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Prepublished online as a Blood First Edition Paper on January 23, 2003; DOI 10.1182/blood-2002-07-2290.
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Blood, 15 May 2003, Vol. 101, No. 10, pp. 4219-4221
TRANSPLANTATION
Brief report
Nephrotic syndrome with crescent formation and massive IgA
deposition following allogeneic bone marrow transplantation for natural
killer cell leukemia/lymphoma
Shinya Kimura,
Akeyo Horie,
Yoshiyuki Hiki,
Chie Yamamoto,
Satoru Suzuki,
Junya Kuroda,
Masayo Deguchi,
Gen-ichi Kato,
Takahiro Karasuno,
Akira Hiraoka,
Toshikazu Yoshikawa, and
Taira Maekawa
From the Department of Transfusion Medicine,
Kyoto University Hospital, Kyoto, Japan; Department of Medicine, Daiko
Medical Center, Daiko, Japan; Department of Clinical and Laboratory
Medicine, Fukui Medical University, Fukui, Japan; Kyoto Second Red
Cross Hospital, Kyoto, Japan; Fifth Department of Internal Medicine,
Osaka Medical Center for Cancer and Cardiovascular Diseases, Osaka,
Japan; and First Department of Internal Medicine, Kyoto Prefectural
University of Medicine, Kyoto, Japan.
We describe herein a case of nephrotic syndrome (NS) following
allogeneic bone marrow transplantation (allo-BMT) for natural killer
cell leukemia/lymphoma. Histologic studies defined the diagnosis as
crescentic glomerulonephritis with massive immunoglobulin A
(IgA) deposition, which has never been reported in NS cases following
allo-BMT. Most of the massive infiltrated cells in the interstice were
CD3+CD4 CD8+ T cells derived from
the donor. We observed mesangial deposition of Haemophilus
parainfluenza outer membrane (OMHP) antigen and decreased
glycosylation of the IgA1 hinge in the recipient's samples is
consistent with the recently reported pathogenesis of IgA nephropathy. Further, the titer of IgA antibody against the donor serum was as high
as other IgA nephropathy cases. These findings suggest that NS and
crescentic glomerulonephritis in this case occurred as one of the forms
of chronic graft-versus-host disease (GVHD), and that IgA
deposition was associated with H parainfluenza and decreased glycosylation of the IgA1 hinge.

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