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Chronic Membranous Glomerulonephritis Caused by Hepatitis B Antigen-Antibody Immune Complexes

PETER F. KOHLER, M.D.; ROBERT E. CRONIN, M.D.; WILLIAM S. HAMMOND, M.D.; DAVID OLIN, M.D.; and RONALD I. CARR, M.D., Ph.D.
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▸Requests for reprints should be addressed to Peter F. Kohler, M.D., Division of Clinical Immunology, University of Colorado Medical Center, 4200 E. 9th Ave., Denver, CO 80220.


Denver, Colorado


Ann Intern Med. 1974;81(4):448-451. doi:10.7326/0003-4819-81-4-448
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The immunopathogenesis of chronic membranous glomerulonephritis was investigated in a 42-year-old man with chronic active hepatitis, type B. In two renal biopsies, 14 months apart, immunofluorescent study showed glomerular deposition of the hepatitis B antigen (HB Ag) and host IgG IgM, and C3 in an irregular "immune complex" pattern. Electron microscopy showed dense deposits in the thickened basement membrane but no morphologic evidence of the intact, spherical, 20-nm HB Ag. Low concentrations of HB Ag were found in serial serum samples whereas total complement and component concentrations were normal. Most significantly, circulating HB Ag-antibody complexes were directly shown by serum cryoprecipitation. Results of in-vitro tests for a cell-mediated immune response to HB Ag were negative. The potential importance of chronic hepatitis B virus infection as a primary cause of human immune-complex glomerulonephritis is supported by our findings.

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