Journal
BIOLOGY OF BLOOD AND MARROW TRANSPLANTATION
Volume 25, Issue 10, Pages 1920-1924Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.bbmt.2019.06.027
Keywords
Graft-versus-host disease; Murine models; Kidney; Complement system; Thrombotic microangiopathy
Categories
Funding
- National Institutes of Health [RO1 CA177909, RO1 CA231141, R21 All 01932]
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Acute graft-versus-host disease (GVHD) affects different organs, including the skin, liver, and gastrointestinal tract. Although kidneys are not among the organs commonly known to be the target of acute GVHD, kidney damage is frequently reported after allogeneic hematopoietic stem cell transplantation (allo-HSCT). We have studied the effect of bone marrow transplantation (BMT) on the kidneys in different murine models of GVHD. We found that glomerular damage in the kidneys is a common pathological finding in mice after BMT. The histopathological features of glomeruli damage included mesengiolysis, mesangial proliferation and edema, subendothelial and endothelial thickening, splitting of capillary walls in glomeruli, narrowing and collapsing of capillary lumens, fibrinoid necrosis of afferent arterioles, intimal hyperplasia, and microthrombi. These pathological features are similar to those detected in kidneys of patients with thrombotic microangiopathy (TMA) after allo-HSCT. We previously showed that activation of the complement system plays a role in GVHD-induced tissue injury in mice. Here we report the presence of complement activation products in the kidney specimens of mice after BMT. We also report that complement deficiency reduced the extent and severity of post-BMT glomerular damage in mice. We conclude that BMT in mice is associated with glomerular injury and tubulointerstitial nephritis, and that kidney damage is at least partially mediated by activation of the complement system. (C) 2019 American Society for Transplantation and Cellular Therapy. Published by Elsevier Inc.
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