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Renal thrombotic microangiopathy associated with chronic humoral graft versus host disease after hematopoietic stem cell transplantation
Author(s) -
Mii Akiko,
Shimizu Akira,
Masuda Yukinari,
Fujino Teppei,
Kaneko Tomohiro,
Utsumi Kouichi,
Arai Takashi,
Ishikawa Arimi,
Wakamatsu Kyoko,
Tajika Kenji,
Iino Yasuhiko,
Katayama Yasuo,
Fukuda Yuh
Publication year - 2011
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2010.02608.x
Subject(s) - thrombotic microangiopathy , peritubular capillaries , pathology , medicine , hematopoietic stem cell transplantation , transplantation , kidney disease , immunology , pathogenesis , graft versus host disease , microangiopathy , renal biopsy , biopsy , disease , diabetes mellitus , endocrinology
Thrombotic microangiopathy (TMA) is a known complication of hematopoietic stem cell transplantation (HSCT). The pathogenesis of TMA is controversial but considered to involve various factors such as total body irradiation, use of calcineurin inhibitors for prophylaxis against graft versus host disease (GVHD), viral infection, and GVHD. Herein we describe a case with renal TMA after HSCT, which was probably associated with antibody‐mediated endothelial cell injury from chronic GVHD (termed here ‘chronic humoral GVHD’). A 49‐year‐old man presented two years after HSCT with renal dysfunction and proteinuria but without the clinical features of TMA. Histopathological examination of renal biopsy showed chronic glomerular endothelial cell injury with double contour of the glomerular basement membrane, microthrombi and the deposition of complement split product C4d along the glomerular capillaries. Renal tubulitis and peritubular capillaritis were also noted with a multilayered basement membrane and patchy C4d deposition on peritubular capillaries. These findings resemble those of chronic antibody‐mediated rejection after kidney transplantation. Furthermore, C4d deposition suggests complement activation. Although circulating anti‐blood type and anti‐human leukocyte antigen antibodies were not detected, the renal TMA in this case was probably associated with chronic humoral GVHD.