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      Glomerulonefritis rápidamente progresiva asociada con vasculitis por ANCA Translated title: Rapidly progressive glomerulonephritis associated with ANCA-vasculitis.

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          Abstract

          Resumen El glomérulo renal, estructura altamente vascularizada, se ve afectado por un grupo de vasculitis de pequeño vaso asociadas con anticuerpos anticitoplasma de neutrófilo (ANCA), descritas por su relativa escasez de depósitos inmunes como pauciinmunes. Estas vasculitis se clasifican según el consenso internacional de Chapel-Hill en poliangeítis microscópica, granulomatosis con poliangeítis, granulomatosis eosinofílica y la llamada vasculitis limitada al riñón. Desde el punto de vista anatomopatológico, la glomerulonefritis rápidamente progresiva puede dividirse en pauciinmune, antimembrana basal glomerular (GBM GN) y mediada por inmunocomplejos. El tratamiento, en general, es con inmunosupresor y terapia renal de soporte desde medidas conservadoras hasta tratamiento de sustitución renal. Se comunica un caso de glomerulonefritis rápidamente progresiva asociada con ANCA por confirmación anatomopatológica.

          Translated abstract

          Abstract The renal glomerulus highly vascularized structure is affected by a small vessel vasculitis group associated with neutrophil cytoplasmic antibodies (ANCA) described by its relative scarcity of pauci-immune deposits as immune. This vasculitis is classified according to international consensus in Chapel-Hill microscopic poliangetitis, granulomatosis with polyangiitis, eosinophilic granulomatosis and the called vasculitis limited to the kidney. From the anatomopathological point of view, the rapidly progressive glomerulonephritis can be divided into pauci-immune, anti glomerular basement membrane and mediated by immune complexes. The treatment is generally based on immunosuppressive therapy and renal therapy support from conservative measures to renal replacement therapy. This paper reports a case of rapidly progressive glomerulonephritis associated with ANCA pathological confirmation.

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          Most cited references19

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          Activated endothelial cells induce neutrophil extracellular traps and are susceptible to NETosis-mediated cell death.

          Neutrophil interaction with activated endothelial cells (EC) is required for transmigration. We examined consequences of this interaction on NETosis. Co-culture of activated EC with neutrophils induced neutrophil extracellular trap (NET) formation, which was partially dependent on production of IL-8 by activated EC. Extended neutophil/EC co-culture resulted in EC damage, which could be abrogated by inclusion of either diphenyleneiodonium to inhibit the NAPDH oxidase pathway required for NETosis, or DNAse to disrupt NETs. These findings offer new insight into mechanisms whereby NETs trigger damage to the endothelium in sepsis, small vessel vasculitis and possibly the villous trophoblast in preeclampsia. Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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            Anti-neutrophil cytoplasmic autoantibodies induce neutrophils to degranulate and produce oxygen radicals in vitro.

            Anti-neutrophil cytoplasmic autoantibodies (ANCA) are in the circulation of most patients with pauci-immune necrotizing vasculitis and pauci-immune crescentic glomerulonephritis. The current study demonstrates an effect of these autoantibodies on neutrophil function in vitro. ANCA cause normal human neutrophils to undergo an oxidative burst and degranulate. Both ANCA phenotypes (i.e., cytoplasmic-pattern ANCA and myeloperoxidase-specific ANCA) induce neutrophil activation. ANCA sera and purified immunoglobulins significantly increase the release of reactive oxygen species when compared with controls. ANCA, in a dose-dependent manner, induce the release of primary granule contents. These effects are markedly enhanced by priming neutrophils with tumor necrosis factor. Flow cytometry studies demonstrate the presence of myeloperoxidase on the surface of neutrophils after cytokine priming, indicating that primed neutrophils have ANCA antigens at their surfaces to interact with ANCA. These observations suggest an in vivo pathogenetic role for ANCA. We propose 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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              Antineutrophil cytoplasmic autoantibodies specific for myeloperoxidase cause glomerulonephritis and vasculitis in mice

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                mim
                Medicina interna de México
                Med. interna Méx.
                Edición y Farmacia S.A. de C.V. (Ciudad de México, Ciudad de México, Mexico )
                0186-4866
                August 2018
                : 34
                : 4
                : 630-637
                Affiliations
                [1] Ciudad de México orgnameHospital Fundación Médica Sur
                [2] Ciudad de México orgnameInstituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán
                Article
                S0186-48662018000400016
                10.24245/mim.v34i4.1241
                1e413961-39e2-4cd9-9fa2-e6e5dc4b65e2

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : February 2017
                : September 2017
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 23, Pages: 8
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                SciELO Mexico

                Categories
                Casos clínicos

                Glomerulonefritis rápidamente progresiva,glomerulonefritis,anticuerpos anticitoplasma de neutrófilo,Rapidly progressive glomerulonephritis,Glomerulonephritis,Neutrophil cytoplasmic antibodies

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