R
Ronald J. Falk
Researcher at University of North Carolina at Chapel Hill
Publications - 268
Citations - 25983
Ronald J. Falk is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Vasculitis & Autoantibody. The author has an hindex of 74, co-authored 259 publications receiving 24202 citations. Previous affiliations of Ronald J. Falk include Icahn School of Medicine at Mount Sinai & Bristol-Myers Squibb.
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Journal ArticleDOI
Nomenclature of systemic vasculitides. Proposal of an international consensus conference
Jc Jennette,Ronald J. Falk,K Andrassy,Pa Bacon,J Churg,J Churg,Wl Gross,Wl Gross,E. C. Hagen,Gs Hoffman,Gg Hunder,Cgm Kallenberg,Rt Mccluskey,Ra Sinico,Ra Sinico,Aj Rees,La Vanes,R Waldherr,Allan Wiik +18 more
TL;DR: The following are some of the conclusions and proposals made at the Chapel Hill Consensus Conference on the Nomenclature of Systemic Vasculitis.
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Anti-neutrophil cytoplasmic autoantibodies with specificity for myeloperoxidase in patients with systemic vasculitis and idiopathic necrotizing and crescentic glomerulonephritis
TL;DR: The presence of the same serologic marker in patients with kidney-limited and arteritis-associated necrotizing and crescentic glomerulonephritis, including Wegener's granulomatosis and polyarteritis nodosa, suggests that these clinically diverse diseases may have a similar pathogenesis, initiated by autoantibody-mediated activation of neutrophils.
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Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro.
TL;DR: It is proposed that, in patients with necrotizing vasculitis, ANCA-induced release of toxic oxygen radicals and noxious granule enzymes from cytokine-primed neutrophils could be mediating vascular inflammation.
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Small-Vessel Vasculitis
TL;DR: Protean clinical manifestations, combined with the etiologic nonspecificity of the histologic lesions, complicate the diagnosis of specific forms of vasculitis.
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Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice
Hong Xiao,Peter Heeringa,Peiqi Hu,Zhi Liu,Minglang Zhao,Yasuaki Aratani,Nobuyo Maeda,Ronald J. Falk,J. Charles Jennette +8 more
TL;DR: This animal model offers strong support for a direct pathogenic role for ANCA IgG in human glomerulonephritis and vasculitis as well as the pathogenic potential of antibodies alone.