It is useful, however, to first review some important general considerations involving the pathology, pathogenesis, and clinical characteristics of the glomerulopathies and an approach to differential diagnosis. Many of the glomerular diseases are defined by the relatively specific pathological changes that are seen on light microscopy, immunofluorescent microscopy, or electron microscopy. Glomerular diseases are usually caused by immunologic factors. On immunofluorescent microscopy, anti-GBM antibody disease is associated with linear immunoglobulin and complement deposition.
Several factors appear to determine the site at which immune deposition is likely to occur.
The rate at which immune complexes are removed also can contribute to the susceptibility to glomerular disease. The latter process is mediated in part by attachment of the complexes to C3b receptors on erythrocytes. Decreased activation of this system is associated with impaired removal of immune complexes and an increased propensity for the development of immune complex diseases. Both the site of immune complex deposition and the factors of the complement system play an important role in the type of glomerular injury that is induced and in the subsequent clinical manifestations. Activation of the complement system leads to the generation of C3a and C5a, which can attract circulating neutrophils and mononuclear cells and lead to a local inflammatory response.