Glomerulonephritis is an immune–inflammatory kidney disease. Affects mainly the renal glomeruli. To a lesser extent, interstitial tissue and kidney tubules are involved in the process. Disease occurs as an independent disease or develops with some systemic pathologies. The clinical picture consists of urinary, edematous and hypertensive syndromes. Diagnostic value has the data of urine tests, samples of Zimnitsky and Rehberg, ultrasound of the kidneys and ultrasound of the renal vessels. Treatment includes drugs for the correction of immunity, anti-inflammatory and symptomatic agents.
Meaning
Glomerulonephritis is a kidney lesion of an immune–inflammatory nature. In most cases, the development of glomerulonephritis is caused by an excessive immune response of the body to antigens of an infectious nature. There is also an autoimmune form of glomerulonephritis, in which kidney damage occurs as a result of the destructive effects of autoantibodies (antibodies to the cells of one’s own body).
Glomerulonephritis ranks second among acquired kidney diseases in children after urinary tract infections. According to the statistics of modern urology, pathology is the most common cause of early disability of patients due to the development of chronic renal failure. The development of acute glomerulonephritis is possible at any age, but, as a rule, the disease occurs in patients under the age of 40 years.
Causes
The cause of the disease is usually acute or chronic streptococcal infection (sore throat, pneumonia, tonsillitis, scarlet fever, streptoderma). The disease can develop as a consequence of measles, chickenpox or SARS. The probability of pathology increases with prolonged exposure to the cold in conditions of high humidity (“trench” nephritis), since the combination of these external factors changes the course of immunological reactions and causes a violation of the blood supply to the kidneys.
There is evidence that glomerulonephritis is associated with diseases caused by certain viruses, Toxoplasma gondii, Neisseria meningitidis, Streptococcus pneumoniae and Staphylococcus aureus. In the vast majority of cases, kidney damage develops 1-3 weeks after streptococcal infection, and the results of studies most often confirm that glomerulonephritis was caused by “nephritogenic” strains of b-hemolytic streptococcus group A.
When an infection caused by nephritogenic strains of streptococcus occurs in the children’s collective, symptoms of acute glomerulonephritis are noted in 3-15% of infected children. During laboratory tests, changes in urine are detected in 50% of children and adults around the patient, which indicates a torpid (asymptomatic or low-symptomatic) course of glomerulonephritis.
After scarlet fever, an acute process develops in 3-5% of children treated at home and in 1% of patients treated in a hospital. ARVI can lead to the development of glomerulonephritis in a child who suffers from chronic tonsillitis or is a carrier of cutaneous nephritogenic streptococcus.
Pathogenesis
Antigen-antibody complexes are deposited in the capillaries of the renal glomeruli, impairing blood circulation, as a result of which the process of primary urine production is disrupted, water, salt and metabolic products are delayed in the body, the level of antihypertensive factors decreases. All this leads to arterial hypertension and the development of renal failure.
Classification
Glomerulonephritis can occur acutely or chronically. There are two main variants of the course of the acute process:
- Typical (cyclic). Characterized by a rapid onset and significant severity of clinical symptoms;
- Latent (acyclic). Erased form, characterized by gradual onset and mild symptoms. It is a significant danger due to late diagnosis and a tendency to transition to chronic glomerulonephritis.
In chronic glomerulonephritis, the following course options are possible:
- Nephrotic. Urinary symptoms predominate.
- Hypertensive. There is an increase in blood pressure, urinary syndrome is poorly expressed.
- Mixed. It is a combination of hypertensive and nephrotic syndromes.
- Latent. A fairly common form characterized by the absence of edema and arterial hypertension with a weakly expressed nephrotic syndrome.
- Hematuric. The presence of erythrocytes in the urine is noted, the remaining symptoms are absent or poorly expressed.
Glomerulonephritis symptoms
Symptoms of an acute diffuse process appear one to three weeks after an infectious disease, usually caused by streptococci (angina, pyoderma, tonsillitis). Acute glomerulonephritis is characterized by three main groups of symptoms: urinary (oliguria, micro- or macrohematuria), edematous, hypertensive. Acute glomerulonephritis in children, as a rule, develops rapidly, flows cyclically and usually ends with recovery. When acute glomerulonephritis occurs in adults, an erased form is more often observed, which is characterized by changes in urine, the absence of general symptoms and a tendency to transition to a chronic form.
