the same time, or after removal of foci of infection (for example, tonsillectomy).
Contraindication to the appointment of corticosteroids in patients with chronic glomerulonephritis is progressive azotemia. In moderate arterial hypertension (BP 180/110 mmHg), treatment with corticosteroid hormones can be carried out while applying antihypertensive drugs. With high hypertension, a preliminary reduction in blood pressure is required. In case of contraindications to corticosteroid therapy or in case of its ineffectiveness, the use of non-hormonal immunosuppressants is recommended: aaiatioprine (imuran), 6-mercaptopurine, cyclophosphamide. These drugs are more effective, and their treatment is better tolerated by patients while taking prednisone in moderate doses (10-30 mg / day), which prevents the toxic effects of immunosuppressants on leukopoiesis. In the later stages - with sclerosis of the glomeruli and their atrophy with the presence of high hypertension - immunosuppressants and corticosteroids are contraindicated, since there is no longer any immunological activity in the glomeruli, and the continuation of such treatment aggravates arterial hypertension.
Immunosuppressive properties are also drugs of 4-aminoquinoline series - hingamin (delagil, resoquine, chloroquine), hydroxychloroquine (plaquenil). Rezokhin (or chloroquine) is applied at 0.25 g 1-2 - 3 times a day for 2-3 - 8 months. Rezokin can cause side effects - vomiting, damage to the optic nerves, therefore, control by an ophthalmologist is necessary.
Indomethacin (metindol, indocide) - a derivative of indole - is a non-steroidal anti-inflammatory drug. It is believed that, in addition to providing anesthetic and antipyretic effects, indomethacin acts on mediators of immunological damage. Under the influence of indomethacin proteinuria is reduced. Assign it inside by 25 mg 2-3 times a day, then, depending on tolerance, increase the dose to 100-150 mg / day. The treatment is carried out for a long time, for several months. The simultaneous use of steroid hormones and indomethacin can significantly reduce the dose of corticosteroids with their gradual abolition.
The deposition of fibrin in the glomeruli and arterioles, the participation of fibrin in the formation of capsular "half moon", a mild increase in the content of fibrinogen in plasma serve as a pathogenetic rationale for the anticoagulant therapy of chronic glomerulonephritis. Strengthening fibrinolysis, neutralizing complement, heparin affects many allergic and inflammatory manifestations and as a result reduces proteinuria, reduces dysproteinemia, and improves the filtration function of the kidneys. Assigned to / to 20 000 IU per day for 2-3 weeks with the subsequent gradual reduction of the dose during the week or IV drip (1000 IU per hour) heparin can be used in combination with corticosteroids and cytotoxic drugs.
In the mixed form of chronic glomerulonephritis (edematous and pronounced hypertensive syndromes), the use of natriuretics is indicated, since they have a pronounced diuretic and hypotensive effect. Hypothiazide administered 50-100 mg 2 times a day, Lasix 40-120 mg / day, ethacrynic acid (uregit) 150-200 mg / day. It is advisable to combine saluretics with a competitive aldosterone antagonist with aldactone (Verohpiron), up to 50 mg4 times a day, which increases the excretion of sodium and reduces the excretion of potassium. The diuretic effect of hypothiazide (and other saluretics) is accompanied by the excretion of potassium with urine, which can lead to hypokalemia with the development of its general weakness, adynamia and impaired cardiac contractility. Therefore, you should simultaneously appoint a solution of potassium chloride. With persistent edema on the background of hypoproteinemia, it is possible to recommend the use of the molecular weight fraction of the polymer glucose-polyglucin (dextran) in the form of intravenous drip 500 ml of 6% solution, which increases the colloid-osmotic pressure of blood plasma, promotes the movement of fluid from the tissues into the blood and causes diuresis. Polyglucin works best on the background of treatment with prednisone or diuretics. Mercury diuretics for renal edema should not be used, since their diuretic effect is associated with a toxic effect on the tubular epithelium and the glomeruli of the kidneys, which, along with an increase in diuresis, leads to a decrease in the filtration function of the kidneys. In the treatment of renal edema, the purine derivatives — theophylline, aminophylline, and others — are ineffective.
