Glomerulonephritis - Causes, symptoms and treatment. MF.

Glomerulonephritis is an immune-inflammatory disease with a predominant lesion of the glomeruli of the kidneys, as well as involving tubules and interstitial tissue.

Glomerulonephritis on the mechanism of development belongs to the group of infectious-allergic diseases. The term "infectious-allergic" reflects the formation of infectious allergies in combination with various non-immune damage to the body. There are also autoimmune forms of the disease, which are caused by damage to the kidney tissue by autoantibodies, i.e.antibodies to its own organ.

Glomerulonephritis is an independent disease, but it can also occur in many systemic diseases such as systemic lupus erythematosus, hemorrhagic vasculitis, infective endocarditis, etc.

Prevalence of glomerulonephritis

Glomerulonephritis is one of the most frequent kidney diseases in children leading to developmentchronic renal failure and early disability. In terms of prevalence, it is the second after an infection of the urinary tract among acquired kidney diseases in childhood.

Acute glomerulonephritis can develop at any age, however most patients are individuals up to 40 years old.

Symptoms of glomerulonephritis

Acute diffuse glomerulonephritis develops 6-12 days after infection, usually streptococcal( tonsillitis, tonsillitis, pyoderma);the most nephritogenic b-hemolytic group A streptococcus, especially strains 12 and 49. The following symptoms are typical:

• hematuria( often macrohematuria);
• edema;
• oliguria;
• increase in blood pressure.

In children, acute glomerulonephritis usually has a cyclic course, with a violent onset, in most cases ends in recovery. In adults, an erased variant with changes in urine without common symptoms is more common, gradually taking on a chronic course.

The first signs of acute glomerulonephritis appear 1-3 weeks after an infectious disease or other factors. The disease begins with a general weakness, headache, nausea, back pain, scrounging, loss of appetite. There can be body temperature rises to very high digits. Pallor of the face, puffiness of the eyelids, a sharp decrease in the amount of excreted urine are noted.

The decrease in the volume of urine can last 3-5 days, after which the diuresis increases, but the relative density of urine, according to the analysis, is reduced.

Another characteristic feature is the presence of blood in the urine - hematuria. Urine acquires the color of "meat slops" or becomes dark brown or black. In cases of microhematuria, the color of urine may not change. At the beginning of the disease, fresh erythrocytes predominate, and subsequently leached out predominantly.

Edema is one of the most characteristic symptoms of glomerulonephritis .They are usually located on the face, appear in the morning, decrease in the evening. Before development of visible edemas about 2-3 liters.fluid can linger in the muscles, subcutaneous tissue. At full preschool age, edema is more difficult to establish, sometimes they are determined only by some compaction of subcutaneous tissue.

Hypertension( increase in blood pressure) is observed in about 60% of cases. In severe glomerulonephritis, an increase in blood pressure may last several weeks. The defeat of the cardiovascular system in acute glomerulonephritis is noted in 80-85% of children.

There may be an increase in the liver, a change in the central nervous system.

With a favorable course of the disease and timely diagnosis and treatment after 2-3 weeks, edema disappears, blood pressure normalizes. Usually recovery in acute glomerulonephritis occurs after 2-2,5 months.

The two most typical forms of acute glomerulonephritis :

1. Cyclic form( starts violently)
2. The latent form( characterized by a gradual onset) is often found, and its diagnosis is of great importance, since often with this form the disease becomes chronic.

Any acute glomerulonephritis , which did not completely disappear within a year, should be considered passed into chronic.

The following clinical forms of the chronic glomerulonephritis are distinguished:

1. The nephrotic form( see Nephritic syndrome) is the most common form of the primary nephrotic syndrome.
2. Hypertensive form. For a long time, hypertension prevails among the symptoms, while the urinary syndrome is not very pronounced.
3. Mixed form. With this form simultaneously there are nephrotic and hypertensive syndromes.
4. Latent form. This is a fairly common form;usually manifested only mildly expressed urinary syndrome without hypertension and edema.

The hematuric form is also distinguished, since in some cases the chronic glomerulonephritis can manifest with hematuria without significant proteinuria and general symptoms.

All forms of chronic glomerulonephritis can periodically give relapses that closely resemble or completely repeat the pattern of the first acute attack of diffuse glomerulorephritis. Especially often, exacerbations are observed in autumn and spring and occur 1-2 days after exposure to the stimulus, most commonly streptococcal infection.

Causes of glomerulonephritis

The development of glomerulonephritis is associated with acute and chronic diseases of various organs, mainly streptococcal nature.