The disease begins with an increase in temperature (significant hyperthermia is possible), cognition, general weakness, nausea, decreased appetite, headache and pain in the lumbar region. The patient becomes pale, his eyelids swell. In acute glomerulonephritis, there is a decrease in diuresis in the first 3-5 days from the onset of the disease. Then the amount of urine excreted increases, but its relative density decreases. Another permanent and obligatory sign of glomerulonephritis is hematuria (the presence of blood in the urine). In 83-85% of cases, microhematuria develops. In 13-15%, it is possible to develop macrohematuria, which is characterized by urine the color of “meat slops”, sometimes black or dark brown.
One of the most specific symptoms is facial swelling, pronounced in the morning and decreasing during the day. It should be noted that the retention of 2-3 liters of fluid in the muscles and subcutaneous fat is possible without the development of visible edema. In overweight preschool children, the only sign of edema sometimes becomes a certain compaction of subcutaneous tissue.
60% of patients develop hypertension, which in severe form of the disease can last up to several weeks. In 80-85% of cases, acute glomerulonephritis causes damage to the cardiovascular system in children. There may be violations of the function of the central nervous system and an increase in the liver. With a favorable course, timely diagnosis and the beginning of treatment, the main symptoms (edema, hypertension) disappear within 2-3 weeks. Full recovery is noted in 2-2.5 months.
All forms of chronic glomerulonephritis are characterized by a recurrent course. Clinical symptoms of exacerbation resemble or completely repeat the first episode of the acute process. The probability of relapse increases in the spring-autumn period and occurs 1-2 days after exposure to an irritant, which is usually a streptococcal infection.
Complications
Acute diffuse glomerulonephritis can lead to the development of acute renal failure, acute heart failure, acute renal hypertensive encephalopathy, intracerebral hemorrhage, transient vision loss. A factor that increases the likelihood of the transition from acute to chronic form is hypoplastic kidney dysplasia, in which the renal tissue develops with a lag from the chronological age of the child.
For a chronic diffuse process characterized by a progressive course and resistance to active immunosuppressive therapy, a secondary shrunken kidney becomes the outcome. Glomerulonephritis occupies one of the leading places among kidney diseases that lead to the development of renal failure in children and early disability of patients.
Diagnostics
The diagnosis is made on the basis of anamnesis (recently transferred infectious disease), clinical manifestations (edema, hypertension) and laboratory data. According to the results of the analyses, the following changes are characteristic:
- micro- or macrohematuria. With macrohematuria, urine turns black, dark brown, or acquires the color of “meat slops”. With microhematuria, there is no change in the color of urine. In the first days of the disease, the urine contains mainly fresh red blood cells, then leached.
- moderate (usually within 3-6%) albuminuria for 2-3 weeks;
- granular and hyaline cylinders in microhematuria, erythrocytic – in macrohematuria according to the results of microscopy of urinary sediment;
- nocturia, decreased diuresis during the Zimnitsky test. The preservation of the concentration capacity of the kidneys is confirmed by the high relative density of urine;
- decreased filtration capacity of the kidneys according to the results of the endogenous creatinine clearance study;
According to the results of a general blood test in acute glomerulonephritis, leukocytosis and increased ESR are detected. A biochemical blood test confirms an increase in the content of urea, cholesterol and creatinine, an increase in the titer of AST and ASL-O. Acute azotemia is characteristic (an increase in the content of residual nitrogen). Ultrasound of the kidneys and ultrasound of the renal vessels is performed. If the laboratory and ultrasound data are doubtful, a kidney biopsy and subsequent morphological examination of the obtained material are performed to confirm the diagnosis.
Glomerulonephritis treatment
Pathology is treated in a hospital setting. Diet No. 7 is prescribed, bed rest. Patients are prescribed antibacterial therapy (ampicillin + oxacillin, penicillin, erythromycin), immunity correction is performed with non-hormonal (cyclophosphamide, azathioprine) and hormonal (prednisolone) drugs. The complex of therapeutic measures includes anti-inflammatory treatment (diclofenac) and symptomatic therapy aimed at reducing edema and normalizing blood pressure.
Subsequently, spa treatment is recommended. After suffering acute glomerulonephritis, patients have been under the supervision of a nephrologist for two years. In the treatment of a chronic process during an exacerbation, a set of measures similar to the therapy of acute glomerulonephritis is carried out. The treatment regimen during remission is determined based on the presence and severity of symptoms.