Evidence map›Paper›PMID 41550499›Full record

ArticleBiochemistry and biophysics reports2026

Functional classification of antineutrophil cytoplasmic antibody (ANCA) and its relation with clinical parameters of ANCA-associated vasculitis.

Mai Taniguchi, China Washio, Momo Uchizawa, Naho Ogawa, Riku Manabe, Suishin Arai, Hodaka Ogawa, Yuka Nishibata, Sakiko Masuda, Daigo Nakazawa and 11 more

Abstract read
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Article in Biochemistry and biophysics reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

21 authors.

Mai TaniguchiDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
China WashioDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Momo UchizawaDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Naho OgawaDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Riku ManabeDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Suishin AraiDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Hodaka OgawaDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Yuka NishibataDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Sakiko MasudaDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.
Daigo NakazawaDepartment of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Utano TomaruDepartment of Surgical Pathology, Hokkaido University Hospital, Sapporo, Japan.
Yoshihiro ArimuraDepartment of Nephrology and Rheumatology, Kyorin University School of Medicine, Tokyo, Japan.
Koichi AmanoDepartment of Rheumatology and Clinical Immunology, Saitama Medical Center, Saitama Medical University, Saitama, Japan.
Yukio YuzawaDepartment of Nephrology, Fujita Health University School of Medicine, Toyoake, Japan.
Ken-Ei SadaDepartment of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
Tatsuya AtsumiDepartment of Rheumatology, Endocrinology and Nephrology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Hiroaki DobashiDivision of Hematology, Rheumatology and Respiratory Medicine, Department of Internal Medicine, Faculty of Medicine, Kagawa University, Kagawa, Japan.
Masayoshi HarigaiDivision of Rheumatology, Department of Internal Medicine, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Seiichi MatsuoTokai National Higher Education and Research System (THERS), Nagoya, Japan.
Hirofumi MakinoOkayama University, Okayama, Japan.
Akihiro IshizuDepartment of Medical Laboratory Science, Faculty of Health Sciences, Hokkaido University, Sapporo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is characterized by serum ANCA and systemic small-vessel vasculitis. Neutrophils are primed to express ANCA antigens on the plasma membrane. ANCA binding to the antigens can transduce signals into neutrophils, releasing reactive oxygen species (ROS) and contributing to AAV development. ANCA-mediated signals are transduced via two pathways: ANCA antigens crosslinked by ANCA, and Fcγ receptor (FcγR), to which the Fc portion of ANCA binds. This study aimed to demonstrate the association of ANCA-mediated neutrophil activation pathways with clinical manifestations of AAV, including renal dysfunction and kidney survival at 6 months after treatment. For this purpose, IgG was extracted from the serum of AAV patients before treatment (n = 112), and ROS production from neutrophils exposed to IgG and its suppression by FcγR inhibitors (FcX) were assessed. IgG exhibiting higher ROS production than control IgG was classified as ROS-inducing ANCA and the others as ROS-noninducing ANCA. The former was subclassified into antigen-driven ANCA and FcγR-driven ANCA according to whether the ROS production suppression rate by FcX was <50 % or ≧50 %, respectively. As a result, ANCA was classified into ROS-inducing antigen-driven ANCA (n = 74), ROS-inducing FcγR-driven ANCA (n = 22), and ROS-noninducing ANCA (n = 16). Serum levels of blood urea nitrogen and creatinine were significantly higher in patients with ROS-inducing FcγR-driven ANCA than in those with ROS-noninducing ANCA. Patients with ROS-inducing FcγR-driven ANCA had a significantly lower kidney survival rate 6 months after treatment than other patients. The collective findings suggest that ROS-inducing FcγR-driven ANCA may predict poor kidney prognosis in AAV.

Indexed as

ANCA-associated vasculitis (AAV)Antineutrophil cytoplasmic antibody (ANCA)Fcγ receptor (FcγR)Reactive oxygen species (ROS)

Identifiers

PMID41550499
PMCPMC12808588

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