Frontiers in nephrology · 2026
Anti-GBM disease shortly after clinically presumed ANCA-associated vasculitis in an 85-year-old patient: a case report and literature review.
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Ito Hiroki, Abe Hiyu, Suzuki Yuya, Yano Kentaro, Sato Fumiya, Numahata Takaki, Ishikawa Risa, Endo-Matsumoto Akari, Matsumoto Keiji, Yuki Tsubasa, Kamada Ayaka, Hashimoto Hideaki, Anan Go, Ishiyama Katsuya, Hirose Takuo, Mori Takefumi
Аннотация
INTRODUCTION: Sequential emergence of anti-glomerular basement membrane (GBM) disease after anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is rare.
CASE PRESENTATION: An 85-year-old woman presented with fever, edema, elevated myeloperoxidase (MPO)-ANCA, mild urinary abnormalities, markedly elevated urinary tubular injury markers, and negative serum anti-GBM antibodies measured by chemiluminescent enzyme immunoassay. Renal biopsy was not performed because of advanced age, severe dementia, antiplatelet therapy, and the family's preference for non-invasive management. She was clinically presumed to have AAV and achieved apparent clinical remission with prednisolone alone, although MPO-ANCA remained positive. However, 2.5 months after the initial AAV diagnosis, she developed rapidly progressive kidney failure requiring dialysis, accompanied by severe hematuria, increased proteinuria, urinary casts, and markedly elevated anti-GBM antibodies. Clinically diagnosed anti-GBM disease was treated with methylprednisolone pulse therapy, prednisolone, plasma exchange, and hemodialysis. Although renal recovery was not achieved, anti-GBM antibodies became negative, and she remained clinically stable on maintenance hemodialysis for over 4 years while receiving low-dose prednisolone.
CONCLUSION: This case suggests that anti-GBM disease can emerge shortly after apparent clinical remission of AAV. ANCA-mediated GBM injury and age-related GBM changes may contribute to subsequent anti-GBM autoimmunity, although these mechanisms remain hypothetical in this patient. Prompt anti-GBM antibody testing should be considered when a rapid, unexplained decline in kidney function occurs during or after AAV treatment.
CASE PRESENTATION: An 85-year-old woman presented with fever, edema, elevated myeloperoxidase (MPO)-ANCA, mild urinary abnormalities, markedly elevated urinary tubular injury markers, and negative serum anti-GBM antibodies measured by chemiluminescent enzyme immunoassay. Renal biopsy was not performed because of advanced age, severe dementia, antiplatelet therapy, and the family's preference for non-invasive management. She was clinically presumed to have AAV and achieved apparent clinical remission with prednisolone alone, although MPO-ANCA remained positive. However, 2.5 months after the initial AAV diagnosis, she developed rapidly progressive kidney failure requiring dialysis, accompanied by severe hematuria, increased proteinuria, urinary casts, and markedly elevated anti-GBM antibodies. Clinically diagnosed anti-GBM disease was treated with methylprednisolone pulse therapy, prednisolone, plasma exchange, and hemodialysis. Although renal recovery was not achieved, anti-GBM antibodies became negative, and she remained clinically stable on maintenance hemodialysis for over 4 years while receiving low-dose prednisolone.
CONCLUSION: This case suggests that anti-GBM disease can emerge shortly after apparent clinical remission of AAV. ANCA-mediated GBM injury and age-related GBM changes may contribute to subsequent anti-GBM autoimmunity, although these mechanisms remain hypothetical in this patient. Prompt anti-GBM antibody testing should be considered when a rapid, unexplained decline in kidney function occurs during or after AAV treatment.