Laboratory and instrumental methods for the diagnosis of glomerulonephritis. Glomerulonephritis: forms, diagnosis, symptoms and treatment. Acute diffuse glomerulonephritis in children and adults

On examination, attention is drawn to the pallor of the skin, swollen face, swollen eyelids, swelling on the body. Due to severe shortness of breath, patients are forced to be in a sitting or half-sitting position. In severe cases, attacks of renal eclampsia may occur. Palpation specifies the prevalence and nature of edema. The apex beat of the heart shifts to the left due to myocardial hypertrophy against the background of arterial hypertension. Percussion can determine the presence of transudate in the pleural cavities and congestion in the lungs. On percussion, the left border of the heart shifts to the left of the mid-clavicular line. During auscultation in the lungs, dry and moist rales are heard if there are congestion in the lungs. When listening to the heart, a weakened I tone and a systolic murmur at the apex are often determined, an accent of the II tone over the aorta.
The ECG revealed signs of left ventricular myocardial overload. Acute glomerulonephritis is characterized by urinary syndrome. If edema occurs, diuresis (oliguria) decreases, the urine of patients contains a large amount of protein and red blood cells. With severe hematuria, urine becomes the color of meat slops. Microscopic examination reveals casts and cells of the renal epithelium in the urine. The nitrogen excretion function of the kidneys is not sharply disturbed. Only in severe cases does the level of residual nitrogen, urea, and creatinine increase.

Diagnosis of any disease includes not only the collection of complaints, anamnesis and clinical examination, but also a wide variety of laboratory tests that allow assessing the general condition of the patient and identifying the leading clinical syndromes. And what tests can tell the doctor about glomerulonephritis, and what examinations need to be done first: let's try to figure it out.

Morphological features of kidney damage in glomerulonephritis

Glomerulonephritis is an acute or chronic immune-inflammatory disease of the renal tissue with a primary lesion of the glomerular apparatus. As the disease progresses, interstitial tissues and renal tubules may be involved in the pathological process. This leads to the development of the following changes:

• increasing the permeability of the wall of the vascular glomerulus for protein and cellular elements;
• the formation of microthrombi that clog the lumen of the supplying arteries;
• slowdown / complete cessation of blood flow in the glomeruli;
• violation of the filtration process in the main functional element of the kidney (nephron);
• death of the nephron with irreversible replacement by its connective tissue;
• a gradual decrease in the volume of filtered blood and the development of progressive renal failure.

All these pathogenetic moments cause the appearance of three main syndromes of the disease (edematous, hypertensive and urinary), as well as a characteristic laboratory picture. To confirm the diagnosis of glomerulonephritis, it is necessary to take blood and urine tests.

Blood test

Blood indicators reflect the general condition of the body and allow us to judge the existing violations of the internal organs. As a rule, laboratory diagnostics in case of suspected glomerulonephritis begins with OAC and BAC, if necessary, these studies can be supplemented by immunological tests.

Clinical Analysis

A general blood test for glomerulonephritis reflects the body's response to pathological changes. It is characterized by the following deviations from the norm:

• a slight acceleration of ESR is a sign of immune inflammation;
• a decrease in hemoglobin is a manifestation of relative anemia caused by an increase in BCC due to a decrease in renal filtration.

The symptoms identified when interpreting the results of the CBC are nonspecific and occur in many diseases. However, a complete blood count helps the doctor make the correct diagnosis as part of a comprehensive examination.

Biochemical analysis

A biochemical blood test, or BAC, is a test that allows you to identify signs of nephrotic syndrome against a background of glomerular inflammation. It is manifested by hypoproteinemia and hypoalbuminemia - a decrease in the concentration of total protein and albumin in the blood. It is this process that leads to the development of oncotic edema in patients with glomerulonephritis.

In addition, using a biochemical blood test, it is possible to diagnose the development of chronic renal failure. It is manifested by an increase in the level of urea and creatinine in the blood.

Immunological study

The autoimmune nature of glomerular inflammation can be confirmed by determining the components of the complement system. An important role in the pathogenesis of glomerulonephritis is played by the C3 component, therefore, at the peak of the disease, its moderate decrease is observed.

Table: Changes in blood tests with glomerulonephritis

Urinalysis

Urine tests are especially demonstrative in case of glomerulonephritis: their indicators have pronounced deviations from the norm. The standard list of diagnostics includes OAM and various tests (Reberg, Nechiporenko, Zimnitsky).

Clinical Analysis

Urinalysis remains the main laboratory method for diagnosing glomerulonephritis. It allows you to identify the patient's urinary syndrome:

• An increase in the relative density of urine associated with the appearance of a large number of cellular elements in it.
• Decreased transparency, turbidity of the fluid secreted by the kidneys.
• Dark colored urine. With an exacerbation of glomerulonephritis, it becomes dirty brown, rusty in color (a shade of "meat slops").
• Macrohematuria and microhematuria - the release of red blood cells associated with an increase in vascular permeability in the renal glomeruli.
• Slight or severe proteinuria is the excretion of protein in the urine.
• Leukocyturia is a nonspecific syndrome, slightly expressed.

Test according to Nechiporenko

Urinalysis according to Nechiporenko allows you to determine the degree of erythrocyturia, proteinuria and cylindruria, which usually correlate with the severity of the disease. Differentiation of glomerulonephritis from other inflammatory diseases of the kidneys allows the combination of excretion of protein and erythrocytes with urine at a low level of leukocyturia.

Zimnitsky test

The study of urine according to Zimnitsky allows you to evaluate the concentration abilities of the kidneys. Since the operation of the tubular apparatus is not impaired in acute glomerulonephritis, there will be no pathological changes in this diagnostic sample. With the progression of sclerotic changes in CGN, patients may experience polyuria (or, conversely, oliguria), nocturia.

Reberg's test

Reberg's test is a diagnostic test that allows you to assess the level of effective blood flow in the kidneys (glomerular filtration). With glomerulonephritis, there is a decrease in creatinine clearance and glomerular filtration rate.

Table: Changes in urine tests with glomerulonephritis

Changes in urine and blood tests are an important diagnostic indicator: they can be used to determine the stage of the inflammatory process, suggest the nature of the course of the disease, and identify leading syndromes. Despite this, the presence of glomerulonephritis in a patient should be confirmed not only by laboratory, but also by clinical and instrumental data. Timely diagnosis and early initiation of therapy can prevent the development of complications, alleviate the patient's well-being and speed up recovery.

21. Topic of the lesson: Acute and chronic glomerulonephritis

21. Topic of the lesson: Acute and chronic glomerulonephritis

1. RELEVANCE OF THE THEME

Knowledge of the topic is necessary for solving professional problems in the diagnosis and treatment of patients with acute and chronic glomerulonephritis. The study of the topic is based on the knowledge of the course of normal anatomy and physiology of the kidneys, pathology of the urinary system, clinical radiology, propaedeutics of internal diseases, clinical pharmacology.

2. PURPOSE OF THE LESSON

Know the etiology, pathogenesis, clinical picture, complications and treatment of acute and chronic glomerulonephritis; be able to collect complaints and anamnesis, conduct a physical and laboratory-instrumental examination of a patient with acute and chronic glomerulonephritis, prescribe therapy.

3. QUESTIONS TO PREPARE FOR THE LESSON

1. Etiology and pathogenesis of acute and chronic glomerulonephritis

that.

2. Clinical manifestations and pathogenesis of the main symptoms of acute and chronic glomerulonephritis.

3. Variants of the course, criteria for chronicization of acute glomerulonephritis, clinical and morphogenetic classification of chronic glomerulonephritis.

4. Treatment of acute and chronic glomerulonephritis.

5. Primary and secondary prevention of acute glomerulone-frit.

4. EQUIPMENT OF THE LESSON

1. Patients with a clinical picture of acute glomerulonephritis and chronic glomerulonephritis: collection of complaints, anamnesis, physical examination, including the use of palpation, percussion and auscultation.

2.Study of the results of laboratory and instrumental examination of a patient with acute and chronic glomerulonephritis: clinical analysis of blood, urine, biochemical and serological blood tests, Reberg's test, urine tests according to Nechiporenko, Zimnitsky, daily proteinuria, ultrasound, dynamic scintigraphy, kidney biopsy.

5. BASELINE TESTS

Choose one correct answer.

1. Glomerulonephritis is an immunoinflammatory disease with the primary involvement of:

A. Klubochkov. B. Kanaltsev.

B.Calyxes.

G. Vas affect. D. Vas effect.

2. The etiological factor of glomerulonephritis can be:

A. Hard physical labor.

B. Strong emotional stress.

B.AG.

D. Stenosis of the renal artery. D. Infection.

3. Nephrotic syndrome is characterized by:

A. Hyperproteinemia. B. Macrohematuria.

B. Arterial hypertension. G. Proteinuria up to 3 g/day.

D. Hyperlipidemia.

4. Acute nephritic syndrome is characterized by:

A. Proteinuria up to 3 g/day.

B. Proteinuria more than 3.5 g/day.

B. Hyperlipidemia.

G. Hypoproteinemia. D. Hyperproteinemia.

5. With glomerulonephritis, edema is characteristic:

A. Calves and feet. B. Loins.

B. Anterior abdominal wall. G. Faces.

D. Shoulder girdle.

6. Select the clinical variant of chronic glomerulonephritis:

A.Latent. B. Fibrous.

B. Capillary.

G. Rapidly progressive. D. Recurrent.

7. The most common etiological cause of acute glomerulonephritis:

A. Hepatitis C virus. B. Hepatitis B virus.

B. Escherichia coli. G. Streptococcus.

D. Staphylococcus.

8. For acute glomerulonephritis the most typical:

A. Nephrotic syndrome. B. Nephritic syndrome.

B. Isolated urinary syndrome. G. HPN.

D. Dyspeptic syndrome.

9. In the analysis of urine in acute glomerulonephritis, the following are found:

A. Glucosuria. B. Oxalates.

B. Urates.

D. Erythrocytes and their casts. D. Leukocytes and their casts.

10.Choose the clinical variant of chronic glomerulonephritis:

A. Stenosing. B. Hematuric.

B. Nephritic. G. Sclerotic. D. Purulent.

11. Specify the glomerular filtration rate at which CRF develops:

A.More than 120ml/min. B. 100-120 ml/min.

B.80-100 ml/min.

D. 60-80 ml/min. D. Less than 60 ml/min.

12. Causes of anemia in chronic azotemia:

A. Vitamin D synthesis is reduced.

B. The synthesis of erythropoietin is reduced.

B. Decreased excretion of electrolytes and water. D. There is platelet dysfunction.

13. Diuretic, which can be taken with glomerulonephritis:

A. Spironolactone. B. Mannitol.

B. Furosemide.

D. Hydrochlorothiazide.

D. Acetazolamide (diacarb*).

14. Target blood pressure in glomerulonephritis:

A. Less than 100/60 mmHg B. Less than 120/70 mm Hg.

B. Less than 125/75 mmHg D. Less than 130/80 mmHg. D. Less than 140/90 mmHg.

15. The means of choice for the treatment of hypertension in chronic glomerulonephritis are:

A. R - Adrenoblockers. B. a - Adrenoblockers.

B. ACE inhibitors. G. Statins.

D. Blockers of slow calcium channels.

16. Select an indicator indicating the activity of jade:

A. Nephrotic syndrome. B. Hyperproteinemia.

B. Proteinuria up to 1 g/day. G. Increase in glucosuria. D. A sharp decrease in blood pressure.

17. Indications for immunosuppressive therapy are as follows:

A. Low creatinine on admission. B. Stenosis of the renal artery.

B.AG.

