It is now generally accepted that a majority of the various forms of the disease glomerulonephritis with perhaps some direct toxic modifications at the onset are primarily immunologic in nature. The work of a number of investigators (1) has pointed out that this immunologic insult may take two basic forms. The first depends upon the production of antigen-antibody complexes which are subsequently trapped in the glomerular capillary walls or filter. The second mechanism may involve the formation of injurious agents (huoral and/or cellular) capable of reacting with the renal basement membrane tissue of the host. The end result of both forms of immunological intrusion is inflammation of the renal tissue, primarily basement membrane, with of course, help from complement components and leukocytes.

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