What causes chronic glomerulonephritis?

The etiologic factor is established in 80-90% of patients with acute glomerulonephritis and only in 5-10% of cases of chronic glomerulonephritis. In 30% of adult patients with membranous nephropathy, it is possible to identify a connection between the disease and hepatitis B virus antigens and drug antigens. There are 4 main groups of etiologic factors that initiate the development of chronic glomerulonephritis.

• Infectious factors:
  • microbial (beta-hemolytic streptococcus group A, staphylococcus, pathogens of tuberculosis, malaria, syphilis);
  • viral (hepatitis B and C viruses, cytomegalovirus, human immunodeficiency virus, herpes viruses, etc.).
• Mechanical and physical impacts:
  • injury;
  • insolation;
  • hypothermia.
• Allergic and toxic effects:
  • food products (obligate allergens, gluten, etc.);
  • chemicals (heavy metal salts, gold preparations);
  • medicines;
  • narcotic substances.
• Vaccinations.

Pathogenesis of chronic glomerulonephritis

Depending on the pathogenetic mechanisms of development of chronic glomerulonephritis, several of its forms are distinguished.

• Glomerulonephritis associated with GBM charge disturbance in children with minimal changes.
• Immune complex glomerulonephritis (which accounts for 80-90% of all glomerulonephritis) is caused by increased formation of pathogenic CIC, formation of immune complexes in situ, and decreased phagocytosis.
• Antibody form of glomerulonephritis caused by the appearance of antibodies to GBM ( Goodpasture's syndrome, some variants of RPGN).

In most cases, these pathogenetic mechanisms are combined, but usually there is one leading one.

In IgA nephropathy, genetic and acquired factors, including immunoregulation disorders, can lead to impaired glycosylation of IgA molecules with their subsequent deposition in the mesangial matrix, contributing to the development of glomerular damage with the activation of various cytokines, vasoactive factors and a number of chemokines. Molecular genetic studies of the blood of patients with familial IgA nephropathy revealed an association of the disease in 60% of patients with a gene mutation on chromosome 6 in the 6q22-23 region. Recently, a connection was established between the development of IgA nephropathy and a gene mutation on chromosome 4 in the 4q22. l-32.21 and 4q33-36.3 loci. IgA nephropathy is a multifactorial disease.

In pathogenesis, the following are important: long-term circulation of causative antigens, development of autoimmune reactions, changes in T-cell immunity, deficiency of T-suppressors, deficiency of C3, C5 components of complement, possibly genetically determined; sharp decrease in serum and leukocyte interferon.

During the exacerbation of chronic glomerulonephritis, all pathogenesis links characteristic of acute glomerulonephritis are important. Of particular importance in progression is the hemodynamic pathway - a violation of intrarenal hemodynamics with the development of intraglomerular hypertension and hyperfiltration. Hypertension leads to progressive damage to the glomeruli and rapid formation of nephrosclerosis, with hyperfiltration and proteinuria being markers of this process. Under the influence of increased intraglomerular pressure, the porosity of the basal membranes of the renal capillaries increases with the subsequent development of their structural disorders. At the same time, mesangial infiltration with plasma proteins increases, which ultimately leads to the development of sclerosis in the renal glomeruli and a decrease in renal function.