G. Persistent nephrotic syndrome. D. Macrohematuria.

18. The following are used as immunosuppressive therapy for glomerulonephritis:

A. Antibiotics.

B. Glucocorticoids.

B. Immunomodulators. G. Diuretics.

D. ACE inhibitors.

19. On the 15th day after the onset of streptococcal infection, a patient developed gross hematuria and paraorbital edema. This episode can be seen as:

D. Urinary syndrome.

20. On the 5th day after the onset of streptococcal infection, a patient developed gross hematuria and paraorbital edema. This episode can be seen as:

A. Acute poststreptococcal glomerulonephritis. B. Exacerbation of chronic glomerulonephritis.

B. Rapidly progressive glomerulonephritis. G. Nephrotic syndrome.

D. Urinary syndrome.

6. MAIN QUESTIONS OF THE THEME

6.1. Definition

The term "nephritis" is currently fully consistent with the term "glomerulonephritis" and includes a group of morphologically heterogeneous immunoinflammatory diseases of the kidneys with a primary lesion of the glomeruli, as well as involving the tubules and interstitial (interstitial) tissue.

Glomerulonephritis is considered an independent nosological entity, but can also occur in many systemic diseases, such as systemic lupus erythematosus, hemorrhagic vasculitis, IE, etc.

6.2. Etiology

.Infections: bacterial (streptococcus, staphylococcus, etc.);

lead, mercury, drugs, etc.).

. Exogenous non-infectious antigens, acting with the involvement of immune mechanisms, including the type of atopy.

. endogenous antigens(rare): DNA, neoplastic, uric acid.

6.3 Pathogenesis

The progression of glomerulonephritis after exposure to various triggering factors is determined by fairly stereotypical processes that gradually lead to sclerosis. These include mesangial cell proliferation and mesangial matrix accumulation, as well as damage to the glomerular capillary wall. In the induction of glomerulonephritis, the leading place is given to immune factors of damage, reactions of humoral and / or cellular immunity; in the future, mediators of inflammation and non-immune mechanisms - hemodynamic and metabolic - acquire an important role in the progression of the process. At all stages of development, the persistence of the etiological factor plays a leading role, which, unfortunately, is known only in 10% of patients.

Immune damage is seen in most glomerular kidney diseases. There are two mechanisms of such damage: the action of nephrotoxic antibodies and the deposition of immune complexes.

Two types of nephrotoxic antibodies are involved in the reaction of antibodies against antigens on the glomerular filtration membrane:

Anti-glomerular basement membrane antibodies;

Antibodies against antigens that do not belong to the glomerular basement membrane.

In cases where the body begins to produce IgG against antigenic glycoproteins of the glomerular basement membrane,

refers to "anti-membrane disease". These changes lead to the development of pronounced proliferative glomerulonephritis with hemorrhages and rapidly increasing renal failure.

There are two types of antigens that do not belong to the glomerular basement membrane:

1) internal (own) antigens;

2) external antigens (formed from drugs, plant lectins, aggregated proteins and infectious agents).

The kidneys are one of the pathways through which immune complexes are normally excreted from the body. The glomeruli are subject to the accumulation of immune complexes, as a large amount of blood is filtered through them. Large immune complexes, which are formed in the presence of antibodies with high affinity for the antigen, settle mainly in the mesangium. After the deposition of pathological immune complexes in the basement membrane, the complement system is activated and vasoactive substances are released. These substances - mediators of acute inflammation - are responsible for damage to the basement membrane.

6.4. Classification of glomerulonephritis

There are three parallel and complementary classifications: etiological, immunological and morphological.

Below is a comprehensive classification of glomerulonephritis based on clinical, morphological and immunological characteristics.

Classification of glomerulopathies.

1. Congenital and acquired glomerulopathies.

2. Clinical types of glomerulonephritis:

Spicy;

Chronic (according to Tareev, 1972): latent, hematuric, nephrotic, hypertonic, mixed, CRF;

Rapidly progressive.

3. Primary kidney diseases (histopathological classification according to Serov).

Diffuse proliferative (acute) glomerulonephritis:

Minimal change disease;

Focal segmental glomerulosclerosis;

Membranous glomerulonephritis (nephropathy);

Mesangioproliferative glomerulonephritis: IgA nephropathy;

Membranoproliferative glomerulonephritis;

Semilunar glomerulonephritis;

Fibroplastic glomerulonephritis (diffuse sclerosis).

4. Glomerulonephritis in systemic diseases:

Lupus jade;

IgA nephropathy, Shenlein-Genoch purpura;

Glomerular lesions in systemic infections: post-streptococcal glomerulonephritis, nephropathy in AIDS, nephropathy in hepatitis B and C.

5. Glomerular lesions in vascular diseases:

Nephrosclerosis benign and malignant;

Anti-neutrophil cytoplasmic antibody-associated nephritis (ANCA);

Thrombotic microangiopathy (hemolytic-uremic syndrome).

6. Hereditary nephropathies:

diabetic nephropathy;

Amyloidosis;

The disease of deferred deposits;

Delayed immunoglobulin disease.

7. Other kidney diseases.

6.5 Clinical syndromes

1.Nephritic Syndrome: recurrent painless hematuria, which can vary from gross hematuria to microhematuria, determined only by special studies; oliguria; proteinuria; cylindruria; AG.

2.Nephrotic Syndrome: swelling; proteinuria above 3.5 g/day; hypoalbuminemia; hyperlipidemia.

3.Asymptomatic kidney disease: proteinuria, hematuria.

4.HPN.

The correlation between the histological variants of glomerulonephritis and the clinical picture of the disease is presented in Table. 48.

6.6 Clinical types of glomerulonephritis

The main clinical types of glomerulonephritis are acute, chronic and rapidly progressive.

6.6.1. Acute glomerulonephritis

6.6.1.1. Definition

Acute glomerulonephritis is an acute diffuse immune-mediated inflammation that develops after sensitization by an antigen (usually bacterial or viral) and is manifested by acute nephritic syndrome.

The ratio of men and women is 2/1. Children 5-15 years old are more often ill. In 10% of cases, adults older than 40 years are affected.

6.6.1.2. Etiology

The most common post-streptococcal glomerulonephritis, Bright's disease. Group A p-hemolytic streptococcus is the most nephritogenic, especially strains 12 and 49.

Other bacterial causes of acute post-infectious glomerulonephritis can be diplococci, streptococci, staphylococci, mycobacteria, Salmonella typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, Actinobacilli, Rickettsia rickettsiae, Mycoplasma species, Meningococcus species, Leptospira species.

Among the viruses that can cause acute glomerulonephritis, noted (with the exclusion of streptococcal etiology) cytomegalovirus,

viruses Coxsackie, Epstein-Barr, hepatitis B and C, HIV, Rubella mumps virus.

Systemic diseases accompanied by the development of acute glomerulonephritis include Wegener's granulomatosis, cryoglobulinemia, systemic lupus erythematosus, polyarteritis nodosa, Henoch-Schonlein purpura, Goodpasture's syndrome.

In addition, abscesses of the internal organs, endocarditis, infected shunts, pneumonia, as well as medications, such as sulfonamides, penicillin, can lead to the development of glomerulonephritis.

6.6.1.3. Pathophysiology

Glomerular damage results from the deposition or formation of immune complexes, complement activation, and inflammatory mediators. Macroscopically, the kidneys can be enlarged by 50%. Under a light microscope, changes in the glomeruli are diffuse generalized, with proliferation of mesangial and epithelial cells. Most often, streptococcus acts as a trigger for the formation of immune complexes. An increase in antibody titers against antistreptolysin-O, antihyaluronidase, and streptokinase also indicates a recent streptococcal infection. Morphological examination most often reveals IgA nephropathy.

6.6.1.4. Clinical picture

The latent period can last up to 3 weeks. If a disease occurs after pharyngitis, the latent period can last up to 2 weeks, after pyoderma - up to 2-4 weeks. The onset of symptoms within the first 4 days of a streptococcal infection is indicative of pre-existing kidney disease.

Acute glomerulonephritis is characterized by acute nephritic syndrome, which includes three main clinical symptoms:

swelling;

macrohematuria; .AG.

Approximately 95% of patients have at least two of the three symptoms.

Edema is observed in 80-90% of patients. Facial edema usually develops, especially periorbital, but may be systemic, accompanied by a decrease in the amount of dark, tea-colored or rusty urine. Severe oliguria indicates the development of rapidly progressive glomerulonephritis.

AH also occurs in 80% of patients.

Nonspecific symptoms are weakness, malaise, lethargy, fever, abdominal pain. Other symptoms may be pharyngitis, respiratory infection, scarlet fever, weight gain, back pain, anorexia, pallor, impetigo. If acute glomerulonephritis develops as part of a systemic disease, then the symptoms of this disease are revealed: for example, rash, arthritis, arthralgia, etc.

With poststreptococcal glomerulonephritis, the oligoanuric phase lasts 3-5 days, after which diuresis increases, and the relative density of urine falls. Urine takes on the color of meat slops. In cases of microhematuria, the color of the urine may not change.

6.6.1.5. Laboratory methods of examination

In the general blood test, normochromic normocytic anemia is noted due to an increase in circulating blood volume. Creatinine and urea reflect the degree of damage to kidney tissue. In 5% of patients, nephrotic syndrome develops, accompanied by hypoproteinemia and hyperlipidemia. The concentration of the third complement fraction increases. With streptococcal etiology of glomerulonephritis, the titer of antistrepto-lysin-O increases in the first 3 weeks, reaching a maximum after 3-5 weeks and returning to normal after six months. In addition, it is necessary to examine the patient's blood for antibodies to DNA, cryoglobulins, hepatitis B and C viruses, HIV, anti-neutrophil cytoplasmic antibodies (ANCA), antibodies to the basement membrane of the renal glomeruli. If infective endocarditis is suspected, blood cultures and echocardiography are required.

Analysis of urine. Dark urine due to erythrocyte hemolysis, specific gravity over 1020, proteinuria, acidosis. At the microscopy of the sediment at the beginning of the disease, fresh erythrocytes predominate, in the future, mainly leached ones are isolated. Hyaline and cellular casts are almost always found. Proteinuria (albuminuria) is usually moderate (up to 3-6 g / l), may disappear in the first

2-3 months, or slowly decline over 6 months. In some patients, proteinuria may recur intermittently for another 1-2 years. Microhematuria disappears after six months. Very rarely, it can persist for 1-3 years. You can think about the transition to a chronic form if proteinuria and hematuria together persist for more than 12 months.

On ultrasound, the kidneys are of normal size or slightly enlarged with increased echogenicity.

Chest x-rays usually show pulmonary venous congestion, and occasionally enlarged heart shadow.

Renal biopsy is indicated to clarify the diagnosis, especially in primary kidney disease. Patients with a history of kidney disease, including those of relatives, and in the case of atypical clinical and laboratory findings, including massive proteinuria, nephrotic syndrome, and a rapid increase in creatinine, are considered candidates for biopsy.

