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Recurrent Membranoproliferative Glomerulonephritis with Glomerular Properdin Deposition in Allografts

[+] Article, Author, and Disclosure Information

Grant support: AM-15159. Dr. Zimmerman is a NIH trainee, grant AM-05582; Dr. Hyman is the recipient of a Special Fellowship, AM-53086, from the U.S. Public Health Service.

Published in abstract form in Clin Res 21:591, 1973.

▸Requests for reprints should be addressed to Stephen W. Zimmerman, M.D., Department of Pathology, University of Wisconsin, 470 North Charter St., Madison, WI 53706.

Madison, Wisconsin

Ann Intern Med. 1974;80(2):169-175. doi:10.7326/0003-4819-80-2-169
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Two children with renal allografts developed membranoproliferative glomerulonephritis that was histopathologically similar to their original disease. Recurrent disease was diagnosed in biopsy specimens from one child with a cadaveric graft, at 2 and at 5½ years after transplantation. The graft remains functional at 6 years, although persistent hematuria, proteinuria, and mild renal failure are evident. The second child received a D-match kidney from her brother. Two years later recurrent glomerulonephritis and chronic graft rejection necessitated a transplant nephrectomy. Immunofluorescence microscopy of renal allografts from both patients showed glomerular deposition of C3 and properdin, with minimal or no deposition of complement-fixing immunoglobulins. Glomerular deposits of properdin factor B (C3 proactivator) were also seen in one of the children. These findings suggest that membranoproliferative glomerulonephritis may recur in renal allografts, possibly through activation of the alternate complement pathway.





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