The most common causes of glomerulonephritis are:

• angina;
• scarlet fever;
• purulent skin lesions( streptoderma);
• pneumonia;

The cause of development of glomerulonephritis can serve as SARS, measles, chicken pox.

Among the etiological factors is the cooling of the organism in a humid environment( "trench" nephrite).Cooling causes reflex disorders of blood supply to the kidneys and affects the course of immunological reactions.

There are reports of the causal role of microorganisms such as Staphylococcus aureus, Streptococcus pneumoniae, Neisseria meningitidis, Plasmodium malaria, Toxoplasma gondii and some viruses.

Usually the onset of the disease on 1-3 weeks is preceded by a streptococcal infection in the form of pharyngitis, tonsillitis, scarlet fever, skin lesions - impetigo-pyoderma. It has been established that acute glomerulonephritis usually causes only "nephritogenic" strains of b-hemolytic streptococcus of group A.

It is believed that if a burst of streptococcal A-infection in a children's team is caused by nephritogenic strains, 3-15% of infected children become nephritis, although among the surrounding sick child adults and children, about 50% show changes in the urine, i.e.they probably tolerate torpid( low-symptom, asymptomatic) nephritis.

Acute glomerulonephritis develops among children who have had scarlet fever, at treatment in hospital and in 3-5% of children treated at home. Respiratory viral infection in a child with chronic tonsillitis or carriage of skin nephritogenic streptococcus A can lead to activation of the infection and cause the emergence of acute glomerulonephritis.

Complications of glomerulonephritis

In acute diffuse glomerulonephritis , the following complications can occur:

1. Acute heart failure( in less than 3% of cases);
2. Acute renal failure( in 1% of patients);
3. Acute renal hypertensive encephalopathy( preeclampsia, eclampsia);
4. Hemorrhage in the brain;
5. Acute visual impairment( rolling blindness);
6. Transition to chronic diffuse glomerulonephritis .

One of the factors of chronic inflammation in the kidneys can serve as the so-called hypoplastic kidney dysplasia, i.e.lag in the development of renal tissue from the chronological age of the child.

With progressing course, not responding to active immunosuppressive therapy, the chronic diffuse glomerulonephritis passes into its final stage - a secondary-wrinkled kidney.

Glomerulonephritis is one of the most frequent kidney diseases in children, leading to the development of chronic kidney failure and early disability.

Diagnosis of glomerulonephritis

Diagnosis of acute glomerulonephritis is based on the appearance in young people after having had angina or acute respiratory viral infection - edema, headache, arterial hypertension and the results of the following laboratory tests.

Characteristic signs of glomerulonephritis are:

1. Hematuria - the presence of blood in the urine. Urine acquires the color of "meat slops" or becomes dark brown or black. In cases of microhematuria, the color of urine may not change. At the beginning of the disease, fresh erythrocytes predominate, and subsequently leached out predominantly.
2. Proteinuria( albuminuria) is usually mild( up to 3-6%), it lasts 2-3 weeks.
3. With microscopy of urinary sediment, hyaline and granular cylinders are found, with macrogemeturia - erythrocyte.
4. The study of the clearance of endogenous creatinine reveals a decrease in the filtration capacity of the kidneys.
5. Zimnitsky's trial shows a decrease in diuresis, nocturia. High relative density of urine indicates the preserved concentration ability of the kidneys.
6. In the blood, the content of residual nitrogen( acute azotemia), urea, the titer of ASL-O and ASG increases. The content of creatinine, cholesterol is increased.
7. When studying the equilibrium of acids and bases in the blood - acidosis;a decrease in albumins, an increase in alpha and beta globulins.
8. In the blood there is leukocytosis, accelerated ESR.
9. In doubtful cases, a kidney biopsy is performed, followed by a morphological study of the bioptic material.

Treatment of glomerulonephritis

Treatment of acute glomerulonephritis :

1. Regimen( all patients with acute glomerulonephritis should be admitted to the nephrologic or therapeutic department, bed rest is prescribed.);
2. Health food( Diet №7);
3. Etiologic( anti-streptococcal) treatment( Penicillin, Ampiox or Erythromycin);
4. Treatment with hormonal( Prednisolone) and non-hormonal immunosuppressants( Imuran, Cyclophosphamide), anti-inflammatory drugs( Voltaren), heparin;
5. Symptomatic treatment( hypertension, edema, etc.);
6. Treatment of complications;
7. Sanatorium treatment( in the sanatoriums of Satarai-Mahi-Khasa, Yangantau, etc.);
8. Clinical examination( observation for 2 years).

In the treatment of chronic glomerulonephritis , the same measures as for acute glomerulonephritis are performed, especially during periods of exacerbation.