After 2-3 weeks, edema disappears, blood pressure returns to normal, and a polyuric crisis occurs. Usually recovery occurs in 2-2.5 months.

6.6.1.5. Treatment

By the time a patient with acute glomerulonephritis develops symptoms, the damage to the glomeruli has already taken place and the healing process has already begun. Therefore, it is too late to act on the cause of the disease. Symptomatic therapy is carried out, aimed at preventing possible complications.

Hospitalization is indicated if there is significant hypertension, massive proteinuria, or a combination of oliguria, generalized pulmonary edema, and elevated serum creatinine or potassium.

In the acute phase, when edema and hypertension are observed, a diet is indicated with salt restriction to 2 g per day and liquid to 1 liter per day (diuresis volume - 400 ml). Longer restrictions are not required.

Limitation of physical activity is indicated in the acute period of the disease, especially in the presence of hypertension. Bed rest can reduce the degree and duration of gross hematuria. Longer bed rest does not affect the course and prognosis of the disease.

With significant edema and / or severe hypertension, loop diuretics are indicated. If hypertension cannot be controlled, then

slow calcium channel blockers or ACE inhibitors. For mild or moderate hypertension, bed rest and fluid restriction are most effective.

The swelling is usually minor and causes little discomfort. It is enough to limit fluid intake. With significant edema, furosemide is indicated. Osmotic diuretics are contraindicated as they may increase blood volume. Potassium-sparing diuretics are contraindicated due to the risk of hyperkalemia.

If a connection with streptococcal infection is proven, titers of antistreptococcal antibodies are elevated and sowing from the pharynx is positive, antibiotic treatment is indicated for 8-12 days. It is necessary to examine family members and the immediate environment of the patient for infection with nephritogenic streptococcus and treat those infected. This event will prevent the spread of nephritogenic strains.

For other infections, appropriate therapy is indicated.

Glucocorticoids and immunosuppressants are indicated for severe proteinuria and a rapid decrease in glomerular filtration rate, which occurs with a non-infectious nature of the disease, in particular, with diffuse connective tissue diseases (systemic lupus erythematosus, vasculitis).

In patients with low physical activity, with prolonged bed rest, heparin and antiaggregants are indicated to prevent venous thrombosis.

Forecast depends on histological examination. An excellent prognosis is in minimal change disease and focal segmental glomerulosclerosis. With mesangial and membranous variants of glomerulonephritis, 25% of patients develop chronic renal failure, with mesangiocapillary - in 70%.

Medical examination. Treatment and observation by a nephrologist. Control of blood pressure, urinalysis and blood creatinine.

Prevention. Streptococcal infection should be aggressively treated.

In most epidemic cases, there is a complete recovery (100%). Sporadic cases in adults in 30% progress to chronic glomerulonephritis.

With non-streptococcal etiology of the disease, the outcome depends on the etiology of glomerulonephritis and may be different. When bacterial

In endocarditis, kidney function returns after successful antibiotic treatment. With AIDS, the process leads to the development of CRF.

6.6.2. Chronic glomerulonephritis

6.6.2.1. Definition

Chronic glomerulonephritis is a chronic immune-mediated inflammation of the glomeruli of the kidneys with persistent changes in urine tests (proteinuria and/or hematuria). It is characterized by irreversible and progressive hyalinization of the glomeruli, fibrosis of the tubulointerstitial apparatus, interstitial fibrosis, leads to a decrease in the glomerular filtration rate and chronic renal failure. Pathological examination reveals membranous glomerulonephritis in 50% of cases, proliferative glomerulonephritis in 20%, and IgA nephropathy (Berger's disease) in 30% with unknown etiology. The course of the disease is a slowly progressive decline in kidney function, usually over 20 years.

6.6.2.2. Pathophysiology

Reducing the mass of nephrons reduces the glomerular filtration rate. Compensatory hypertrophy and hyperfiltration of the remaining nephrons occur, and intraglomerular hypertension is triggered. These changes lead to further progression of glomerulosclerosis and loss of nephron mass.

In the initial stages of the disease, a significant decrease in glomerular filtration rate may lead to a slight increase in serum creatinine. Azotemia develops when the glomerular filtration rate decreases to less than 60-70 ml/min. Along with an increase in urea and creatinine levels with a decrease in glomerular filtration rate:

The synthesis of erythropoietin decreases, which leads to anemia;

The synthesis of vitamin D decreases, which leads to hypocalcemia, hyperparathyroidism, hyperphosphatemia and renal osteodystrophy;

The excretion of acids, potassium, salt and water decreases, which leads to acidosis, hyperkalemia, hypertension and edema;

Platelet dysfunction is observed, which leads to increased bleeding.

Uremic toxins affect all organs and systems. Uremia develops at a glomerular filtration rate of about 10 ml/min.

Clinical symptoms of uremia: weakness, fatigue, loss of appetite, weight loss, itching, nausea and vomiting in the morning, taste disturbance, insomnia at night and drowsiness during the day, peripheral neuropathy, seizures, tremors, edema and hypertension, shortness of breath or chest pain cell, depending on the position of the body, suggest the presence of stagnation or pericarditis. Leg cramps may indicate an electrolyte imbalance.

6.6.2.3. Clinical picture

On examination: Hypertension, jugular venous distention (in severe heart failure), crackles in the lungs (in pulmonary edema), pericardial friction rub in pericarditis, epigastric tenderness, or blood in the stool suggest uremic gastritis or enteropathy.

6.6.2.4. Laboratory diagnostics

Urinalysis: the presence of altered erythrocytes, erythrocyte casts, albumin, low specific gravity. Proteinuria more than 1 g/day is considered a predictor of the rapid development of CRF.

Blood test: anemia as a result of a violation of the synthesis of erythropoietin, an increase in the levels of urea and creatinine, retention of potassium, fluid and acids leads to hyperkalemia, hyponatremia, and a decrease in bicarbonate levels. Violation of the synthesis of vitamin D 3 leads to hypocalcemia, hyperphosphatemia, increased levels of parathyroid hormone. The low level of albumin is due to the diet or increased excretion in nephrotic syndrome.

6.6.2.5. Instrumental research methods

Ultrasound: a decrease in the size of the kidneys indicates the irreversibility of the process.

Morphological examination reveals the following variants.

.Minimal glomerular change disease It is more common in children, but it also occurs in adults. The expressed nephrotic syndrome with massive hypostases is characteristic; erythrocyturia and hypertension are rare. It is with this form that glucocorticoids are most effective.

cocorticoids, which sometimes allow stopping edema in 1 week. The prognosis is quite favorable, CRF rarely develops.

.Focal segmental glomerulosclerosis: 80% of patients develop chronic renal failure within 10 years. The course is progressive, the prognosis is serious, it is one of the most unfavorable morphological variants, rarely responding to active immunosuppressive therapy.

.Membranous glomerulonephritis(membranous nephropathy). Within 10 years, chronic renal failure develops only in 20-30% of patients. In a third of patients, it is possible to establish a connection with known antigens: hepatitis B or E viruses, tumor, drugs (captopril, gold, lithium, mercury, penicillamide). In addition, the reasons for the development of this form of chronic glomerulonephritis can be systemic diseases of the connective tissue, infectious agents.

.Membranoproliferative glomerulonephritis- the most common morphological type of glomerulonephritis. There is a familial form that is inherited in an autosomal dominant manner. In addition, this variant of chronic glomerulonephritis can occur with systemic lupus erythematosus, Sjogren's syndrome, rheumatoid arthritis, hereditary complement deficiency, scleroderma, chronic infections: hepatitis B and C, cryoglobulinemia, malaria, schistosomiasis, mycoplasmosis, endocarditis, multiple abscesses of internal organs; with cirrhosis of the liver, hemolytic-uremic syndrome, thrombotic thrombocytopenic purpura, antiphospholipid syndrome, radiation nephritis, etc. Within 10 years, 40% of patients develop chronic renal failure.

. IgA nephritis or Berger's disease- a separate variant of membrane-proliferative glomerulonephritis with deposition of immunoglobulin A in the glomeruli. The disease develops at a young age, more often in men, the leading symptom is hematuria. In 50% of patients, recurrent gross hematuria occurs in the first days or even hours of febrile respiratory diseases. The prognosis is favorable, but worsens significantly with the addition of nephrotic syndrome and / or hypertension. Within 10 years, CRF develops in 10% of patients.

. Mesangiocapillary glomerulonephritis may be associated with hepatitis C virus, as well as with cryoglobulinemia. This is unfavorable

ny variant of glomerulonephritis with a progressive course and the development of CRF, poorly responding to therapy.

Renal biopsy is not indicated for reduced kidney size. A small number of patients who have experienced a sharp exacerbation of the disease need a biopsy. In the early stages, it is still possible to evaluate the primary process. In the later stages, hyalinosis and glomerular degeneration, tubular atrophy, significant interstitial fibrosis, and arteriolosclerosis are detected.

Depending on the clinical manifestations and course, the following clinical variants of chronic glomerulonephritis are distinguished (according to Tareev, 1972):

Latent;

Hematuric;

Nephrotic;

Hypertensive;

Mixed; .HPN.

Latent glomerulonephritis- the most common form of chronic glomerulonephritis, manifested only by changes in urine (proteinuria up to 2-3 g / day, slight erythrocyturia), sometimes AH I degree. The course is usually slowly progressive.

Hypertensive glomerulonephritis- this is a latent glomerulonephritis with more pronounced hypertension and minimal urinary syndrome.

Hematuric glomerulonephritis manifested by constant hematuria, often with episodes of gross hematuria, proteinuria does not exceed 1 g / day, the course is quite favorable.

Nephrotic glomerulonephritis characterized primarily by nephrotic syndrome, usually relapsing in nature. In the absence of erythrocyturia and hypertension (which is commonly seen in children), the prognosis is relatively good. In adults, isolated nephrotic syndrome is rare, the combination with erythrocyturia and / or hypertension significantly worsens the prognosis; when combined with hypertension, they speak of mixed glomerulonephritis.

6.6.2.6. Treatment

Progression to CKD can be slowed by various interventions, including aggressive control of diabetes, hypertension, proteinuria, dietary protein, phosphate, lipid control.

blood. Specific therapy is indicated for systemic diseases (eg, systemic lupus erythematosus). Anemia and renal osteodystrophy should be aggressively controlled. Target BP less than 130/80 mm Hg.

ACE inhibitors are considered the treatment of choice for hypertension. They have a renoprotective effect, reduce proteinuria by reducing the tone of the descending arteriole and reducing intraglomerular pressure. An alternative may be the use of angiotensin receptor blockers. Perhaps the combined use of drugs of these groups.

Furosemide has been shown to control edema and blood pressure. This drug may reduce hyperkalemia caused by ACE inhibitors. To achieve the target blood pressure, other antihypertensive agents (slow calcium channel blockers, β-blockers) may also be prescribed.

Correction of renal osteodystrophy is carried out by prescribing vitamin D.

Before prescribing erythropoietin drugs, other possible causes of anemia should be excluded.

All potentially nephrotoxic drugs should be avoided. NSAIDs, aminoglycosides, intravenous contrast agents can lead to the development of acute renal failure.