In the treatment of hypertensive forms of chronic glomerulonephritis, hypotensive agents used in the treatment of hypertension can be prescribed: reserpine, reserpine with hypothiazide, adelfan, trirezide, cristapin, dopegmt. However, sharp fluctuations in blood pressure and orthostatic fall, which can impair renal blood flow and filtration function of the kidneys, should be avoided. In the pre-eclampsia period and in the treatment of eclampsia, which can occur during exacerbation of chronic glomerulonephritis, magnesium sulfate can be prescribed to patients, with intravenous and intramuscular administration it can reduce blood pressure in the form of a 25% solution and improve kidney function with a diuretic effect, and also help swelling of the brain. Treatment in the final stage of chronic nephritis, see Chronic renal failure.
Forecast. The end result of chronic glomerulonephritis is wrinkling of the kidneys with the development of chronic renal failure - chronic uremia. Immunosuppressive therapy significantly changed the course of the disease. There are cases of complete remission of the disease with the disappearance of both general and urinary symptoms.
Nephrotic syndrome (NS) is a nonspecific clinical and laboratory symptom complex, expressed in massive proteinuria (5 g / day or more), disorders of protein-lipid and water-salt metabolism. These disorders are manifested by hypoalbuminemia, dysproteinemia (with a predominance of (Xd-tobulins), hyperlipidemia, lipiduria, as well as edema to the degree of anasarca with edema of serous cavities.
The term NA is widely used in the WHO classifications of diseases and has almost supplanted the old term nephrosis. NA is primary and secondary. Primary NA develops in actual kidney diseases (all morphological types of Bright glomerulonephritis, including the so-called lipoid nephrosis, membranous nephropathy, nephropathic form of primary amyloidosis, congenital and hereditary NA). Secondary NA rarer, though the band causing its diseases very numerous: collagen (SLE, periarteritis nodosa, systemic scleroderma), hemorrhagic vasculitis, rheumatism, rheumatoid arthritis, bacterial endocarditis, diabetic glomerulosclerosis, blood diseases (lymphoma), chronic suppurative diseases (lung abscess , bronchiectasis, etc.), infections (tuberculosis), including parasitic (malaria) and viral, tumors, drug disease and allergies. Histological and cytological studies primarily reveal changes characteristic of nephropathy, which caused the development of NA. The histological features of the NA itself include the fusion of the foot processes and the spreading of the podocyte bodies in the glomeruli, hyaline and vacuolar dystrophy of proximal tubule cells, and the presence of foamy cells containing lipids.
The pathogenesis of NA is closely related to the underlying disease. Most of the diseases listed above have an immunological basis, i.e. they result from the deposition in the organs (and kidney) of complement fractions, immune complexes or antibodies against the glomerular basement antigen of the glomerular membrane with concomitant violations of cellular immunity.
The main link in the pathogenesis of the leading symptom of NA - massive proteinuria - is the reduction or disappearance of a constant electrical charge of the wall of the capillary loop of the glomerulus. The latter is associated with the depletion or disappearance of sialoprotein from it, normally with a thin layer of clothing on the epithelium and its processes lying on the basal membrane, and which is contained in the membrane itself. As a result of the disappearance of the "electrostatic trap" proteins in large quantities go into the urine. Вскоре происходит "срыв" процесса реабсорбции белков в проксимальном канальце нефрона. Нереабсорбированные белки попадают в мочу, обусловливая своим составом селективный (альбумин и трансферрин) или неселективный (высокомолекулярные белки, например, альфа (два)-М Г) характер протеинурии.
Все остальные многочисленные нарушения при НС являются вторичными по отношению к массивной протеинурии. So, as a result of hypoalbuminemia, reduction of colloid osmotic pressure of plasma, hypovolemia, reduction of renal blood flow, enhanced production of ADH, renin and aldosterone with sodium hyperreabsorption develop edema.
