Chapter 22. Glomerulonephritis
Glomerulonephritis (GN) is a group of morphologically heterogeneous immuno-inflammatory diseases with a predominant lesion of glomeruli, but with mandatory involvement of tubules and interstitial tissue. GN can be either independent nosological entities, or one of the manifestations of systemic autoimmune diseases (SLE, systemic vasculitis, etc.), paraneoplastic syndrome (solid and hematological tumors), systemic infections (viral, bacterial, fungal, parasitic, etc.).
Etiology
Etiologic factor can be identified in 80–90% of cases of acute glomerulonephritis (AGN) and in 5–10% of chronic glomerulonephritis (CGN). In other patients, the cause remains unknown. GN development can be caused by infections (bacterial, viral, fungal, parasitic, protozoal). The etiological factors may also include toxic substances, medications, allergens, tumors acting indirectly through immune mechanisms including as part of immediate hypersensitivity, as well as endogenous Ag (tumor, DNA, etc.). Exposure to cold is an important trigger factor in the occurrence and exacerbation of GN, sometimes having an independent value, as well as insolation (for example, in lupus GN).
Classification
Classification of GN is based on the identification of:
- variant of the course (acute, subacute/rapidly progressive, chronic);
- leading clinical syndrome or a combination of them (for more detailed clinical classification, see section “Chronic Glomerulonephritis”);
- type of morphological changes (for more detailed morphological classification, see section “Chronic Glomerulonephritis”).
As the outcome of any form of GN, generalized renal tissue fibrosis (nephrosclerosis) may develop, which clinically corresponds to chronic renal failure (CRF), including terminal stage.