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Experimental Streptococcal Glomerulonephritis: Longitudinal Study of a Laboratory Model Resembling Human Acute Poststreptococcal Glomerulonephritis
An experimental model of acute poststreptococcal glomerulonephritis is described by an early transient phase of minimal proteinuria which was not restricted to the nephritogenic strain, a latent period, and a secondary recrudescence of a much greater proteinuria only in animals exposed to the nephri...
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Published in: | The Journal of infectious diseases 1970-10, Vol.122 (4), p.249-259 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | An experimental model of acute poststreptococcal glomerulonephritis is described by an early transient phase of minimal proteinuria which was not restricted to the nephritogenic strain, a latent period, and a secondary recrudescence of a much greater proteinuria only in animals exposed to the nephritogenic strain. This secondary phase of proteinuria developed shortly after the onset of measurable type-specific serum antibodies and at the same time that fixed gamma-globulins, streptococcal M protein, and beta-1-C globulins were first detected in the region of the basement membrane of the glomerulus. The gamma-globulins were eluted from the kidneys of these animals and reacted only with type 12 streptococcal M protein. These findings suggest that the secondary phase of proteinuria, which was restricted to the nephritogenic strain, is mediated by the fixation of complexes of type 12 streptococcal M protein and type-12-specific antibody in the region of the basement membrane of the glomerulus. In contrast, the early transient phase of proteinuria, which was not restricted to the nephritogenic strain, occurred in the absence of such immunologic changes and is presumed to reflect a toxic response to some cellular or extracellular product of the streptococcus. The resemblance of this model to a similar disease observed in man suggests that the same pathogenetic mechanisms may be operative. |
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ISSN: | 0022-1899 1537-6613 |
DOI: | 10.1093/infdis/122.4.249 |