scispace - formally typeset
Journal ArticleDOI

Production of nephrotic syndrome in rats by Freund's adjuvants and rat kidney suspensions.

TLDR
The small amounts of rat kidney proteins used, support the interpretation that an isoand autosensitization mechanism is at play, and help clarify the mechanism behind the severe nephrotic syndrome noted in 20 rats given Freund's adjuvants and a supernate of rat kidneys suspension by intraperitoneal injection.
Abstract
Summary1) A severe nephrotic syndrome was noted in 20 rats given Freund's adjuvants and a supernate of rat kidney suspension by intraperitoneal injection. When kidney tissue was replaced by liver, only 3 of 21 animals developed a much milder renal disease. Lung or muscle suspensions failed to induce proteinuria in 10 rats. 2) In large doses (0.5 ml) Freund's adjuvants alone produced a mild nephrotic disease in 3 of 10 rats. Even though the smaller amounts of the adjuvants usually used (0.25 ml) never produced proteinuria, slight histological alterations of the glomerular structure were frequently noted. 3) In contradistinction to other tissue suspensions addition of rat kidney supernate enhanced the effect of adjuvants markedly and regularly. 4) The small amounts of rat kidney proteins used, support the interpretation that an isoand autosensitization mechanism is at play.

read more

Citations
More filters
Journal ArticleDOI

Treatment of primary membranous nephropathy: where are we now?

TL;DR: New data on the use of rituximab suggest it should be considered as a potential initial therapy in the treatment of patients with primary MN and quantification and follow-up of antiPLA2R Abs levels can help in assessing prognosis and evaluate the response to treatment.
Journal ArticleDOI

Suppression of experimental membranous glomerulonephritis in rats by an anti-MHC class II antibody.

TL;DR: It is demonstrated that the MHC class II molecule itself is directly involved in the pathogenesis of HN, and suggested that this therapy would be any better (or less toxic) than nonselective immunosuppressants in the treatment of IMN.
Journal Article

Role of dipeptidyl peptidase IV (gp 108) in passive Heymann nephritis. Use of dipeptidyl peptidase IV-deficient rats.

TL;DR: The results indicate that DPP IV may contribute to, but is not essential for, the induction of PHN.
Journal ArticleDOI

Glomerular T cells in Heymann nephritis.

TL;DR: Investigation of T cells infiltrating the glomerulus in HN in Lewis rats by polymerase chain reaction (PCR) of their Vβ chains, CDR3 spectratyping and sequencing found at least two, and possibly more, Vβ genes are involved in the pathogenesis of HN.
Journal ArticleDOI

Proteinuria induced by anti-dipeptidyl peptidase IV (gp108); role of circulating and glomerular antigen

TL;DR: Results suggest that proteinuria is induced by direct binding of anti‐ DPPIV antibody to the membrane antigen of glomerular cells.
Related Papers (5)