Symptoms, course. The clinical picture of NA, lame swelling, dystrophic changes of the skin and mucous membranes, may be complicated by peripheral phlobothrombosis, bacterial, viral, fungal infections of various localization, brain edema, fundus retina, nephrotic crisis (hypovolemic shock). In some cases, the symptoms of NA can be combined with arterial hypertension (mixed form of NA).
Diagnosis of glomerulonephritis
Diagnosis of NA is not difficult. The diagnosis of the underlying disease and nephropathy causing NA is made on the basis of anamnestic data, clinical research data and data obtained using a puncture biopsy of the kidney (less often than other organs), as well as additional laboratory methods (LE cells in the presence of SLE).
The course of NA depends on the form of nephropathy and the nature of the underlying disease. In general, NA is a potentially reversible state. Thus, spontaneous and medicinal remissions are characteristic of lipoid nephrosis (even in adults), although there may be recurrences of NS (up to 5-10 times within 10-20 years). With the radical elimination of the antigen (timely surgery for the tumor, the exclusion of the drug-antigen) complete and stable remission of NS is possible. The persistent course of NS is found in membranous, mesangioproliferative, and even in fibroplastic glomeruponephritis. The progressive nature of the course of NA with the outcome in chronic renal failure in the first 1.5-3 years of the disease is observed with focal-segmental hyalinosis, extracapillary nephritis, and subacute lupus nephritis.
Treatment of patients with NS is diet therapy - limiting sodium intake, consumption of animal protein to 100 g / day. The stationary mode without strict bed rest and physical therapy to prevent venous thrombosis of the extremities. Mandatory rehabilitation of latent infection foci. Of the drugs used: 1) corticosteroids (prednisone 0.8-1 mg / kg for 4 weeks, in the absence of the full effect - a gradual decrease to 15 mg / day and continued treatment for 1-2 months, 2) cytostatics (azathioprine - 2-4 mg / kg or leukeran - 0.3-0.4 mg / kg) up to 6-8 months, 3) anticoagulants (heparin -20,000-50,000 IU per day), sometimes indirect anticoagulants, 4) anti-inflammatory drugs (indomethacin - 150-200 mg per day, Brufen - 800-1200 mg per day), 5) diuretic (saluretics - alone or in combination with intravenous infusions of albumin, furosemide, ver shpiron). The effectiveness of therapy is determined by the nature of the underlying disease and the morphological features of nephropathy. Spa treatment (sanatoriums Bairam-Ali, Sitorai Mahi-Hasa, Bukhara during remission and the southern coast of Crimea) was shown to patients with NA depending on the type of the underlying disease and the degree of its activity.
The prognosis for the timely and adequate treatment of the underlying disease can be favorable.
Etiology and provoking factors
The etiology of CGN is as follows:
- Infectious agents - bacterial (Str, Staf, Tbs, etc.), viral (hepatitis B, C, cytomegalovirus, HIV)
- Toxic agents - alcohol, drugs, organic solvents, mercury
The reason in most cases is beta-hemolytic streptococcus group A.
Diseases contributing to the development of pathology:
• Angina and chronic tonsillitis,
• Scarlet fever,
• Infectious heart disease,
• Rheumatological diseases,
• Autoimmune pathology.
Classification of chronic glomerulonephritis
1. Acute glomerulonephritis
- with nephritic (hematuric) syndrome
- with nephrotic syndrome
- with isolated urinary syndrome
- with nephrotic syndrome, hematuria and hypertension
2. Chronic glomerulonephritis
- hematuric form
- nephrotic form
- mixed form
Morphological classification of CGN
- With minimal changes
The classification is based on the assessment of clinical and laboratory syndromes, pathogenesis (primary, secondary), the functional ability of the kidneys (with loss, without loss, CRF) and morphology.
CG course occurs:
• Recurrent (remission is replaced by exacerbation).
• Persistent, (constant activity of immune inflammation in the glomeruli while maintaining the functional abilities of nephrons for a long time).
• Progressive (constant activity of the process with a tendency to renal failure, and a gradual decrease in glomerular filtration).
• Rapidly progressive (the process is so active that after a short period of time the CRF is formed).