6.6.3. Rapidly progressive glomerulonephritis

In addition to acute and chronic glomerulonephritis, there are rapidly progressive (subacute) glomerulonephritis, characterized by a decrease in glomerular filtration rate of about 50% in a short period - from several days to 3 months - and rapidly progressive renal failure without episodes of latent course or remission. Microscopy reveals fibrinoid necrosis, 50% of the glomeruli show "crescents". These patients have anti-basement membrane antibodies. Rapidly progressive glomerulonephritis can develop after infections, contact with organic solvents, but more often it is caused by systemic vasculitis and systemic lupus erythematosus. In the mid 70s. 20th century a group of patients with rapidly progressive glomerulonephritis was identified, in which deposits in the glomeruli were not found. 80% of them had circulating A1HSA.

6.6.3.1. Classification

1. Diseases associated with antibodies against the basement membrane of the renal glomeruli: Goodpasture's syndrome and disease with antibodies against the basement glomerular membrane (involving only the kidneys).

2. Diseases associated with immune complexes: post-infectious, post-streptococcal, visceral abscesses, systemic lupus erythematosus, Henoch-Schonlein purpura, mixed cryoglobulinemia, IgA nephropathy, membranoproliferative glomerulonephritis.

3. Diseases associated with A1HSA: Wegener's granulomatosis, microscopic polyangiitis, necrotizing glomerulonephritis with crescents, Churg-Strauss syndrome. The most common cause of death in these patients is massive pulmonary hemorrhage. If immunosuppressive therapy is started, they are more likely to die from infectious complications.

Men and women of all ages are equally affected.

6.6.3.2. Clinical picture

Some patients come with manifestations of kidney disease: anemia, hematuria, edema, oliguria, uremia. Most often, nephritic syndrome develops (rarely nephrotic), there is a rapid progression to CRF. Symptoms of weakness, nausea, vomiting usually dominate the clinical picture.

In other patients, the signs and symptoms of the underlying disease come first.

In still others, the prodromal period is characterized by flu-like symptoms: malaise, fever, arthralgia, myalgia, anorexia, and weight loss. This is followed by abdominal pain, painful skin nodules or ulcerations, migratory polyarthropathy. AG is not typical. Further, vasculitis progresses with the defeat of all organs and systems.

In 15% of patients, the onset of the disease may be asymptomatic.

Symptoms of CRF develop over several weeks or months: weakness, fatigue, nausea, vomiting, anorexia, malignant hypertension, retinopathy with retinal detachment, joint and abdominal pain, hemoptysis in Goodpasture's syndrome, oliguria, proteinuria, hematuria.

6.6.3.3. Examination methods

In terms of examination, in addition to routine tests, it is necessary to identify diseases that led to the development of rapidly progressive glomerulonephritis, as well as the study of A1HSA and kidney biopsy.

6.6.3.4. Treatment

The start of therapy should not be delayed until the results of the biopsy are available.

Most forms of rapidly progressive glomerulonephritis are more or less progressive diseases; the most reliable way to stop progression is to identify and eliminate the etiological factor. If it is impossible to establish the etiology, efforts should be aimed at suppressing the activity and stopping the exacerbation, which makes it possible to stabilize the course of the disease.

The prognosis is very serious, only massive immunosuppressive therapy can stop the progression. Glucocorticoids and cytostatics are used to suppress activity.

Glucocorticoids, which have immunosuppressive and anti-inflammatory effects, have been the main means of pathogenetic therapy for nephritis for several decades. Renal failure requiring dialysis is not considered a contraindication to initiating therapy.

Cytostatics in the treatment of nephritis are used somewhat less frequently due to the greater severity of side effects. As a rule, alkylating compounds are used - cyclophosphamide and chlorambucil; the antimetabolite azathioprine is less effective, although less toxic.

The presence of the following complications remains an indication for urgent dialysis: metabolic acidosis, pulmonary edema, pericarditis, uremic encephalopathy, uremic gastrointestinal bleeding, uremic neuropathy, severe anemia and hypocalcemia, hyperkalemia.

6.7. Prevention

There is no specific prophylaxis for most cases of glomerulonephritis. In some cases, it is likely that stopping or limiting contact with organic solvents, mercury, and non-steroidal anti-inflammatory analgesics can help.

6.8. Clinical examination

A patient with suspected kidney disease should be seen by a nephrologist. Early referral to a nephrologist improves prognosis and outcome.

7. CURATION OF PATIENTS

1. Under the supervision of a teacher, collect complaints, anamnesis and examine a patient with a clinical picture of acute and chronic glomerulonephritis, you should pay attention to:

Non-specific nature of complaints: weakness, decreased ability to work, dyspeptic complaints, etc.;

Risk factors for nephrological pathology: severe hypothermia, especially in conditions of high humidity, infectious diseases, allergic reactions, intoxication, occupational hazards, etc.;

Characteristic symptoms: pallor with an icteric tint and dryness of the skin, rarely erythema, swelling of the face, limbs, rarely ascites and anasarca, urinary disorders with a decrease in the amount of urine (oliguria, anuria), increased urination, especially at night, and a change in transparency and urine color, fever, subfebrile condition, shortness of breath, palpitations, hypertension.

2. Development of methods of physical examination of patients: palpation, percussion, auscultation (including renal arteries).

3. Drawing up a plan for examining a nephrological patient.

4. Evaluation of the results of laboratory and instrumental examination of a patient with acute and chronic glomerulonephritis with the determination of the leading nephrological syndrome: nephritic, nephrotic, urinary, hypertonic, tubular disorders (tubulopathy syndrome), acute or chronic renal failure.

5. Discussion of the basic principles of treatment of the examined patient.

8. CLINICAL ANALYSIS OF THE PATIENT

Clinical analysis is carried out by a teacher or students under the direct supervision of a teacher.

Tasks of clinical analysis.

Demonstration of the methodology for questioning and examining patients with acute and chronic glomerulonephritis.

Control of the skills of examination and questioning by students of patients with acute and chronic glomerulonephritis.

Demonstration of a method for diagnosing acute and chronic glomerulonephritis based on the data of a survey, examination and examination of a patient.

Demonstration of the method of drawing up a plan of examination and treatment.

During the lesson, the most typical and / or complex cases of acute and chronic glomerulonephritis from a diagnostic and / or therapeutic point of view are analyzed. At the conclusion of the clinical review, a structured final or preliminary diagnosis should be formulated and a plan for the examination and treatment of the patient should be drawn up. The results of the work are recorded in the curation diary.

9. SITUATIONAL TASKS

Clinical challenge? one

Patient D., 32 years old, turned to the local doctor with complaints of general malaise, feeling of weakness, decreased efficiency, swelling of the eyelids, face, dull, aching, prolonged pain of low intensity in the lumbar region, change in the color of urine (the color of "meat slops") .

The patient suffered a sore throat and two weeks after it began to notice a decrease in efficiency, a change in the color of urine, swelling of the eyelids. Sick for 2 days.

Past diseases: childhood infections, tonsillitis, acute respiratory viral infections, pneumonia. The patient works as a controller, he does not notice any occupational hazards. Bad habits are denied. Family history: mother has hypertension, father has gastric ulcer, daughter is healthy. Allergological anamnesis is not burdened.

On examination: a state of moderate severity. Body temperature 36.8 °C. The face is pale, puffy, the eyelids are swollen, the eyes are narrowed. The skin and mucous membranes are pale, clean, moist. Respiratory rate - 20 per minute. On auscultation of the lungs: hard breathing.

The heart sounds are muffled, there are no noises, the rhythm is correct, 78 beats per minute. BP - 130/80 mm Hg.

General blood test: hemoglobin - 120 g/l, erythrocytes - 4.1 x 10 9 /l. Color indicator - 0.9, leukocytes - 6.8x 10 9 /l, segmented - 76%, stab - 1%, eosinophils - 2%, monocytes - 2%, lymphocytes - 15%. ESR - 25 mm/h.

Urinalysis: relative density - 1018, protein - 1.066 g/l, erythrocytes - 10-12 in the field of view, leukocytes - 2-4 in the field of view.

Urinalysis according to Nechiporenko: erythrocytes - 6000 in 1 ml, leukocytes - 3000 in 1 ml, no cylinders were found. Daily proteinuria - 1.8 g.

Biochemical blood test: total protein - 70 g/l, albumin - 33 g/l, urea - 7.9 mmol/l, creatinine - 102 µmol/l, potassium - 4 mmol/l.

Bacteriological examination of a throat swab: no pathological microflora was detected.

1. What symptoms and syndromes are determined in the patient?

4.Prescribe a treatment.

Clinical challenge? 2

In patient S., 47 years old, during a dispensary examination, an increase in blood pressure up to 200/110 mm Hg was revealed. With a more thorough questioning, it was possible to establish that the patient has been worried about headaches, dizziness, flies before his eyes for 4-5 years. Deterioration in the last six months. Due to busyness, I did not go to the doctor. Continued to work.

Past diseases: childhood infections, SARS, tonsillitis, appendectomy 10 years ago. The patient works as an economist, he does not notice any professional hazards. Bad habits are denied. Family history: mother is healthy, father has gastric ulcer, son is healthy. Allergological anamnesis is not burdened.

On examination: the condition is relatively satisfactory. Body temperature 36.5 °C. Skin and mucous membranes of normal color, clean, moist. There are no edema.

Respiratory rate - 19 per minute. On auscultation of the lungs: vesicular breathing, no wheezing.

The left border of the relative dullness of the heart is 2 cm outward from the midclavicular line in the fifth intercostal space. Auscultation of the heart: clear heart sounds, accent II tone over the aorta, no noise. The rhythm of the heart is correct. Pulse - 68 per minute, satisfactory filling, tense. BP - 200/110 mm Hg.

The abdomen is soft and painless. Liver at the edge of the costal arch.

The area of ​​the kidneys is not changed, the kidneys are not palpated, the symptom of effleurage is negative on both sides.

Clinical blood test: hemoglobin - 118 g / l, erythrocytes - 4.2x 10 9 / l, leukocytes - 5.8x 10 9 / l, stab - 4%, segmented - 56%, lymphocytes - 33%, monocytes - 7%. ESR - 16 m m / h.

Urinalysis: relative density - 1016, protein - 4.3 g/l. leukocytes - 1-2 in the field of view, erythrocytes - 6-8 in the field of view. Daily proteinuria - 2.2 g.

Zimnitsky's test: daytime diuresis - 1060 ml, nighttime - 1400 ml, fluctuations in the relative density of urine from 1006 to 1018.

Reberg's test: glomerular filtration - 60 ml / min, tubular reabsorption - 98%.

Biochemical blood test: creatinine - 138 µmol/l.

2. Formulate a clinical diagnosis.

3. What additional investigations should be performed for the patient to confirm the diagnosis?

4.Prescribe a treatment.

Clinical challenge? 3

Patient M., 35 years old, turned to the local doctor with complaints of general malaise, weakness, fatigue, decreased performance, nausea, vomiting, lack of appetite, swelling of the eyelids, face, dull, aching, prolonged pain of low intensity in the lumbar region, discoloration urine (“meat slops”), a decrease in the amount of urine, swelling of the face, legs and feet, an almost constant headache in the occipital region, flies before the eyes.

