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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.

© 2003 by The American Society of Hematology.
 

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