In most cases, pathology is characterized by slow development. Many patients can not remember when it was the beginning and after which they became ill.
The most typical symptoms are:
• Diuresis depends on the severity of chronic renal failure: a decrease in daily diuresis (oliguria) at the initial stage, with progression - polyuria (a lot of urine) with outcome in anuria in the terminal stage of chronic renal failure, in the clinical analysis of urine pathological content of erythrocytes and protein.
• Urination mostly prevails at night: nocturia.
• Edema: from minor to severe, localization is different.
• Weakness, fatigue.
• Increased temperature response.
• Development of persistent hypertension.
• Thirst, the smell of acetone in the exhaled air, itching skin indicate the neglect of the disease and the progress of ESRD.
There are several forms of chronic glomerulonephritis.
Glomerulonephritis with isolated urinary syndrome
Isolated urinary syndrome is characterized by the following features:
• Lack of edema, AH
The most common variant is distinguished by a benign course (aggressive treatment is not prescribed). Patients have no complaints with this form.
During the examination in the urine protein is found in small quantities and red blood cells.
Since the disease proceeds covertly, and the progression of renal failure is slow, but constant, sometimes all laboratory and clinical signs of CRF are detected in the first-time patients.
The latent form of chronic glomerulonephritis, despite the benign course with timely diagnosis, can be the cause of renal failure.
Nephrotic form of glomerulonephritis
It takes a little more than 20% of cases. It has pronounced clinical manifestations, the leading symptom is the appearance of significant edema.
In the clinical analysis of urine, the loss of protein (predominantly, albumin) is more than 3 g / day, which is why, on the contrary, there are not enough protein substances in the plasma.
Increased blood cholesterol, triglycerides and low density lipoproteins.
The nephrotic form of glomerulonephritis is an indication for emergency hospitalization of the patient, as his condition is regarded as severe due to the development of ascites, pleurisy, etc. against the backdrop of massive edema. In addition, the patient is at risk of developing secondary infection on the background of reduced immunity, osteoporosis, thrombosis, hypothyroidism, atherosclerosis, heart attack, stroke.
All of the above pathology is a consequence of impaired water – electrolyte balance (loss of zinc, copper, vitamin D, calcium, thyroid-stimulating hormones, etc.) with urine.
The most terrible complications of nephrotic forms of glomerulonephritis are brain swelling and hypvoemia shock.
Mixed version or hypertensive glomerulonephritis
It is characterized by a combination of nephrotic syndrome and persistent hypertension (increased blood pressure). Typically, rapid progression with outcome in CRF, due to the detrimental effect of hypertension on the kidney vessels.
Hematuric form of glomerulonephritis
Chronic glomerule nephritis in men is more often in hematuric form.
Edema does not appear, there is no increase in blood pressure.
There is no pronounced proteinuria (no more than 1 g / day), but there is hematuria (erythrocytes in the urine).
The factors provoking hematuric chronic glomerulonephritis include:
• alcohol intoxication,
• poisoning with any substances
• colds with Berger's disease.
Nephrologists note this pattern: the brighter the clinical manifestations, the greater the chances of complete restoration of the functional ability of the kidneys.
It must be remembered that any form of chronic hepatitis, with the confluence of certain circumstances, can move into an acute stage with a clinic typical of acute glomerulonephritis.
Chronic glomerulonephritis in the acute stage will be treated according to the scheme used in the treatment of acute immune inflammation of the kidneys.
How to diagnose chronic glomerulonephritis
An important role in the diagnosis of chronic hepatitis is assigned to clinical and laboratory research. During the conversation between the doctor and the patient, attention is paid to the presence of infectious diseases in history, concomitant pathology, in particular, systemic diseases, and the urological history is clarified.
• General urinalysis
Urine in chronic glomerulonephritis is variable, it depends on the morphology of the pathological process. Typically, a decrease in specific gravity, the greater the amount of protein in the urine (up to 10 g / day), the more data for the nephrotic form.
Erythrocytes are present: gross hematuria or microhematuria. In the urine sediment detect hyaline and granular cylinders (nephrotic and mixed form), fibrin.
