It is now firmly established that a variety of immune mechanisms are responsible for most glomerulonephritides, and that they act largely through the activation of complement, recruitment of leukocytes and macrophages, stimulation of clotting, and liberation of vasoactive kinins. The etiological factors which originate the process can be either infectious agents, endogenous antigens (DNA, tumoral antigens), or exogenous toxins. The activation of the immune system may take different forms, including: the production of anti-GBM antibodies which may at times cross-react with other tissues or organs; the formation of antigen-antibody complexes of specific solubility, molecular size, permeability, which will variously tend to localize in the mesangium, in subepithelial, or subendothelial deposits; the development of antibodies which specifically react with native antigens present in the GBM in a discontinuous manner; the trapping of antigens within the GBM, which then act as "planted" antigens. The morphologic type of glomerulonephritis and its clinical course will probably depend upon the predominant type of antigen produced, its persistence, its mode of action, and the concurrent degree of activation of complement, recruitment of PMNs and macrophages, stimulation of the clotting system, as well as upon the development of hypertension and the functional response of the kidney to reduced renal mass. Whether or not it will be possible, in the future, to relate directly each type of glomerulonephritis to specific etiologic agents, to the type of immune response, and to genetic predisposition is unclear, but this will determine whether it will be possible to devise specific treatment strategies for each condition.(ABSTRACT TRUNCATED AT 250 WORDS)
