ArticleInternational journal of experimental pathology2003
Production of a new model of slowly progressive Heymann nephritis.
Article in International journal of experimental pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Antibody-initiated beneficial and harmful immune responses.Immunologic research · 2018Review
- Tolerance, loss of tolerance and regaining tolerance to self by immune-mediated events.Immunologic research · 2017Article
- Regaining tolerance to a self-antigen by the modified vaccination technique.Clinical reviews in allergy & immunology · 2013Review
- Production of heterologous IgG antibody against Heymann nephritis antigen by injections of immune complexes.International journal of experimental pathology · 2012Article
- Preventative and therapeutic vaccination to combat an experimental autoimmune kidney disease.Biologics : targets & therapy · 2007Article
- Down-regulation of pathogenic autoantibody response in a slowly progressive Heymann nephritis kidney disease model.International journal of experimental pathology · 2004Article
- Presence of immunoglobulin M antibodies around the glomerular capillaries and in the mesangium of normal and passive Heymann nephritis rats.International journal of experimental pathology · 2004Article
- Production of Heymann nephritis by a chemically modified renal antigen.International journal of experimental pathology · 2004Article
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Authors and funding
4 authors.
Funding
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Abstract
A slowly progressive autoimmune kidney disease was induced in Sprague Dawley rats by subcutaneous injection of a chemically modified kidney antigen (rKF3), incorporated into Alum and Distemper complex vaccine, followed by subcutaneous injections of an aqueous preparation of the same antigen. Pathogenic autoantibodies developed, which reacted with fixed glomerular nephritogenic antigen. Subsequently, immunopathological events lead to chronic progressive immune complex glomerulonephritis and proteinuria. The slowly developing disease was morphologically and functionally similar to Heymann nephritis (HN). The damage observed in the kidneys of experimental animals at 8 weeks and at the end of the experiment was examined by direct fluorescent antibody test, histology and electron microscopy. The changes were similar to the typical lesions found in HN rat kidneys, but less severe. Animals became proteinuric from 17 weeks onward (instead of the usual 4-8 weeks). By the end of the experiment, at 8 months, 100% of the rats were proteinuric. This new experimental model of autoimmune kidney disease, which is not complicated by intraperitoneal deposition and retention of Freund's complete adjuvant and renal tubular antigens, allowed us to investigate the pathogenesis of the disease processes from a different aspect, and promises to be a useful and improved model for the investigation of future treatment options.
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