Argument for the Classical Concept:

Passive Anti-GBM Nephritis

(Masugi Nephritis)

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The experimental induction of anti-GBM nephritis is not dependent on Freundīs adjuvant because it is also seen after injection of foreign anti-GBM antibodies alone (foreign, or heterologous: from another animal species), just as passive Heymann nephritis can be produced by injecting foreign anti-kidney antibodies (Unanue & Dixon 1962).


Counter-Argument


Again, just as in passive Heymann nephritis, this type of glomerulonephritis can be separated into two steps. The first step, the heterologous phase, is followed by trace proteinuria at most and no renal damage is seen. At this stage only rabbit antibodies can be seen in the glomeruli. A few days later a serious glomerulonephritis may develop. At this stage, the autologous phase, the rabbits own antibodies can be seen in the glomeruli also, obviously attacking the foreign antibodies that are located along the glomerular basement membrane. Thus, two immunological process are taking place in the glomeruli: immune complex formation between the foreign (heterologous) anti-GBM antibodies and the GBM, which is harmless; and immune complex formation between the ratīs own (autologous) antibodies and the foreign antibody. And again, the second reaction can be abolished if the animals are made tolerant to the injected, foreign antibodies before the experiment (Hammer & Dixon 1963).

 

Once again it has been demonstrated that a direct attack on the kidney by oneīs own antibodies does not produce glomerulonephritis. A crucial factor is missing.

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