Ultrastructural studies in passive in situ immune complex glomerulonephritis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1989-12

AUTHORS

M. Sasaki, S. Batsford, F. Thaiss, T. Oite, A. Vogt

ABSTRACT

Morphologic studies were performed in a passive model of in situ immune complex glomerulonephritis in rats. The formation and fate of subepithelial immune complexes as well as the role of glomerular polyanion in the induction of disease were examined. Unilateral in situ immune complex glomerulonephritis was induced in rats by perfusion of cationised horse spleen ferritin (pI > 9.5) (400 μg/rat) into the left kidney followed by systemic injection of 0.2 ml (= 400 μg precipitating antibody) of sheep anti-ferritin antiserum 2 h later. This schedule induced glomerulonephritis with proteinuria (mean maximum 100 mg/24 h between the 5th and the 12th day). Rats were sacrificed at intervals between 1 h and 42 days after induction of glomerulonephritis, samples of renal tissue were examined by light, immunofluorescence and electron microscopy (including staining of anionic sites by polyethyleneimine). The lesion induced closely resembled that of membranous glomerulonephritis in man as massive subepithelial deposits were seen with very little cellular infilatration or proliferation. The antigen (ferritin) deposits were initially located subepithelially; from 2 weeks onwards intramembranous deposits in the thickened basement membrane were present, the apparent translocation being due to excessive newly synthesised basement membrane material which encloses the deposits. A loss of anionic sites in the lamina rara interna, lamina rara externa and on the epithelial cell surface coat preceeded the development of proteinuria. More... »

PAGES

173

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf02890068

DOI

http://dx.doi.org/10.1007/bf02890068

DIMENSIONS

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