What causes chronic glomerulonephritis?

Etiological factor is established in 80-90% of patients with acute glomerulonephritis and only 5-10% of cases of chronic glomerulonephritis. In 30% of adults with membranous nephropathy, it is possible to identify the association of the disease with antigens of the hepatitis B virus, drug antigens. There are 4 main groups of etiological factors initiating the development of chronic glomerulonephritis.

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

Pathogenesis of chronic glomerulonephritis

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

• Glomerulonephritis, associated with a violation of the charge of GBM in children with minimal changes.
• Immunocomplex glomerulonephritis (making up 80-90% in the structure of all glomerulonephritis), caused by increased formation of pathogenic CECs, formation of immune complexes in situ, and reduction of phagocytosis.
• The anti-inflammatory form of glomerulonephritis, caused by the appearance of antibodies to GBM ( Goodpasture syndrome, some variants of the GPGN).

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

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

In the pathogenesis, long circulation of cause-significant antigens, development of autoimmune reactions, changes in T cell immunity, deficiency of T suppressors are important. Deficiency of C3, C5 of complement components, possibly genetically conditioned; a sharp decrease in serum and leukocyte interferon.

In the period of exacerbation of chronic glomerulonephritis, all links of pathogenesis characteristic of acute glomerulonephritis are important. Of particular importance in progression is the hemodynamic pathway - the violation of intrarenal hemodynamics with the development of intra-cerebral hypertension and hyperfiltration. Hypertension leads to progressive glomerular damage and the rapid formation of nephrosclerosis, with hyperfiltration and proteinuria markers for this process . Under the influence of increased intra-cerebral pressure, the porosity of the basal membranes of the renal capillaries increases with the subsequent development of their structural disturbances. Simultaneously, infiltration of mesangium with plasma proteins intensifies, which ultimately leads to the development of sclerosis in the renal glomeruli and the reduction of renal functions.