For hypertensive forms, a decrease in glomerular filtration is typical.
1. increased levels of cretinin, urea,
2. hypoproteinemia and dysproteinemia,
4. increase of antibody titer to streptococcus (ASL-O, antihyaluronidase, anti-streptokinase),
5. a decrease in the level of C3 and C4,
6. increase of all immunoglobulins M, G, A
7. electrolyte imbalance.
• Sow urine on flora and drug sensitivity.
• Zimnitsky test.
• Nechiporenko test.
• Reberg test.
• Kidney ultrasound with doppler
At the initial stages, ultrasound diagnostics does not reveal any pronounced changes.
If there is a progression of chronic glomerulonephritis, sclerotic processes in the kidneys with a decrease in their size are possible.
• Review and excretory urography, radioisotope scintigraphy allow to evaluate the function of each kidney separately and the general state of the parenchyma.
If the patient has persistent hypertension, electrocardiography confirms hypertrophy (increase in size) of the left ventricle.
• examination of the fundus
Symptoms are similar to those with hypertension:
1. narrowing of the arteries
2. varicose veins
3. point hemorrhages,
To determine the morphological component of the CG form, it is possible to conduct a diagnostic biopsy. According to the results of the morphological conclusion, the treatment tactics are chosen.
The procedure is considered invasive and has a number of contraindications:
• Single kidney or lack of collateral kidney function.
• Right ventricular insufficiency.
• Infectious processes.
• Renal artery thrombosis.
• Kidney cancer.
• Heart attacks, stroke in the acute stage.
Differential diagnosis is carried out with the following diseases:
• chronic pyelonephritis,
• hemorrhagic fever with renal syndrome,
• hypertensive disease,
• tuberculous lesions of the urinary organs, etc.
Treatment for chronic glomerulonephritis
The scheme of therapy will depend on the form of the disease, clinical manifestations, comorbidity, the presence of complications.
The main aspects of treatment in chronic glomerulonephritis are normalization of blood pressure, elimination of edema and maximum lengthening of the predialysis period of time.
It is recommended to normalize the mode of work and rest, to avoid hypothermia, work with toxic substances.
Pay attention to the timely reorganization of foci of possible infection: caries, tonsils, throat, etc.
Diet for chronic glomerulonephritis
Great importance is attached to proper diet.
Chronic renal failure leads to a violation of the electrolyte balance of the blood, self-poisoning of the body as a result of accumulation of toxic substances.
Properly selected nutrition is able to correct the adverse effects of toxins on the body at the initial stage of CRF. Yes, and at all other stages of chronic renal failure without a diet anywhere.
What can you eat for glomerulonephritis - combines diet (table number 7).
Its main points are:
• Refusing salt.
• Reduced fluid intake.
• Introduction to the diet of foods with a high content of potassium and calcium.
• Limiting animal protein intake.
• Introduction to the diet of vegetable fats and carbohydrates.
Proper nutrition in chronic hepatitis will allow longer do without hemodialysis or kidney transplantation
Medication for chronic glomerulonephritis
First-line drugs are immunosuppressive agents. Due to the overwhelming effect on the activity of immunity, the pathological processes in the glomerular apparatus of the kidney are slowed down.
The dosage of prednisolone is calculated individually, 1 micron / kg per day, for 2 months, with a gradual decrease in order to avoid withdrawal syndrome. Periodically prescribed pulse therapy (the introduction of corticosteroid drugs in a high dose short-term). With the irregularity of the reception, improper dosage, untimely started therapy and with a severe degree of immune disorders, the efficiency decreases.
Contraindications for the treatment of non-steroid hormones are the following conditions:
• tuberculosis and syphilis in active form,
• viral ophthalmic diseases,
• infectious processes,
With caution, steroids are used for diabetes, thromboembolism, herpes,
systemic candidiasis, hypertension, Itsenko-Cushing's disease, severe form of CRF.
Applied with progressive forms of chronic pyelonephritis in men and women, and in all cases when there are contraindications to the prescription of steroid drugs, or the appearance of complications, or in the absence of the effect of therapy.
