Evidence map›Paper›PMID 25003769›Full record

ReviewNature reviews. Rheumatology2014

Pathogenesis of antineutrophil cytoplasmic autoantibody-mediated disease.

J Charles Jennette, Ronald J Falk

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed, 3 pooled it
28.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

233 citing papers in PubMed, 3 syntheses or guidelines pooled it, 485 citations in OpenAlex.

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  7. Recognition of ear, nose and throat involvement in patients with ANCA-associated vasculitis: from in-depth interviews to insights for the future.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026
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173 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

J Charles JennetteDepartment of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina at Chapel Hill, 308 Brinkhous-Bullitt Building, CB#7525, Chapel Hill, NC 27599-7525, USA.
Ronald J FalkDepartment of Pathology and Laboratory Medicine, School of Medicine, University of North Carolina at Chapel Hill, 308 Brinkhous-Bullitt Building, CB#7525, Chapel Hill, NC 27599-7525, USA.
University of North Carolina at Chapel Hill · US

Funding

Translation of Knowledge on the Pathogenesis of ANCA Disease into NovelP01DK058335 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JENNETTE, CHARLES · 2000 to 2019
$25.9M
NIDDK NIH HHS P01 DK058335NIDDK NIH HHS P01-DK058335‑11
6 · The paper itself

Abstract

Antineutrophil cytoplasmic autoantibodies (ANCAs) are the probable cause of a distinct form of vasculitis that can be accompanied by necrotizing granulomatosis. Clinical and experimental evidence supports a pathogenesis that is driven by ANCA-induced activation of neutrophils and monocytes, producing destructive necrotizing vascular and extravascular inflammation. Pathogenic ANCAs can originate from precursor natural autoantibodies. Pathogenic transformation might be initiated by commensal or pathogenic microbes, legal or illegal drugs, exogenous or endogenous autoantigen complementary peptides, or dysregulated autoantigen expression. The ANCA autoimmune response is facilitated by insufficient T-cell and B-cell regulation. A putative pathogenic mechanism for vascular inflammation begins with ANCA-induced activation of primed neutrophils and monocytes leading to activation of the alternative complement pathway, which sets in motion an inflammatory amplification loop in the vessel wall that attracts and activates neutrophils with resultant respiratory burst, degranulation, extrusion of neutrophil extracellular traps, apoptosis and necrosis. The pathogenesis of extravascular granulomatosis is less clear, but a feasible scenario proposes that a prodromal infectious or allergic condition positions primed neutrophils in extravascular tissue in which they can be activated by ANCAs in interstitial fluid to produce extravascular necrotizing injury that would initiate an innate granulomatous inflammatory response to wall off the necrotic debris.

Indexed as

AnimalsAntibodies, Antineutrophil CytoplasmicBiomarkersDisease Models, AnimalEvidence-Based MedicineGlomerulonephritisHumansImmunologic FactorsVasculitisAntibodies, Antineutrophil CytoplasmicBiomarkersImmunologic Factors

Identifiers

PMID25003769
OpenAlexW2082322877

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.