The patient had a sore throat and two weeks after suffering a sore throat began to notice a decrease in efficiency, a change in the color of urine, swelling of the eyelids. Sick for a week.

Past diseases: childhood infections, tonsillitis, SARS. The patient works as an official, does not note any occupational hazards. Bad habits are denied. Family history: parents are healthy, daughter is healthy. Allergological anamnesis is not burdened.

On examination: a serious condition. Body temperature 37.8 °C. The face is pale, puffy, the eyelids are swollen, the eyes are narrowed, the legs and feet are swollen. The skin and mucous membranes are pale, clean, moist. Respiratory rate - 22 per minute. On auscultation of the lungs: hard breathing.

Heart sounds are muffled, there are no noises, the heart rhythm is correct. Heart rate - 78 per minute. BP - 200/120 mm Hg. Art.

The abdomen is soft and painless. The lower edge of the liver is palpable at the edge of the costal arch, painless.

The area of ​​the kidneys is not changed, the kidneys are not palpable, the symptom of effleurage is weakly positive on both sides.

Complete blood count: hemoglobin - 102 g / l, erythrocytes - 3.1x 10 9 / l, leukocytes - 7.6x 10 9 / l, segmented - 70%, rod-nuclear - 2%, eosinophils - 2%, monocytes - 4%, lymphocytes -

22%. ESR - 32 mm/h.

Urinalysis: relative density - 1018, protein - 2.066 g/l, erythrocytes - 10-12 per field of view, leukocytes - 2-3 per field of view.

Urinalysis according to Nechiporenko: erythrocytes - 6000 in 1 ml, leukocytes - 3000 in 1 ml, no cylinders were found. Daily proteinuria - 2.8 g.

The glomerular filtration rate is 50 ml/min, tubular reabsorption is 80%.

Biochemical blood test: total protein - 68 g/l, albumin - 30 g/l, cholesterol - 5.2 mmol/l, urea - 10.9 mmol/l, creatinine - 402 µmol/l, potassium - 4 mmol / l.

1. What symptoms and syndromes are observed in the patient?

2. Formulate a clinical diagnosis.

3. What additional investigations should be performed for the patient to confirm the diagnosis?

4.Prescribe a treatment.

10. STANDARDS OF ANSWERS

10.1. Answers to test tasks of the initial level

1.A.

2.D.

3.D.

4.A.

5.G.

6.A.

7.G.

8.B.

9.G.

10.B.

11.G.

12.B.

13.B.

14.G.

15.B.

16.A.

17.G.

18.B.

19.A.

20.B.

10.2. Answers to situational tasks

Clinical challenge? one

1. A patient has nephritic syndrome: macrohematuria, proteinuria 1.8 g/day.

2. Diagnosis: acute post-streptococcal glomerulonephritis with nephritic syndrome.

3. Ultrasound of the kidneys, kidney scintigraphy.

4. Treatment.

Bed rest.

ACE inhibitor with nephroprotective purpose.

Clinical challenge? 2

1. The patient has a urinary syndrome: proteinuria 2.2 g/day, hematuria, AH - 200/110 mm Hg, CRF: decrease in glomerular filtration rate to 60 ml/min, increase in serum creatinine to 138 µmol/l.

2. Chronic glomerulonephritis, hypertonic form. HPN.

3. Additional studies: fundus examination, ECG, echocardiography, renal ultrasound, kidney scintigraphy.

4. At this stage, symptomatic therapy is carried out.

Table? 7 (restriction of salt consumption to 3-5 g.

Antihypertensive therapy: ACE inhibitors, slow calcium channel blockers, β-blockers, angiotensin receptor antagonists.

During therapy, it is necessary to reduce the pressure to a level of less than 130/80 mm Hg.

Clinical challenge? 3

1. The patient has a nephritic syndrome: gross hematuria, proteinuria 2.8 g/day, arterial hypertension up to 200/120 mm Hg; CRF: an increase in urea - 10.9 mmol / l, creatinine - 402 μmol / l, a decrease in glomerular filtration to 50 ml / min and tubular reabsorption up to 80%, anemia - 102 g / l,

2. Diagnosis: post-streptococcal glomerulonephritis with nephritic syndrome, rapidly progressive. CRF, mild anemia.

3. Kidney ultrasound, kidney scintigraphy, kidney biopsy, fundus examination, blood test for serum iron, total iron-binding capacity of blood serum, ferritin, erythropoietin.

4. Treatment.

Table? 7. Reducing the intake of fluids, salt, protein foods.

Bed rest.

Diuresis control (accounting for drunk and excreted fluid).

Furosemide to reduce edema and lower blood pressure.

Nephroprotective therapy: ACE inhibitor and angiotensin receptor blocker (and to lower blood pressure), heparin.

Blockers of slow calcium channels, p-blockers to reduce blood pressure.

Erythropoietin in the exclusion of iron deficiency.

Immunosuppressive therapy: glucocorticoids, cytostatics.

Internal diseases: a guide to practice. classes in faculty therapy: textbook. allowance A. A. Abramov; ed. Professor V. I. Podzolkov. - 2010. - 640 p.: ill.

Glomerulonephritis and pregnancy - is there a danger to the woman and the fetus? A serious pathological deviation in the functioning of the filtration apparatus of the kidneys is glomerulonephritis. Pregnancy, as a special condition of a woman's body, often increases the risk of this pathology. This is primarily due to weakened immunity in pregnant women and their vulnerability to infections. The hormone progesterone, which is actively produced to preserve the fetus, reduces the elasticity of the tissues of the ureters, which leads to disruption of urodynamics and stagnation of urine in the pyelocaliceal complex of the kidneys. In addition, the uterus with a growing fetus puts pressure on the organs of the woman's urinary system, which can also provoke congestion in the urinary tract, and cause coccal infection to enter the body. It is also natural during pregnancy that the kidneys of the expectant mother work with an increased load, cleansing not only the mother's body, but also the amniotic fluid.

1. Causes of glomerulonephritis
2. Possible complications of glomerulonephritis
3. Symptoms of glomerulonephritis
4. Diagnosis and treatment of glomerulonephritis
5. Prevention of glomerulonephritis

Causes of glomerulonephritis

Glomerulonephritis is an autoimmune disease that affects the renal glomeruli responsible for the blood filtering process, and it occurs due to an acute immune response of the human body to a streptococcal infection. The formed immune complexes “antigen-antibody” settle in the renal glomeruli and, mistaking glomerular cells for foreign proteins, begin to destroy them in case of any infection entering the body. Very often glomerulonephritis is preceded by angina.

What can become a "push" for the occurrence of glomerunefrit in pregnant women:

Under the influence of these factors, acute glomerulonephritis of pregnant women may occur or an exacerbation of a chronic one may occur.

Possible complications of glomerulonephritis

Glomerulonephritis during pregnancy has an adverse effect on its course and the development of the fetus.

With glomerulonephritis, the following complications may occur:

1. Preeclampsia, pereklamsia, eclampsia, nephropathy.
2. Acute renal failure.
3. Heart failure.
4. Anemia.
5. Arterial hypertension.
6. Visual impairment.
7. Hemorrhages.

Pathological conditions of the mother with glomerulonephritis lead to premature detachment of the placenta, oxygen starvation of the fetus and delays in its development, and also cause severe congenital anomalies, including the organs of the genitourinary system.

The risk of an adverse pregnancy outcome is assessed in three degrees:

1. The first is that the risk is minimal and no more than twenty percent of women are exposed to it.
2. The second is expressive. There is a real danger of retardation in the development of the fetus, its intrauterine death or premature birth.
3. The third is the maximum degree of risk. There is a real danger of the death of a woman and a fetus during childbirth, a high risk of intrauterine death of a child and the birth of a baby with severe anomalies.

Symptoms of glomerulonephritis

With glomerulonephritis, symptoms and treatment depend on the form and severity of the disease. Signs of pathology are very pronounced in the acute form of the disease and less noticeable in the chronic form. With a latent course of glomerulonephritis, the symptoms are very mild, but even in this case, a woman needs to be monitored in a hospital.

What signs indicate a developing pathology:

1. There are pulling pains in the lower back.
2. The face is swollen. Fluid accumulates in the subcutaneous fat and pleural region.
3. Severe headaches are difficult to relieve with painkillers.
4. High body temperature is one of the signs of acute glomerulonephritis.
5. Violation of urination (reduction of daily diuresis) or its complete absence.
6. Blood impurities in the urine. Urine has the color of "meat slops."
7. High blood pressure.
8. Signs of intoxication are nausea and vomiting.

In addition, the woman experiences weakness, dizziness.

The chronic course of the disease depends on the form of pathology:

1. Latent. Symptoms are mild, but there are minor deviations in urine tests (protein is detected).
2. Nephrotic. Pronounced swelling.
3. Hypertensive. Persistent high blood pressure, but no changes in the urine.
4. Terminal. There are signs of kidney failure.

Diagnosis and treatment of glomerulonephritis

Before prescribing treatment for the expectant mother, the doctor conducts the necessary diagnostics, which includes:

• general urine analysis - for the content of protein, blood cells (leukocytes, erythrocytes) and cylinders;
• urine culture when an infection is detected;
• urinalysis according to Nechiporenko;
• blood tests to determine the presence of protein (absence of albumin confirms the diagnosis), antibody levels, cholesterol, fibrinogen levels;
• ultrasound examination of the kidneys and other organs of the urinary system.

Treatment of pregnant women with glomerulonephritis has a number of features and is carried out in a hospital:

1. First of all, a woman is prescribed bed rest to ensure uniform heating of the body and peace.
2. Diet. It is supposed to strictly limit the amount of salt, control the amount of fluid and protein products consumed.
3. Medical therapy. The doctor prescribes drugs to correct blood pressure, relieve swelling, antibiotics to eliminate the infection (currently there are drugs that are completely safe for the fetus), drugs to increase the level of albumin in the blood, drugs to improve blood flow between the mother and fetus (acetylsalicylic acid).

Without fail, the doctor prescribes vitamins, minerals and antioxidants necessary to strengthen the body of the expectant mother and child. Depending on the effectiveness of the course of therapy, it is subsequently decided how the birth will take place (naturally or by caesarean section).

Prevention of glomerulonephritis

To do this, you must follow simple rules:

• always dress according to the weather - do not allow hypothermia, do not neglect gloves and a hat, do not allow shoes to get wet;
• monitor your diet, eat less seasonings and salt;
• give up alcohol, smoking and other bad habits;
• timely and correctly treat colds, diseases of the ENT and organs of the genitourinary system;
• plan pregnancy in the presence of kidney disease after a thorough examination.

Due to the fact that glomerulonephritis is a complex and dangerous disease, you can not self-medicate, and when the first warning signs appear, you should seek qualified help from a clinic.

In addition, while carrying a baby, a woman cannot fight the disease with standard methods, since most medications pose a potential danger to the unborn child. Therefore, it is very important to remember that being in a special situation, one should not neglect the precautionary measures and ignore regular visits to the antenatal clinic and the timely delivery of all tests.