Sometimes in the treatment regimen include both hormones and cytostatics.
Contraindications: pregnancy and the active phase of infectious processes.
With care: the expressed dysfunctions of a liver and kidneys, blood pathology.
The list of cytostatics for chronic glomerulonephritis in men and women:
Complications: hemorrhagic cystitis, pneumonia, agranulocytosis (pathological changes in the blood, oppression of blood formation).
When side effects have developed, treatment with cytostatics for chronic glomerulonephritis in men and women is canceled.
Nonsteroidal anti-inflammatory drugs
It was believed that Indomethacin, Ibuklin, Ibuprofen can suppress the autoimmune response. NSAIDs are not prescribed by all nephrologists, since drugs from the NSAID group have a toxic effect on the kidneys and often provoke the development of drug nephropathy even without glomerulonephritis.
Anti-coagulants and antiplatelet agents
Contribute to the improvement of the rheological properties of blood. Interfere with the processes of thrombosis in the renal glomeruli and the adhesion of blood vessels. Heparin is most often used in a course of 3 to 10 weeks in individual dosages, which depend on many factors, including coagulogram indicators.
Symptomatic therapy depends on the clinical manifestations of chronic glomerulonephritis and includes:
• Antihypertensive drugs.
• Diuretic drugs.
Some forms of GM are characterized by a persistent increase in blood pressure, therefore, the appointment of antihypertensive drugs from the group of ACE inhibitors is justified:
To activate the flow of fluid in the nephron, diuretics are used:
Sometimes CG occurs on the background of any infections; in this case, antibacterial drugs are prescribed to prevent secondary infection. Protected penicillins are more commonly prescribed, since the drugs are less toxic and effective against beta-hemolytic streptococcus group A.
For penicillin intolerance, cephalosporins antibiotics can be used. The use of antibiotics has been substantiated for the proven association of the development of glomerulonephritis with the infectious process, for example, in a man or a woman, glomerulonephritis after streptococcal angina appeared 14 days later.
The outcome of chronic diffuse glomerulonephritis is always secondary wrinkling of the kidneys and the onset of chronic renal failure.
If chronic kidney disease has led to significant disruptions in the body, programmed hemodialysis is indicated when the creatinine level reaches 440 µmol / L. In this case, the direction of the patient for examination for disability is justified. By itself, the diagnosis of chronic hepatitis, without impaired renal function, does not give the right to disability.
For hypercholesterolemia, statins are prescribed to lower cholesterol.
Есть хорошие отзывы от применения плазмофереза при гломерулонефрите.
Хронический гломерулонефрит у детей
В педиатрии гломерулонефрит у детей занимает второе место после инфекций мочевыводящих путей. Often the disease affects children aged 3 to 9 years.
Boys are faced with immune inflammation in the kidneys 2 times more often than girls. In some cases, the pathology develops 10-14 days later after the childhood infection. As in adult men and women, chronic glomerulonephritis is the outcome of an acute immunological process in the kidneys.
Clinical manifestations, forms, signs are identical.
The treatment is less aggressive due to age.
Chronic glomerulonephritis in children is treated by a nephrologist.
Prevention of exacerbations in chronic glomerulonephritis comes down to timely rehabilitation of inflammation foci, regular monitoring of clinical and laboratory parameters, dieting, avoidance of hypothermia, and timely treatment.
The prognosis of chronic glomerulonephritis, depending on the morphological variant
• GN minimal changes - preservation of renal function after 5 years - 95%,
• Membranous GN - preservation of renal function after 5 years - 50-70%
• FSGS - preservation of renal function after 5 years - 45 -50%
• Mesangioproliferative - preservation of renal function after 5 years - 80%
• Membranous and proliferative - the preservation of renal function after 5 years - 45 - 60%
Life expectancy depends on the clinical variant of the disease and the features of the functional state of the kidneys.
Favorable prognosis for the latent variant (subject to timely treatment), dubious for hematuric and hypertonic variants.
The prognosis is unfavorable for nephrotic and mixed form of glomerulonephritis.
