Masugi Nephritis Produced by the Antiserum to Heterologous Glomerular Basement Membrane

Nishihara, Tohru; Kusuyama, Yoshio; Gen, Eisei; Tamaki, Nobuhiko; Saito, Koji

doi:10.1111/j.1440-1827.1981.tb00986.x

Cited by 8 publications

(2 citation statements)

References 8 publications

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“…Although no quantitative assessment of these infil trated cells was made, the potency of the NT given in the present study may possibly mask the role of these factors. Related details have been described elsewhere [12]. In addi tion, CPM treatment enhances delayed hypersensitive reac tion in mice [5].…”

Section: Discussionmentioning

confidence: 99%

Effect of Cyclophosphamide on Murine Nephrotoxic Nephritis

Kusuyama¹,

Nishihara²,

Gen³

et al. 1983

Nephron

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We studied the effect of cyclophosphamide (CPM) on development of severe glomerular lesions in a model of murine nephrotoxic nephritis (NTN). CPM treatment (300 mg/kg) before initiation of the first phase on NTN showed no host antibody depositions along the glomerular basement membrane, as revealed by immunofíuorescence; however, the histological study revealed no significant difference in the degree of renal damage between the control and the CPM-treated mice. Therefore, the severe glomerular lesions in murine NTN may be induced without antibody response to nephrotoxin, in the glomerulus.

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Section: Discussionmentioning

confidence: 99%

Effect of Cyclophosphamide on Murine Nephrotoxic Nephritis

Kusuyama¹,

Nishihara²,

Gen³

et al. 1983

Nephron

Self Cite

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“…The other is that the drugs which are often used as a remedy for nephritis in clinical cases show the remission of this RGG accelerated NTS nephritis. Little attention has been paid to the experi mental nephritis in mice (9)(10)(11)(12)(13)(14).…”

Section: Discussionmentioning

confidence: 99%

Experimental glomerulonephritis in mice as a model for immunopharmacological studies.

et al. 1982

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Abstract-The experimental glomerulonephritis was caused by the intra venous injection of a subnephrotoxic dose of nephrotoxic serum in the mice which had been previously immunized with rabbit IgG and complete Freund's adjuvant.The elevation of urinary protein excretion, serum blood urea nitrogen level and cholesterol level and the decrease of serum albumin level were demonstrated in nephritic mice. Hypercellularity in the glomerulus and hyalinosis in tubular system were observed in histopathological studies. The clinical signs in this experimental model were similar to human glo merulonephritis.In a transfer experiment, sensitized lymphocytes against rabbit IgG were necessary for the onset of disease.Clear remission of glomerulonephritis was indicated by the administration of cyclophosphamide or 6-mercaptopurine.Glucocorticoids showed moderate suppression of the development of this nephritis. These evidences suggest that this experimental model is useful for the immunopharmacological research of glomerulonephritis.

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Anti-GBM nephritis in the mouse: severe proteinuria in the heterologous phase

Assmann

Tangelder

Lange

et al. 1985

Vichows Archiv A Pathol Anat

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Highly reproducible anti glomerular basement membrane (GBM) nephritis has been induced in the mouse after a single injection of rabbit or goat antibody against purified homologous GBM. The severity of albuminuria was closely related to the amount of antibody given. With doses of 4 mg or more, low serum albumin concentrations, sometimes accompanied by ascites and oedema, were observed after 1 week. Glomerular injury was characterized by an initial accumulation of polymorphonuclear granulocytes followed by thrombosis and necrosis, the extent of which defined the outcome of the glomerulonephritis. With high doses of antibody the exudative lesions entered a chronic phase, while at doses lower than 2 mg remission of the lesions occurred. Immunofluorescence studies showed prompt linear fixation of the injected antibodies to the glomerular capillary wall, accompanied by immediate binding of C3 in a fine granular pattern. Fibrin deposits appeared at 2 h in some glomeruli, increased thereafter, and were present after one day in more than 90% of the glomeruli in mice that had received 4 mg of antibody. This new reproducible model in the mouse is suited for the study of the relationship between activation of mediator systems, histological lesions, and proteinuria.

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Masugi Nephritis Produced by the Antiserum to Heterologous Glomerular Basement Membrane

Cited by 8 publications

References 8 publications

Effect of Cyclophosphamide on Murine Nephrotoxic Nephritis

Effect of Cyclophosphamide on Murine Nephrotoxic Nephritis

Experimental glomerulonephritis in mice as a model for immunopharmacological studies.

Anti-GBM nephritis in the mouse: severe proteinuria in the heterologous phase

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