Anti-Glomerular Basement Membrane Antibody Disease Complicated by Complement-Mediated Thrombotic Microangiopathy: A Case Report
Abstract
Anti-glomerular basement membrane (GBM) antibody disease rarely causes thrombotic microangiopathy (TMA). We herein report the case of a 75-year-old Japanese woman who developed refractory TMA during treatment for anti-GBM antibody disease. Although secondary TMA was initially suspected, persistent hemolytic anemia and thrombocytopenia despite plasma exchange, glucocorticoids, and cyclophosphamide led us to suspect complement-mediated TMA. Eculizumab was initiated after genetic testing for complement regulatory factors was performed. The patient became transfusion-independent within one week, and genetic testing identified the c.293C＞T (p.Thr98Ile) variant in CD46. Complement-mediated TMA should thus be considered in refractory cases, and anti-C5 monoclonal antibodies may be an effective therapeutic option.
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BibTeX
@article{okino2026antiglomerular,
title = {{Anti-Glomerular Basement Membrane Antibody Disease Complicated by Complement-Mediated Thrombotic Microangiopathy: A Case Report}},
author = {Ryo Okino and Yoshitada Toyota and Takaaki Kaji and Ryo Nishioka and Ichiro Mizushima and Norihiko Sakai and Yasunori Iwata},
journal = {Internal Medicine},
year = {2026},
month = aug,
doi = {10.2169/internalmedicine.7718-26},
url = {https://www.jstage.jst.go.jp/article/internalmedicine/advpub/0/advpub_7718-26/_article},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Anti-Glomerular Basement Membrane Antibody Disease Complicated by Complement-Mediated Thrombotic Microangiopathy: A Case Report
AU - Ryo Okino
AU - Yoshitada Toyota
AU - Takaaki Kaji
AU - Ryo Nishioka
AU - Ichiro Mizushima
AU - Norihiko Sakai
AU - Yasunori Iwata
PY - 2026
DA - 2026/08/19
JO - Internal Medicine
DO - 10.2169/internalmedicine.7718-26
UR - https://www.jstage.jst.go.jp/article/internalmedicine/advpub/0/advpub_7718-26/_article
AB - Anti-glomerular basement membrane (GBM) antibody disease rarely causes thrombotic microangiopathy (TMA). We herein report the case of a 75-year-old Japanese woman who developed refractory TMA during treatment for anti-GBM antibody disease. Although secondary TMA was initially suspected, persistent hemolytic anemia and thrombocytopenia despite plasma exchange, glucocorticoids, and cyclophosphamide led us to suspect complement-mediated TMA. Eculizumab was initiated after genetic testing for complement regulatory factors was performed. The patient became transfusion-independent within one week, and genetic testing identified the c.293C＞T (p.Thr98Ile) variant in CD46. Complement-mediated TMA should thus be considered in refractory cases, and anti-C5 monoclonal antibodies may be an effective therapeutic option.
SN - 1349-7235
SN - 0918-2918
ER -