What a disease
Glomerulonephritis is an immune-inflammatory disease of the kidneys, in which the glomeruli of the organ are affected and the small vessels are affected. According to the mechanism of the development of the disease attributed to infectious-allergic pathologies.
Less common is autoimmune glomerulonephritis, in which the cause of the disease is the effect of its own antibodies to the organ.
This disease can occur on its own. There are cases when glomerulonephritis developed on the basis of other inflammatory diseases.
In men, glomerulonephritis develops more often than in women. Children are diagnosed quite often. In adults, pathology is found, as a rule, up to 40 years. The disease is so common that the frequency of such a diagnosis is second only to infectious pathologies of the urinary tract.
Glomerulonephritis is accompanied by disorders in the formation of urine and in cleansing the body. Impulse to the beginning of the pathological process can be a postponed infection.
Different forms of the disease
Glomerulonephritis can occur in both acute and chronic form. Acute glomerulonephritis is well treatable. If the pathology becomes chronic, most patients have renal failure. This is the most unpleasant complication of glomerulonephritis.
There are different opinions about how much they live with glomerulonephritis. However, the prognosis may differ, depending on what methods of treatment the patient uses, how carefully he watches his lifestyle and at what stage of the disease he has discovered the problem.
The classification includes several clinical varieties of glomerulonephritis:
Nephrotic glomerulonephritis is a hematuric form of the disease. Accompanied by persistent hematuria (presence of blood in the urine). On the body can form voluminous edema. The most dangerous consequences are cerebral edema and retinal edema. At best, this leads to disability, but death is also possible.
In hypertensive form there is a steady increase in blood pressure. The composition of urine is almost unchanged.
For the mixed form is characterized by the presence of symptoms of several forms. For example, blood in the urine and hypertension can be observed.
In the latent form of pathology, patients show only weak changes in urine excretion. This is the most common form of chronic glomerulonephritis.
Causes of pathology
In order to cure the disease as soon as possible, it is necessary to eliminate the causes. There are three main factors:
The more risk factors there are, the greater the likelihood of getting sick.
It is possible to diagnose glomerulonephritis soon after infection with such infections:
- beta hemolytic streptococcus group A,
Note! Symptoms of glomerulonephritis develops 3 weeks after the initial infection of the infection.
Insect bites, work in hazardous production, alcohol overdose can lead to toxic damage to the body. Sometimes the body may react negatively to the introduction of serum for vaccination and certain medications.
If the child or adult is overcooled, the kidney nursing vessels narrowed. This led to a deterioration in the blood supply and, as a result, contributed to the development of glomerulonephritis.
Features of the acute form
Symptoms of the acute form of glomerulonephritis include:
- swelling, especially on the face in the morning (seen in the photo),
- oliguria (small amount of urine excreted),
- high blood pressure
- lower back pain on the sides.
Important! If any symptoms occur in a child shortly after transferring scarlet fever or sore throat, an emergency consultation with a doctor is necessary.
Features of the subacute form
Subacute glomerulonephritis is considered the most complex form of the disease. Often put such a diagnosis in adults. Symptoms are scarce, but changes can be seen in the general urine analysis. It is manifested not only by edema and an increase in pressure, but also by a slight increase in body temperature.
Subfebrile condition lasts for several weeks. If first aid is not provided, no medication will help and the patient will receive a kidney transplant.
Features of the chronic form
Chronic diffuse glomerulonephritis develops slowly. For a long time, the symptoms are absent. Because of this, diagnosis is complicated, and it is possible to start treating the disease only in the latter stages. Most often, the pathological process starts after the acute infection.
Against the background of chronic glomerulonephritis, chronic renal failure develops. In this case, home treatment is not possible. If you do not remove the aggravation, the patient’s death occurs.
One of the complications of the chronic form of the disease is uremia. In this condition, a large amount of urea accumulates in the blood. As a result, develop severe damage to the internal organs, especially the brain. From the symptoms can be identified:
- blurred vision
- smell of urine from the mouth,
- dry mouth
- lethargy and low performance.
