Glomerular membrane attack complex is not a reliable marker of ongoing C5 activation in lupus nephritis.


Journal

Kidney international
ISSN: 1523-1755
Titre abrégé: Kidney Int
Pays: United States
ID NLM: 0323470

Informations de publication

Date de publication:
03 2019
Historique:
received: 02 05 2018
revised: 26 09 2018
accepted: 27 09 2018
pubmed: 19 1 2019
medline: 15 2 2020
entrez: 19 1 2019
Statut: ppublish

Résumé

Complement plays an important role in the pathogenesis of lupus nephritis (LN). With the emergence of therapeutic complement inhibition, there is a need to identify patients in whom complement-driven inflammation is a major cause of kidney injury in LN. Clinical and histopathological data were obtained retrospectively from 57 biopsies with class III, IV, and V LN. Biopsies were stained for complement components C9, C5b-9, C3c, and C3d and for the macrophage marker CD68. C9 and C5b-9 staining were highly correlated (r = 0.92 in the capillary wall). C5b-9 staining was detected in the mesangium and/or capillary wall of both active and chronic proliferative LN in all but one biopsy and in the capillary wall of class V LN in all biopsies. C5b-9 staining intensity in the tubular basement membrane correlated with markers of tubulointerstitial damage, and more intense capillary wall C5b-9 staining was significantly associated with nonresponse to conventional treatment. Glomerular C5b-9 staining intensity did not differ between active and chronic disease; in contrast, C3c and CD68 staining were associated with active disease. Evaluation of serial biopsies and comparison of staining in active and chronic LN demonstrated that C5b-9 staining persisted for months to years. These results suggest that C5b-9 staining is almost always present in LN, resolves slowly, and is not a reliable marker of ongoing glomerular C5 activation. This limits the utility of C5b-9 staining to identify patients who are most likely to benefit from C5 inhibition.

Identifiants

pubmed: 30655025
pii: S0085-2538(18)30789-0
doi: 10.1016/j.kint.2018.09.027
pmc: PMC6389546
pii:
doi:

Substances chimiques

Biomarkers 0
Complement C5 0
Complement Membrane Attack Complex 0
Immunosuppressive Agents 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

655-665

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom

Informations de copyright

Copyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.

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Auteurs

Hannah R Wilson (HR)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Nicholas R Medjeral-Thomas (NR)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Alyssa C Gilmore (AC)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Pritesh Trivedi (P)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Kathleen Seyb (K)

Ra Pharmaceuticals, Inc., Cambridge, Massachusetts, USA.

Ramin Farzaneh-Far (R)

Ra Pharmaceuticals, Inc., Cambridge, Massachusetts, USA.

Iva Gunnarsson (I)

Division of Rheumatology, Department of Medicine, Karolinska Institutet and Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Agneta Zickert (A)

Division of Rheumatology, Department of Medicine, Karolinska Institutet and Rheumatology, Karolinska University Hospital, Stockholm, Sweden.

Thomas D Cairns (TD)

Centre for Inflammatory Disease, Imperial College London, London, UK.

Liz Lightstone (L)

Centre for Inflammatory Disease, Imperial College London, London, UK.

H Terence Cook (HT)

Centre for Inflammatory Disease, Imperial College London, London, UK. Electronic address: t.h.cook@imperial.ac.uk.

Matthew C Pickering (MC)

Centre for Inflammatory Disease, Imperial College London, London, UK.

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Classifications MeSH