Abstract
It appears that in human renal isografts glomerulonephritis in the transplant may be a recurrence of the original disease. In the allograft, nephritis may be either recurrence, an intrinsic part of the rejection process itself, or acquisition de novo of the disease. A number of parallels to both antiglomerular basement membrane disease and circulating antigen-antibody complex disease in the animal model are suggested, but with the possible exception of an occasional demonstration of anti-GBM disease, proof that such mechanisms operate in the glomerulonephritis developing in the human allograft is at present lacking.
MeSH terms
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Acute Disease
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Adrenal Cortex Hormones / pharmacology
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Antigen-Antibody Complex
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Antigens, Bacterial
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Antilymphocyte Serum / pharmacology
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Autoantibodies
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Basement Membrane / immunology
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Chronic Disease
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Disease Models, Animal
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Fibrin
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Glomerulonephritis / etiology*
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Glomerulonephritis / immunology
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Glomerulonephritis / pathology
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Graft Rejection / complications*
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Graft Rejection / immunology
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Humans
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Kidney / drug effects
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Kidney Glomerulus / immunology
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Kidney Glomerulus / pathology
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Kidney Transplantation*
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Recurrence
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Streptococcus / immunology
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Transplantation, Homologous
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Transplantation, Isogeneic
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Virus Diseases / complications
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Virus Diseases / immunology
Substances
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Adrenal Cortex Hormones
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Antigen-Antibody Complex
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Antigens, Bacterial
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Antilymphocyte Serum
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Autoantibodies
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Fibrin