If you have any complaints, you should consult a doctor, as only a specialist can identify the disease and its appearance in the early stages and find the right prescription.
To prescribe medication, it is necessary to conduct such studies:
- examination of the fundus of the eye in order to detect changes in the structure of retinal vessels,
- urinalysis for red blood cell count and creatinine,
- Ultrasound of the kidneys to determine the size of the organ and the state of its surface,
Kidney biopsy for glomerulonephritis is not always performed, but only if a tumor process is suspected to determine its benignity.
To get rid of the disease, the treatment of folk remedies is not recommended. Some folk methods are applicable only after consultation with the doctor and only along with the main therapy.
Complete clinical recommendations can be given only by the attending physician after the examination. Depending on what caused the pathology and on what stage of development the disease is, can be applied:
- antibiotics ("Amoxicillin"),
- glucocorticoids (drugs containing cortisone, prednisone),
- cytostatics ("Busulfan", "Anastrozole").
May be prescribed drugs that have a suppressive effect on the immune system.
It is mandatory for patients to follow a diet. It is important to reduce the amount of salt, water and protein products consumed. Food in any case should not include meat soups.
During pregnancy, glomerulonephritis can cause complications, so treatment can be given in the hospital. Antibiotic therapy is not always used. The treatment is aimed at eliminating the symptoms and causes of the inflammatory process.
Prevention is in compliance with the regime of sleep and rest, proper nutrition and maintenance of water-salt balance in the body.
If symptoms occur, it is important to immediately consult a doctor. This is the only way to prevent the development of renal failure and to protect the organ from irreversible damage.
How to identify glomerulonephritis
If glomerulonephritis is suspected, the forms of the disease are determined after the diagnosis has been accurately established. Despite the brilliance of the clinical picture, similar symptoms can be detected in other diseases. Therefore, the diagnosis of glomerulonephritis should be comprehensive. The range of activities includes the following:
- survey (if it’s about the child, the doctor receives the necessary information from the parents). Important information - for the first time suspected such a diagnosis or pathology of the kidneys occurred in the past. Next, the doctor finds out whether the relatives have a similar disease, whether the patient has had infectious diseases in the recent past, all this is necessary to suggest the cause of the pathology,
- A medical history is compiled. The doctor finds out when the symptoms appeared, how badly they felt, if the patient took symptomatic medications and how they helped.
- inspection. The doctor assesses the presence of swelling, measures the pressure of the patient, can visually assess the changed color of urine,
- analyzes. If glomerulonephritis is suspected, the diagnosis includes urine analysis for protein and blood, blood analysis for leukocytes and ESR, blood biochemistry for protein and cholesterol, as well as immunoassay for suspected autoimmune cause of the disease,
- hardware diagnostics. An ultrasound scan is performed where an increase in the size of the kidneys and other characteristics of the organ is detected.
Before treating glomerulonephritis, the doctor may refer the patient to a rheumatologist, cardiologist, ophthalmologist, infectious diseases specialist, and other specialists as needed.
Complications of glomerulonephritis
Doctors immediately warn people treated for glomerulonephritis that a neglect of their health can provoke a relapse or the onset of other diseases.
For example, if a woman lived for a long time without caring about her health, then the complications of glomerulonephritis in this case would be serious.
The healthier the body, the less pronounced the effects of kidney disease.
Among the main complications are the following:
- pulmonary edema. The manifestation of this complication of acute glomerulonephritis occurs in patients with hypertension, heart disease,
- renal failure in acute form. Kidneys stop working on the background of post-streptococcal glomerulonephritis,
- eclampsia. In humans, the pressure increases dramatically, epilepsy and convulsions may occur, hypertensive crisis,
- uremia. In this case, acute glomerulonephritis causes complications in the form of serious intoxication of the whole organism,
- the transition of the disease to the chronic form.
Usually, in the diagnosis of acute glomerulonephritis, the prognosis is favorable, but there is simply no reason for panic and a question to the doctor - how many people live with glomerulonephritis. A timely diagnosis and competent medical care will quickly be lifted onto the patient’s feet.