Experimental IgA Nephropathy Induced by Coxsackie B4 Virus in Mice

Viruses have been suspected to be etiological agents of IgA nephropathy. Recently, viruses were detected in renal tissues from patients with IgA nephropathy. We tried to cause lesions similar to IgA nephropathy by inoculating virus into mice and to detect virus RNA in the lesion by in situ hybridiza...

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Published inAmerican journal of nephrology Vol. 17; no. 1; pp. 81 - 88
Main Authors Yoshida, Kazuo, Suzuki, Junzo, Suzuki, Shigeo, Kume, Kazunari, Mutoh, Shigeo, Kato, Kazuo, Suzuki, Hitoshi
Format Journal Article
LanguageEnglish
Published Basel, Switzerland Karger 01.01.1997
S. Karger AG
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Summary:Viruses have been suspected to be etiological agents of IgA nephropathy. Recently, viruses were detected in renal tissues from patients with IgA nephropathy. We tried to cause lesions similar to IgA nephropathy by inoculating virus into mice and to detect virus RNA in the lesion by in situ hybridization. A group of mice were inoculated intravenously with coxsackie B 4 virus once a month from 1 to 5 months of age and sacrificed monthly from 6 to 12 months of age. Mesangial proliferation and deposits that stained positive with periodic acid-Schiff in light microscopy and electron-dense deposits in electron microscopy were found from 6 months of age. Positive findings for IgG and IgA deposition in the mesangium were noted and the intensity of IgA deposition was predominant after 10 months of age. The signals of coxsackie B 4 virus by in situ hybridization were observed in the lesions. These observations indicate that coxsackie B 4 virus inoculated repeatedly into mice induces lesions similar to IgA nephropathy. The depositions of the lesions may be immune complexes of coxsackie B 4 virus and these immune complexes injure renal tissues.
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ISSN:0250-8095
1421-9670
DOI:10.1159/000169076