Proper treatment for acute pyelonephritis

Acute pyelonephritis is an inflammatory disease of the tissues of the kidneys and the pyelocaliceal system, and is usually recorded in the patient's card according to the microbial code 10. Currently, acute pyelonephritis is the most common kidney disease that occurs in medical practice. Such a disease is often found among children, when the load on the kidneys is intense, while their development has not yet been fully formed.

As for adults, the disease most often affects women under forty years of age, however, in old age it is more common among men, due to the prevalence of prostate adenoma, which creates obstacles to urine output, which, accordingly, is a favorable condition for the reproduction of pathogenic bacteria.

In fifty percent of cases, acute pyelonephritis occurs due to the penetration of Escherichia coli into the tissues of the kidneys. There are three ways of penetration of microorganisms into the urinary system: ascending, hematogenous and contact. The most common among them is ascending, due to the structural features of the female urethra, pathogenic bacteria easily penetrate the bladder, especially during intercourse, so women who have an active sex life are more likely to get the disease than others. As for men, the risk of getting acute pyelonephritis is much lower, due to the peculiarities of the structure of the urinary system.

The course of the disease and the risk of complications are usually determined by the primary and secondary nature of the infection. Uncomplicated acute pyelonephritis responds well to therapy and does not affect the kidney tissue, as for secondary infection, severe kidney damage and paranephritis are likely. In diagnosing such a disease, the dynamics of the development of symptoms and their nature of occurrence play a very important role.

Usually, during the initial examination, the attending physician asks the patient if he has recently had any purulent or infectious diseases of the urinary system and genital organs. After that, based on the results, tests and data collected, it is already possible to make an adequate diagnosis and appropriate treatment.

Main symptoms

Usually the initial stage of acute pyelonephritis is characterized by a sharp rise in body temperature up to forty degrees. After a certain period of time, the patient develops aching pains in the lumbar region, a rapid and painful act of urination, which indicates that cystitis has also joined the underlying disease. Doctors usually divide the nature of the symptoms that arise into two types: local and general. Acute pyelonephritis symptoms:

• excessive sweating;
• Rapid fatigue and general malaise;
• chills and fever;
• Loss of appetite, vomiting and diarrhea;
• feeling of thirst;
• Dull pain in the lumbar region, which intensifies during movement or palpation;
• Usually on the fifth day of the course of the disease, tension in the muscles of the abdominal wall is observed.

At the moment, there are also several forms of acute pyelonephritis that must be taken into account during the diagnosis and the correct code of the ICD:

• The most acute form is characterized by a severe general condition of the patient. The patient has an increase in body temperature, accompanied by chills, which is repeated up to three times a day;
• Acute - lies in the fact that the patient has pronounced local symptoms of the disease, such as mild intoxication of the body and increased thirst;
• The subacute form of the disease is characterized by the fact that local symptoms come to the fore, while the general ones practically disappear;

The latent form proceeds practically without symptoms and does not pose a direct threat to the patient's health, but can develop into a chronic condition, exacerbations of which can lead to the development of a wrinkled kidney.

It is important to understand that if a person discovers at least one of the above symptoms, an immediate appeal to a qualified specialist should follow, since untimely treatment of acute pyelonephritis can lead to very serious consequences, including: kidney failure and chronic pyelonephritis.

Necessary treatment

Acute and chronic pyelonephritis is a disease with which people most often turn to doctors, and the cure for the disease largely depends on the correct diagnosis and the correctly chosen microbial code. As a rule, patients are prescribed a complex method of treatment, which includes: adherence to the regimen, diet and drug use of drugs.

Treatment of acute pyelonephritis is carried out only in a hospital under the supervision of the attending physician, who strictly monitors the course of the disease, since the disease can cause many complications. If acute pyelonephritis is suspected, the patient is immediately taken to a hospital, where a medical card is issued for him. The case history of acute pyelonephritis according to the ICD code is classified under number ten. Treatment is usually directed primarily at fighting the infection in order to restore kidney function.

Acute pyelonephritis treatment includes: bed rest, which must be strictly observed until the end of fever and chills, diet and drug therapy. The main role in the treatment is played by drug therapy, while the main emphasis is on those drugs that can be excreted together with urine in high concentration. A positive result is also achieved with the appointment of certain medicinal herbs and fees, such as St. John's wort, diuretic tea, rose hips.

Reception of infusions from such medicinal collections is recommended to take four tablespoons a day for three or more months. Vitamins are also prescribed, and in case of intoxication of the body, intravenous solutions are used. In cases where severe purulent foci are found in the kidneys, surgical intervention is necessary.

With properly prescribed treatment, acute pyelonephritis can be cured in the first days of onset, as a rule, chills and fever disappear first, and then local symptoms.

Despite the fact that the main symptoms may disappear after a few days, antibiotics are continued for at least six weeks with their constant change.

It is worth remembering that self-treatment is extremely dangerous, you should not experiment on yourself and look for reasons, it is better to immediately contact a medical institution for qualified assistance. Proper and timely treatment eliminates the risk of possible complications and positively affects the course of the disease.

To prevent the prevention of the disease, systematic examination and monitoring is necessary, especially for pregnant women, who are most susceptible to diseases of the kidneys and urinary system. Urine tests should be taken not only during gestation, but also after childbirth, since the possible course of the disease that began during pregnancy might not show any symptoms.

As for the prognosis for acute pyelonephritis, in general, with timely assistance and a correctly diagnosed microbial code, it is very favorable.

Diet for this type of disease

The diet for acute pyelonephritis should include food that is easily digested by the patient's body. In addition to being easily digestible, it should also be with a sufficient amount of vitamins and calories, but salt intake is recommended to be minimized, since its excessive content makes the kidneys work in an enhanced mode, which is contraindicated in the acute course of the disease.

In the first days of hospitalization, due to the high probability of intoxication of the body, the patient is recommended to eat fresh vegetables and fruits, it is also necessary to drink at least two liters of liquid, which helps to remove harmful substances from the body. Best of all, they cope with this task: sweet tea, compotes and infusions of medicinal herbs.

In the future, as the patient's condition improves, the specialist transfers him to a therapeutic diet at number seven, with a gradual increase in fluid intake and the inclusion of vegetable, dairy and sour-milk products in the daily diet, usually an appointment is made after about ten days of hospital stay.

In acute pyelonephritis, which is recorded in the patient's medical history, the following foodstuffs are strictly prohibited according to microbial code 10: rich broths from meat and fish, canned foods, mustard, horseradish, sorrel and garlic.

After the patient is discharged, a diet is prescribed, which includes the use of proteins, fats and carbohydrates, the patient should eat fractionally about five times a day. The doctor takes into account the general condition of the patient and, on the basis of this, draws up an individual diet, which should include a variety of consumed products, especially dairy and sour-milk.

Strict adherence to such dietary nutrition allows you to maintain the weakened body of the patient and his immunity at the required level, which contributes to a speedy recovery.

Glomerulonephritis with a predominance of nephrotic syndrome

Glomerulonephritis is a group of diseases that are expressed by a predominant lesion of the glomerular apparatus of the kidneys. This pathology is inflammatory in nature and manifests itself in different ways. Glomerulonephritis is accompanied by isolated urinary, nephritic or nephrotic syndromes. It progresses rapidly and can turn into nephrosclerosis or chronic renal failure. Most often they suffer from children of primary school age and adult men.

The share of glomerulonephritis with nephrotic syndrome accounts for about 20% of all cases of glomerulonephritis. When prescribing therapy, the doctor should pay special attention to the diet. A special diet for nephrotic syndrome has been developed.

Reasons for development

The most common cause of acute autoimmune damage to the glomeruli of the kidneys is considered to be β-hemolytic streptococcus group A. But these bacteria do not directly affect the basement membrane of the glomeruli. It's all about the antigen-antibody reaction and the formation of cyclic immune complexes.

When a streptococcal infection enters the body, defense mechanisms are activated. The cells of the immune response begin to produce antibodies that bind to the antigen and form cyclic immune complexes (CICs). The latter settle on the glomerular membrane, the defeat of which leads to an increase in permeability and the formation of an inflammatory focus. As a result, nephrotic syndrome develops, in which blood proteins are excreted in large quantities.

Not only streptococcal infection causes kidney failure. Herpes viruses (herpes simplex, Epstein-Barr virus, cytomegalovirus), staphylococci, enterococci, hepatitis B and many others are capable of this.

Other factors in the occurrence of glomerulonephritis include drugs that have a potential nephrotoxic effect. This means that some antibiotics (aminoglycosides, sulfonamides), non-steroidal anti-inflammatory drugs can provoke the development of acute glomerulonephritis. Of great importance in the occurrence of the dosage form of the disease is individual sensitivity to drugs, the presence of concomitant pathologies of the kidneys or other organs.

Glomerulonephritis in children with nephrotic syndrome sometimes occurs after childhood infections, tonsillitis, tonsillitis, and in the presence of congenital anomalies of the urinary system.

Nephrotic syndrome in chronic glomerulonephritis often develops with insufficient or untimely treatment of infectious diseases of the kidneys.

Classification

According to nosologies, primary (etiology is unknown) and secondary glomerulonephritis are distinguished. The former accounts for about 80% of all cases. If the doctor can accurately identify the cause of the disease, then we can talk about the development of secondary glomerulonephritis.

According to the type of flow, there are:

1. Acute: the duration of the condition is up to 3 months.
2. Subacute - from 3 months to 1 year.
3. Chronic - the disease progresses for more than a year and there is a possibility of developing renal failure.

Clinical manifestations

The onset of acute and chronic glomerulonephritis with nephrotic syndrome is usually different. The clinical picture is also different. But in all cases there are changes in the urine, hypertensive and edematous syndromes.

Acute glomerulonephritis begins with a sharp increase in temperature and weakness. The patient complains of pronounced symptoms of intoxication: dizziness, nausea, loss of appetite, pale skin. Nephrotic syndrome is characterized by the presence of edema, increased blood pressure and certain changes in the urine. In acute glomerulonephritis, this syndrome is considered primary.

An increase in blood pressure occurs due to an imbalance of vasoactive substances (renin, angiotensin), which are produced in the kidney parenchyma. An increase in renin production affects the vascular wall, causing spasm. This, in turn, leads to a significant increase in blood pressure. For children, this condition is not typical.

The nephrotic form of chronic glomerulonephritis does not have such a violent onset. Its symptoms are more diverse and correspond to the form, stage of the disease and the degree of kidney damage. Chronization of the process in children is very dangerous.

Edema

Extrarenal changes (edema, hypertension) occur gradually. Initially, the patient notes the appearance of small edema on the face and only in the morning, but then they progress up to anasarca and intracavitary manifestations. A person suffering from a nephrotic form of glomerulonephritis has a characteristic appearance, which will allow the doctor to suspect the development of pathology. Such people are pale, the face is swollen, puffy. The skin at the site of edema is cold to the touch, trophic disorders (dryness, peeling) are observed.

It must be remembered that in children, edema appears spontaneously and is already very pronounced at the very beginning. They can be asymmetrical, but more often they are generalized (spread throughout the body).

The release of fluid from the bloodstream is due to an increase in the excretion of protein along with urine. A certain amount of proteins in the blood plasma maintains an optimal colloid osmotic pressure. If their number noticeably decreases, then the pressure, respectively, falls. The compensatory mechanism is activated, which is based on the maintenance of oncotic pressure. The fluid passes into the intercellular space to restore processes.

