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Transfer of anti‐glomerular basement membrane antibody‐induced glomerulonephritis in inbred rats with isologous antibodies from the urine of nephritic rats
Author(s) -
Sado Yoshikazu,
Naito Ichiro,
Okigaki Tohru
Publication year - 1989
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.1711580410
Subject(s) - nephritis , glomerulonephritis , antibody , glomerular basement membrane , basement membrane , antigen , urine , autoantibody , proteinuria , nephritic syndrome , immunology , medicine , kidney , pathology
Anti‐glomerular basement membrane antibody‐induced glomerulonephritis (anti‐GBM nephritis) was transferred from nephritic rats to normal recipient rats with isologous antibodies obtained from the urine of the nephritic rats. The original actively‐immunized anti‐GBM nephritis was induced in inbred WKY/NCrj rats by injecting the nephritogenic antigen from bovine renal basement membranes. Excreted urinary antibodies were collected, purified, and then injected into recipient rats of the same strain, Haematuria and proteinuria appeared on day 2 and day 3, respectively; both became heavier and reached a plateau by day 5. Endocapillary hypercellularity of mononuclear cells in glomeruli was the first histological change, which was observed from day 2, and later extracapillary changes such as fibrin deposition, capsular adhesion, and crescent formation were observed. These histological changes were the same as those seen in the actively‐immunized nephritis. The results demonstrate that anti‐GBM nephritis is clearly induced by autoantibodies. This new passively‐immunized model of anti‐GBM nephritis makes it possible and easier to analyse further the mechanism of anti‐GBM nephritis because only isologous antibodies are used. This study also indicates that the urine of the nephritic rat is a good source of autoantibodies.