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Nephrotic Syndrome after Hematopoietic Cell Transplantation: Do Glomerular Lesions Represent Renal Graft-versus-Host Disease?

Kirsten Brukamp^*, Alden M. Doyle^*, Roy D. Bloom^*, Nancy Bunin, John E. Tomaszewski, and Borut iman^*

^* Renal-Electrolyte and Hypertension Division, Department of Medicine, Division of Oncology, The Children’s Hospital of Philadelphia, and Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Address correspondence to: Drs. Kirsten Brukamp and Borut iman, Renal-Electrolyte and Hypertension Division, Department of Medicine, University of Pennsylvania School of Medicine, 700 Clinical Research Building, 415 Curie Boulevard, Philadelphia, PA 19104. Phone: 215-573-1830; Fax: 215-898-0189; E-mail: brukampk{at}uphs.upenn.edu, bcizman{at}cceb.med.upenn.edu

Glomerular disease associated with nephrotic syndrome has rarely been recognized as a distinct complication of allogeneic hematopoietic cell transplantation. Case reports in the English and Japanese literature since 1988 have described variable glomerular histology, comprising mainly membranous glomerulonephritis (MGN) in almost two thirds and minimal change disease (MCD) in nearly one quarter of patients. Review of the literature reveals a close temporal relationship between the development of nephrotic syndrome shortly after cessation of immunosuppression and the diagnosis of chronic graft-versus-host disease (GVHD). An association of glomerular disease with simultaneous GVHD was seen in 47% of patients overall. Nephrotic syndrome followed GVHD within 5 months in 60% of the combined MCD and MGN reports. A decrease in immunosuppressive medication use was linked to nephrotic syndrome occurrence within 9 months in 63% of patients with MCD and MGN. MCD occurred earlier after hematopoietic cell transplantation, was diagnosed sooner after medication change, and exhibited a better prognosis in comparison with MGN. Glomerular lesions after hematopoietic cell transplantation may therefore represent the renal manifestation of GVHD. Further studies are warranted to delineate the pathogenesis of this complication.

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