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
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Advances in membranous nephropathy: Success stories of a long journey
TL;DR: 1. embranous nephropathy is characterized by an accumulation of immune deposits on the outer aspect of the glomerular basement membrane.
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Immunopathology of the nephrotic syndrome associated with renal vein thrombosis. Report of two cases and brief review of the literature.
TL;DR: Renal tissue from two patients with the nephrotic syndrome and renal vein thrombosis was studied by immunofluorescence microscopy in addition to conventional histologic and electron microscopic technics, finding the pathogenesis of the lesion must remain in doubt.
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New 'Antigens' in Membranous Nephropathy.
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Regulatory gamma delta T cells in Heymann nephritis express an invariant Vγ6/Vδ1 with a canonical CDR3 sequence
TL;DR: The restriction in γδ TCR seen in two completely different models of kidney injury and the expression of an innate activating molecule NKG2D suggests that the γ δ T cells may be responding to tissue stress from injury and producing a regulatory response.
Journal ArticleDOI
A Small N-Terminal 60-kD Fragment of gp600 (Megalin), the Major Autoantigen of Active Heymann Nephritis, Can Induce a Full-Blown Disease
TL;DR: Results indicate that this small fragment, retaining the natural disulfide bonds and probably its overall structure, contains those B and T cell epitopes that are sufficient to produce this organ-specific autoimmune disease.