Pathogenesis

Almost all of the primary glomerulonephritides and the majority of the secondary glomerulonephritides have an immunological basis. Immune damage may be either antibody, cell or complement mediated. However the most important mechanism is antibody mediated glomerular damage.

Antibody mediated damage is due to either one OR both of the following mechanisms:

• injury by antibodies reacting in situ with either fixed insoluble glomerular antigens or with circulating antigens which have become planted in the glomerulus; examples include anti-GBM disease (the cause of glomerular injury in Goodpasture's syndrome) and post-streptococcal glomerulonephritis
• injury resulting from the deposition within the glomerulus of circulating soluble antigen-antibody immune complexes; examples include post-streptococcal glomerulonephritis and the glomerulonephritis associated with SLE

Glomerular damage by T cell-mediated immunity is less understood but the hypothesis is an attractive one and there are clues to its existence as a mechanism in both experimental and human glomerulonephritis.

Complement mediated glomerular damage occurs in type II membranoproliferative and other proliferative glomerulonephritides.

Following the initial immunological insult further glomerular damage may be brought about by one or more of the following:

• neutrophils (stimulated by complement components)
• terminal membrane attack complex of complement (C5b-C9)
• platelets, monocytes and macrophages
• the coagulation system via fibrin deposition