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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.

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EXPERIMENTAL G LOMERULONEPHRIT IS II. ImamoLoolc EVENTS IN THE PATHOGENESIS OF NEPttROTOXIC SERUM NEPHRITIS IN TttE RAT

TL;DR: The possibility of an immunologic basis for human glomerulonephrifis is supported by a number of imrnunologieally induced forms of experimental glomeruIL, and one of the most thoroughly studied of these experimental models is nephrotox~c serum nephritis.
Posted ContentDOI

Clinical characteristics and outcomes of idiopathic membranous nephropathy with glomerular IgM deposits

TL;DR: Glomerular IgM deposition is associated with younger age, more severe FSGS lesions and C1q deposition, and worse renal outcomes in IMN, and was an independent risk factor of eGFR decline of ≥5 mL/min/1.73 m2 per year during follow-up.

Pathological studies on nephrotoxic serum nephritis accelerated with rabbit γ-globulin in mice.

TL;DR: It appears this nephritic model shares a common pathology with human membranoproliterative glomerulonephritis type 1 and crescentic glomersul onephritis and can be considered an appropriate model for producing severe nephritis for short periods.
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