With the progression of the disease with nephrotic syndrome, edema increases. They are already localized not only on the upper half of the body. Swelling of the lumbar region, legs along the entire length. In very advanced cases, cracks can form on the lower extremities with the leakage of serous fluid.

No less dangerous intracavitary edema. Excess fluid accumulates in the abdominal, pleural and cardiac cavities, disrupting the functioning of vital organs. Children with ascites may develop abdominal pain syndrome.

Diagnostic measures

Definition of a nephrotic syndrome does not cause big difficulties. The main criterion is the characteristic changes in the composition of urine.

When conducting a general analysis, it is revealed:

• massive proteinuria (from 3 g/day and above);
• the main part of the protein fractions is albumin;
• the excretion of the daily amount of urine decreases due to the formation of edema;
• urine density increases, due to increased protein loss;
• under the microscope, hyaline cylinders are found;
• due to the high permeability of the glomerular membranes in the urine, altered red blood cells can be seen.
• erythrocyturia is characteristic of mixed nephrotic syndrome, which is also accompanied by arterial hypertension.

In the nephrotic form of acute and chronic glomerulonephritis, an assessment of the work of the kidneys is carried out to detect renal failure. The signal for this is a decrease in the amount of urine separated. It is necessary to determine the glomerular filtration rate of creatinine.

In a general blood test with nephrotic syndrome, a sharp increase in ESR (above 30 mm / h) is found. More revealing are the data of biochemical analysis. For nephrotic syndrome, a decrease in protein fractions, namely albumin, will be characteristic (total protein - less than 60 g / l, albumin - less than 40 g / l). Increasing levels of lipids and cholesterol. The electrolyte balance of the blood is disturbed: potassium is excreted in large quantities in the urine, and sodium is retained.

As additional research methods, ultrasound of the kidneys and renal vessels is prescribed. To determine the exact cause of the development of nephrotic syndrome, a fine-needle biopsy of the damaged organ is prescribed. To exclude congenital pathology of the urinary system, excretory urography with intravenous contrast is used.

Differential diagnosis of nephrotic syndrome in acute and chronic glomerulonephritis is carried out with amyloidosis, diabetic glomerulosclerosis, collagen nephropathy and myeloma kidney disease.

Therapy Methods

Treatment of glomerulonephritis with nephrotic syndrome is carried out in a hospital under the supervision of a doctor. In specialized hospitals, therapy is prescribed by a nephrologist. Children are hospitalized in the nephrology department of pediatrics. The patient must strictly adhere to bed rest and prescribed diet.

Medical nutrition is aimed at:

1. Increase your daily protein intake. The diet must be selected so that the body receives about 1.4 g of protein per 1 kilogram of weight, taking into account its loss in urine. Animal proteins make up 2/3 of this amount. Patients on a diet number 7 B are recommended to eat cottage cheese, egg whites, lean meats or fish. If kidney function decreases, then the amount of protein consumed decreases.
2. The diet involves reducing fat intake. This is due to an increase in total cholesterol and triglycerides in the blood. On average, the daily norm of fats is about 80 g, of which 35% are vegetable.
3. The diet provides for a sharp restriction of table salt. All food is cooked without adding it. The use of salty sauces, marinades is contraindicated.
4. With food, you can restore the missing potassium. The therapeutic diet includes a large number of vegetables and fruits. The patient is recommended to eat honey, potatoes, legumes, bananas, greens.
5. Despite swelling, the amount of fluid consumed is limited slightly. The daily norm is about 1 liter. In children, it is calculated according to weight. But the doctor must monitor the ratio of absorbed and excreted fluid.

With a therapeutic diet, it is forbidden to eat fresh bread, meat, mushroom broths, fatty meats and offal, spicy and salty types of cheese, smoked meats. You can not eat chocolate and cream confectionery. A gentle temperature regime is optional. A therapeutic diet is prescribed until a complete remission occurs.

Conservative treatment

First of all, it is necessary to prescribe pathogenetic therapy. Glucocorticosteroids, cytostatics, and selective immunosuppressants are used as immunosuppressants.

Glucocorticoids (prednisolone, dexamethasone) are considered the drugs of choice. They prevent the entry of immune complexes into the inflammatory focus. At the beginning of treatment of the nephrotic form of glomerulonephritis, large doses of prednisolone are prescribed, gradually reducing them. This is called pulse therapy. Before starting treatment, the doctor should warn the patient about the development of possible side effects. These include changes in appetite, sleep deprivation, increased pressure, the occurrence of steroid diabetes, and others. With great care it is necessary to use these drugs in children.

Diuretics are prescribed to reduce swelling. The advantage is given to potassium-sparing. In nephrotic syndrome, in rare cases, forced diuresis is carried out with the help of diuretics to drastically reduce edema. The appointment of diuretics occurs under the control of the level of sodium and potassium in the blood.

All drug treatment is carried out against the background of diet, bed rest and monitoring of key indicators.

Prognosis and possible complications

In acute and chronic glomerulonephritis, which are accompanied by the occurrence of nephrotic syndrome, it is necessary to take into account the possibility of complications.

With severe edema, the likelihood of developing pneumonia or pneumonitis increases. If patients develop cracks in the area of ​​pronounced edema, then they must be carefully treated to avoid infection.

The most formidable complication is the nephrotic crisis. It is accompanied by severe pain and a drop in blood pressure. In children and adults, it is necessary to be wary of the formation of chronic renal failure in glomerulonephritis with nephrotic syndrome.

With timely treatment, compliance with all medical recommendations and diet, the prognosis is favorable.

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The site provides reference information for informational purposes only. Diagnosis and treatment of diseases should be carried out under the supervision of a specialist. All drugs have contraindications. Expert advice is required!

Diagnosis of acute and chronic glomerulonephritis

diagnostic symptoms ( or patient complaints) glomerulonephritis are:

• general weakness and malaise;
• swelling of the face, feet, legs;

• change in color and transparency of urine - urine may acquire a red, brown or cloudy hue, become foamy, contain sediment;
• difficulty urinating ( sluggish jet);
• decrease in daily diuresis ( urine volume);
• sometimes polyuria, that is, an increase in the daily volume of urine;
• arterial hypertension ( increased blood pressure).

Tests for glomerulonephritis

The second most important laboratory sign is hematuria - the presence of red blood cells in the urine. This symptom is most characteristic of acute glomerulonephritis and is less common in chronic.
Glomerulonephritis is accompanied by changes not only from the general analysis of urine, but also from the blood test.

Blood changes in glomerulonephritis are:

• hypoalbuminemia- Decrease in blood albumin less than 65 grams per liter), occurs due to the massive loss of proteins in the urine;
• anemia- a decrease in the concentration of hemoglobin and erythrocytes, due to their loss in the urine with hematuria;
• dysproteinemia- violation of the ratio of albumins and blood globulins, occurs due to the massive loss of albumins;
• increase in the concentration of urea, ammonia, creatinine ( signs of uremia) ;
• leukocytosis- an increase in blood leukocytes is an indicator of an acute process.

Research in glomerulonephritis

The main method for examining kidney function is the measurement of glomerular filtration rate, abbreviated as GFR. In order to calculate this indicator, a Reberg test is performed, which is carried out according to the concentration of creatinine and the volume of urine released per unit of time. Normal GFR ranges from 80 to 140 milliliters per minute in men and from 75 to 130 in women. GFR is elevated in diseases such as diabetes mellitus, hypertension, and in the early stages of nephrotic syndrome. A decrease in GFR indicates renal failure, that is, the final stage of glomerulonephritis.

GFR indicators ( glomerular filtration rate) in renal failure are:

• initial stage (compensated) renal failure - from 30 to 50 milliliters per minute;
• moderate stage (subcompensated) renal failure - from 15 to 30 milliliters per minute;
• final stage (decompensated) renal failure - less than 15 milliliters per minute.

Treatment of glomerulonephritis

If there are chronic foci of infection in the body, for example, tonsillitis or otitis media, then antibacterial treatment is prescribed to eliminate them. As a rule, antibiotics of the penicillin series are recommended. Penicillin is prescribed for a period of 7 to 10 days. The dose of the drug is selected exclusively individually - based on the vastness of the focus of infection and concomitant diseases. If the patient has high blood pressure, then diuretics are prescribed ( diuretics), enhancing the excretion of sodium from the body.

With severe edema and a decrease in daily diuresis to 500 ml, hypothiazide and furosemide are indicated, sometimes in combination with veroshpiron. Sometimes, namely with the nephrotic form of acute glomerulonephritis, glucocorticoids are indicated. As a rule, prednisolone or dexamethasone is prescribed. The scheme of their appointment is also strictly individual. It is important to know that drugs from this category are prescribed no earlier than 3 to 4 weeks from the onset of the disease.

Treatment of glomerulonephritis with folk remedies

Groups of folk remedies for glomerulonephritis are:

• means to increase immune function;
• medicines to reduce the inflammatory process;
• products against puffiness.

Medications to enhance immune function
To strengthen the barrier function, traditional medicine offers various recipes based on foods rich in vitamins and other valuable substances. Popular with glomerulonephritis are vitamin mixtures based on honey with the addition of dried fruits and nuts, as all this has a pleasant taste. In addition, such products do not contain liquid, so they can be used without restrictions ( according to prescription). With glomerulonephritis, patients are advised to increase the amount of sugar, which is contained in sufficient quantities in these mixtures, which is also their plus.

The components of the recipe for strengthening immunity are:

• dried apricots;
• raisin;
• figs;
• prunes;

To prepare the mixture, all components, except honey, should be passed through a meat grinder. Then the mass must be poured with honey and put in a convenient container. The product is stored in the refrigerator for 1 - 2 months. You need to take a vitamin mixture in a teaspoon half an hour before a meal. The duration of therapy is 2 - 3 months.

Medications to reduce inflammation
With glomerulonephritis, herbal decoctions are used, which contain various active compounds that suppress the inflammatory process. A drink is prepared from a tablespoon of a crushed plant and 500 milliliters of water. The suspension must be kept in a steam bath, filtered and drunk half a glass three times a day.

Plants that are used for anti-inflammatory infusions are:
In addition to decoctions of herbs with anti-inflammatory action, you can prepare alcohol tinctures. The use of tincture will reduce the amount of fluid consumed, which is important for many patients with glomerulonephritis. For tincture, it is necessary to use only dry plants, which are poured with alcohol in a ratio of 10 to 1 and infused for 2 weeks. The filtered suspension is taken 10-15 drops three times a day 20-30 minutes before a meal.

anti-puffiness products
With glomerulonephritis, the inclusion in the diet of various natural products that have a diuretic effect is shown. Increasing the amount of urine produced can reduce swelling of the tissues and normalize the level of pressure. In addition to the diuretic effect, such products are distinguished by a valuable composition of vitamins and other substances necessary for the body.

