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Renal thrombotic microangiopathy associated with chronic graft‐versus‐host disease after allogeneic hematopoietic stem cell transplantation
Author(s) -
Mii Akiko,
Shimizu Akira,
Kaneko Tomohiro,
Fujita Emiko,
Fukui Megumi,
Fujino Teppei,
Utsumi Kouichi,
Yamaguchi Hiroki,
Tajika Kenji,
Tsuchiya Shinichi,
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.1440-1827.2011.02704.x
Subject(s) - thrombotic microangiopathy , graft versus host disease , medicine , hematopoietic stem cell transplantation , pathology , transplantation , stem cell , haematopoiesis , microangiopathy , disease , immunology , biology , diabetes mellitus , endocrinology , genetics
Thrombotic microangiopathy (TMA) is a major complication after hematopoietic stem cell transplantation (HSCT). In this study, we examined the clinical and pathologic features of 2 patients and 5 autopsy cases with HSCT‐associated renal TMA to clarify the association between graft‐versus‐host disease (GVHD) and renal TMA. The median interval between HSCT and renal biopsy or autopsy was 7 months (range 3–42 months). Clinically, acute and chronic GVHD occurred in 7 and 4 patients, respectively. Clinical evidence for TMA was detected in 2 patients, while chronic kidney disease developed in all patients. The main histopathological findings were diffuse endothelial injury in glomeruli, peritubular capillaries (PTCs), and small arteries. In addition, all cases showed glomerulitis, renal tubulitis, and peritubular capillaritis with infiltration of CD3+ T cells and TIA‐1+ cytotoxic cells, suggesting that GVHD occurred during the development of TMA. Diffuse and patchy C4d deposition was noted in glomerular capillaries and PTCs, respectively, in 2 biopsy and 2 autopsy cases, suggesting the involvement of antibody‐mediated renal endothelial injury in more than 50% of renal TMA cases. In conclusion, the kidney is a potential target of chronic GVHD that may induce the development of HSCT‐associated TMA. Importantly, some cases are associated with chronic humoral GVHD.