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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Avacopan improves anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis by selectively antagonizing the C5a receptor, thereby inhibiting neutrophil migration and the induction of adhesion molecule expression. Although avacopan reduces glucocorticoid-related toxicity and significantly improves renal function, a high incidence of liver injury has been reported in avacopan-treated patients. Nevertheless, the pathophysiological mechanisms and clinical manifestations of liver injury associated with avacopan therapy have not been fully elucidated.
Case report
An 83-year-old woman was diagnosed with microscopic polyangiitis (MPA) and treated daily with prednisolone (PSL) 30 mg and avacopan 60 mg. Furthermore, rituximab was administered twice at a dose of 500 mg. Her renal function improved rapidly, and the prednisolone dose was tapered to 5 mg/week. Forty-three days after initiating PSL and avacopan, her laboratory tests revealed liver injury with aspartate aminotransferase 655 IU/L, alanine aminotransferase 504 IU/L, and γ-glutamyl transpeptidase 402 IU/L. In addition to discontinuing avacopan, acyclovir (ACV) and ganciclovir (GCV) were initiated due to the marked elevation of liver enzymes, suggesting viral hepatitis rather than drug-induced hepatic injury. The elevation of liver enzymes improved 2 days after treatment. Myeloperoxidase-ANCA and cytomegalovirus antigenemia tests were negative; therefore, GCV was discontinued on day 7, and avacopan was not resumed. ACV was discontinued on day 14, and the patient was discharged on day 17. A liver biopsy revealed nonspecific inflammatory changes, complicating the differentiation between viral- and drug-induced hepatitis. However, the rapid improvement in liver enzyme levels suggests that the liver injury in the present case was attributable to viral infection, particularly a herpes virus, rather than a drug-induced mechanism.
Liver injury has been reported in approximately 20% of patients with vasculitis treated with avacopan, with both hepatocellular and cholestatic patterns observed. Conversely, patients with vasculitis who receive corticosteroids and rituximab may be more susceptible to drug-induced viral hepatitis. Although avacopan is not considered a major contributor to viral reactivation, the C5a receptor is involved in hepatocyte regeneration and protection. Thus, avacopan may delay recovery or exacerbate viral hepatitis. In patients receiving avacopan in combination with other immunosuppressants for vasculitis, considering not only avacopan-induced liver injury, but also the possibility of viral reactivation is important.