Products that should be used against edema are:

• Watermelon. With glomerulonephritis, fasting days are recommended, during which you should eat from 1.5 to 2 kilograms of watermelon pulp. Such events should be carried out no more than once every 2-3 weeks. Watermelon peel also has a diuretic effect. To eat the peel, the flesh should be cut from it, dried and then ground into dust. Take one tablespoon inside, washing down the powder with water.
• Pumpkin, carrot. Pumpkin and / or carrot juice will help reduce swelling, which should be prepared independently and taken 100 milliliters per day. Vegetables can also be baked or eaten raw.
• Kalina, cranberry. These berries have a pronounced diuretic effect, and also have an anti-inflammatory effect. You can take viburnum and cranberries inside in the form of a fruit drink, for which the berries should be ground with sugar and poured with warm water. Also, grated berries with sugar can be consumed in their pure form ( tablespoon after meal).
• Leafy greens. Fresh parsley, celery and dill should be added to salads and other dishes, as these plants help reduce swelling and normalize blood pressure. You can make juice from celery stalks, which should be taken at 100 - 200 milliliters per day.

Sanatorium-resort treatment for glomerulonephritis

Indications for treatment in a sanatorium with glomerulonephritis
For patients who have suffered acute glomerulonephritis, a visit to a sanatorium is indicated if residual effects of the disease persist for a long time. Also, resorts are recommended for those patients whose treatment of the disease has been delayed for more than six months. In the chronic form, sanatorium treatment is relevant for any form of the disease if there are no contraindications. The best time to visit the resort areas is spring, summer and early autumn.

Procedures in sanatoriums for glomerulonephritis
In addition to the beneficial effects of the dry climate, the healing effect in sanatoriums is achieved through various physiotherapy procedures. The impact of electric current, magnetic field and other factors can reduce swelling, reduce the inflammatory process and strengthen the patient's immunity. There is a wide variety of physiotherapy procedures that can be performed on patients with glomerulonephritis. In most cases, patients are prescribed a complex of several procedures, which are carried out at different time intervals. The treatment regimen is drawn up by a doctor who takes into account the form of the disease, the patient's condition and other factors.

Types of physiotherapeutic procedures for glomerulonephritis are:

• exposure to a low frequency magnetic field ( conductors are located in the projection zone of the kidneys);
• the introduction of pharmacological drugs through the skin using current ( electrophoresis);
• exposure to an electric field of ultrahigh frequency ( UHF therapy);
• exposure to ultrasound on the lumbar region;
• paraffin and ozocerite applications ( medicinal resin);
• use of medicinal leeches hirudotherapy);
• visiting the steam room, infrared sauna;
• ingestion of medicinal mineral waters.

Spa treatment is contraindicated in the case when the patient has blood in the urine, which is visible to the naked eye ( gross hematuria). Severe edema and severe renal failure are also conditions in which spa treatment is not recommended. In the case when the blood pressure indicators exceed 180/105 millimeters of mercury, visiting resorts is also not recommended.

Diet for glomerulonephritis

Nutrition for glomerulonephritis

General guidelines for the diet for glomerulonephritis are as follows:

• food temperature should be medium;
• salt is used only to salt cooked food;
• the number of meals should vary from 5 to 6 per day;
• the consumption of foods high in dyes, flavor enhancers and other additives should be kept to a minimum;
• preference should be given to seasonal vegetables and fruits;
• products and dishes of exotic origin should be limited.

Diet for acute glomerulonephritis

• Squirrels. In acute glomerulonephritis, the rate of pure protein is 20 grams, and half of them should be of animal type.
• Fats. About 80 grams of fat should be consumed per day, of which 15 percent should be vegetable.
• Carbohydrates. The norm of carbohydrates per day is 350 grams, of which 25 percent should be sugar. The norm of sugar should be replenished by consuming sweet fruits and berries. Sugar can also be used to sweeten foods and drinks.
• The energy value. The total calorie content of products should not exceed 2200 calories.
• Liquid. In acute glomerulonephritis, the amount of fluid you drink may exceed the total amount of urine excreted for the previous day by no more than 300 milliliters. The recommended rate of liquid includes not only drinking in its pure form, but also the water that was used to prepare the first courses.
• Salt. The daily salt intake varies from 1.5 to 2 grams.

Products for acute glomerulonephritis

An example of a daily menu for acute glomerulonephritis may be:

• First breakfast. Porridge from any cereal with butter, weak tea.
• Lunch. Salad of fresh fruits or vegetables. Sour cream, vegetable oil can be used as a dressing.
• Dinner. Vegetable soup, boiled meat with potato garnish, jelly.
• afternoon tea. Pancakes from zucchini, carrots or pumpkins.
• Dinner. Macaroni with milk. Dessert can be jelly or jelly.
• Late dinner. Vegetable salad, fruit juice.

Diet for chronic glomerulonephritis

• Squirrels. The rate of pure protein increases to 40 grams per day.
• Fats. The amount of fat in chronic glomerulonephritis should vary from 90 to 100 grams, of which at least 25 percent should be vegetable.
• Carbohydrates. At least 500 grams of carbohydrates should be consumed per day, among which there should be foods containing any form of sugar ( fructose, glucose).
• The energy value. The calorie content of the diet can vary from 2700 to 3000 calories.
• Liquid. The amount of liquid you drink should correspond to the amount of urine excreted the day before or be 300-400 milliliters more.
• Salt. The daily amount of table salt consumed should not exceed 3 grams.

Supplements to the daily diet for chronic glomerulonephritis are as follows:

• the norm of meat / fish increases to 100 grams;
• cottage cheese is introduced into the diet in an amount of not more than 100 grams;
• it is allowed to include one whole egg in the menu;
• the amount of potatoes increases to 300 grams;
• the norm of apples increases to 2 - 3 pieces.

Prevention of glomerulonephritis

Primary prevention of glomerulonephritis

Measures for the primary prevention of glomerulonephritis are as follows:

• timely treatment of infectious diseases;
• control of the state of foci of chronic infection;
• increasing the body's resistance to cold.

The general rules for the treatment of infectious diseases are as follows:

• identification of the causative agent of the disease and the application of appropriate treatment ( antibiotics or antivirals);
• compliance with bed rest for the entire period of treatment;
• compliance with the deadline for taking the prescribed drugs, even if the patient's well-being has improved significantly;
• maintenance therapy after completion of treatment ( vitamins, immunomodulators) in order to prevent recurrence of the disease and the transition of the disease to the chronic stage;
• during and after treatment after 10 - 30 days) should take a urine test.

Common signs of chronic infection are as follows:

• subfebrile temperature ( 37 to 38 degrees);
• trouble falling asleep or waking up, shallow sleep;
• increased cereals, whole grain products). You also need to control the consumption of foods high in modified fats, caffeine, chemical additives, sugar, salt. A prerequisite for strong immunity is regular physical activity ( sports, dancing, swimming, hiking).

  In the presence of chronic infections, a person is recommended anti-relapse therapy, which is aimed at preventing exacerbations. For this, the patient is prescribed medication to strengthen the immune system. Various physical therapy procedures may also be indicated ( irrigation, washing, heating). Anti-relapse therapy is carried out most often in spring and autumn before the onset of seasonal exacerbations.

  Increasing the body's resistance to cold
  Hypothermia increases the risk of developing respiratory diseases, which, in turn, can lead to glomerulonephritis. Therefore, the development of resistance to cold is an important preventive measure for this pathology of the kidneys. It is possible to reduce the body's sensitivity to low temperatures and increase immunity by hardening. In order for the hardening of the body not to cause harm and be effective, it must be carried out based on a number of rules.

  The rules for hardening the body are as follows:

  • you can not start procedures in the stage of exacerbation of diseases;
  • at first, the duration of any procedure should not exceed 1 - 2 minutes;
  • subsequently, the time of procedures should be gradually increased - 5 - 7 minutes for water sessions, 20 - 30 minutes for all other procedures;
  • tempering activities should be carried out regularly ( daily or every other day);
  • when feeling worse ( fever, chills) during or after the procedure, hardening should be stopped.
  There are several hardening methods, but you should start with one simple procedure, gradually increasing the complexity and number of hardening activities.

  Hardening procedures include:

  • walking barefoot on grass, sand;
  • wiping with a towel dipped in cool water;
  • dousing with cool water;
  • air baths ( exposure of the torso at an air temperature of 20 degrees, which should be gradually reduced to 14 degrees).

  Secondary prevention of glomerulonephritis

  The goal of secondary prevention is to prevent the transition of glomerulonephritis to the chronic stage. If the patient has already been diagnosed with the chronic stage of the disease, preventive measures are taken in order to prevent an exacerbation of the disease.

  Measures for secondary prevention of glomerulonephritis are as follows:

  • compliance with a special regime in everyday life;
  • refusal of certain working conditions;
  • following the rules of the diet;
  • doctor's observation.
  In addition to these provisions, the patient must also strictly comply with all primary prevention measures.

  Compliance with a special regime in everyday life
  One of the important conditions for the prevention of glomerulonephritis is the observance of a special regimen. Physical and nervous strain adversely affects the functionality of the kidneys. Therefore, people who have had this disease should control the level of stress and provide the body with high-quality and timely rest.

  Patients who have had an acute form of glomerulonephritis need for a certain period ( duration is determined by the doctor) observe the most sparing mode of physical activity. Subsequently, physical activity should be gradually increased. In the morning, it is recommended to perform a set of simple exercises, and in the evening to take walks. In this case, patients are shown an afternoon rest in a horizontal position. It is also recommended to rest after any physical activity. In the supine position, the blood supply and metabolic processes in the kidneys become more intense, as a result of which their functionality improves. In addition to the regime of rest and physical activity, the prevention of glomerulonephritis requires compliance with a number of other rules.

  The provisions for the prevention of glomerulonephritis in everyday life are as follows:

  • refusal of water sports and any activities associated with a long stay in the water;
  • prevention of hypothermia, especially during daytime and nighttime rest;
  • control of drafts and humidity levels in the rooms where the patient is located;
  • female patients after the acute phase of the disease should refuse to plan pregnancy for a period of at least 3 years.
  Refusal of certain working conditions
  People who have suffered glomerulonephritis should avoid large physical and mental stress at work. Do not stay in a damp room for a long time or be exposed to cold. Secondary prevention of glomerulonephritis requires the rejection of work that involves contact with harmful and toxic substances. Work at night is contraindicated, as well as those activities that are associated with long business trips.

  Following the rules of the diet
  Prevention of glomerulonephritis requires a special diet, which reduces the load on the kidneys and improves their functionality. Preventive nutrition in this disease involves a decrease in the volume of protein foods ( fish, dairy and meat products) and an increase in the amount of carbohydrates ( fruits, vegetables, cereals) in the diet. The norm of table salt, which is allowed to be consumed without harm to the kidneys, is 2-3 grams per day.
  With the appearance of edema and an increase in blood pressure, it is recommended to completely refuse food for 1-2 days, and reduce the daily volume of fluid to 250-300 milliliters. Subsequently, the amount of fluid increases in accordance with the volume of urine excreted.

  Doctor's observation
  Regular testing and monitoring of one's own condition is an important condition for the prevention of glomerulonephritis. Patients who have suffered an acute form of this disease, after discharge from the hospital, are shown to be monitored by a doctor for 3 years, during which a series of examinations should be carried out. During the first 2 months after discharge, once every 2 weeks, a general analysis of urine and blood should be taken. In the future, the regularity is reduced to once every 2 months, and after the first year, tests should be taken every 6 months. In addition to urine and blood tests, it is necessary to visit such specialists as an otolaryngologist every six months.