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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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Early initiation of immunosuppressive treatment in membranous nephropathy patients

TL;DR: In contrast to Western countries, early immunosuppression (even steroid monotherapy) in patients is associated with better remission in the 1st year and renal preserve, especially with oriental ethnic background.
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Effects of systemic complement activation on renal circulation of rats.

TL;DR: The results suggest that injection of CVF and the liberation of high amounts of the anaphylatoxins, C3a and C5a, induces the release of TXA2, which contributes to the early renal effects and the formation of cysteinyl‐leukotrienes which play an important role in the late phase of systemic complement activation.
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Autoimmune diseases of the kidney.

TL;DR: The various autoimmune renal diseases are arbitrarily classified as if they were induced by a single pathogenic mechanism (Table I) and two groups of animal models of nephritis will be described.
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Aliskiren Regulates Neonatal Fc Receptor and IgG Metabolism with Attenuation of Anti-GBM Glomerulonephritis in Mice

TL;DR: Results suggest that suppression of FcRn and PRR and regulation of IgG metabolism may be related to the attenuation of anti-GBM GN by aliskiren.
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