Evidence map›Paper›PMID 24790181›Full record

ArticleJournal of the American Society of Nephrology : JASN2014

Glomerular autoimmune multicomponents of human lupus nephritis in vivo: α-enolase and annexin AI.

Maurizio Bruschi, Renato Alberto Sinico, Gabriella Moroni, Federico Pratesi, Paola Migliorini, Maricla Galetti, Corrado Murtas, Angela Tincani, Michael Madaio, Antonella Radice and 19 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02403115 (Validation of the Assay of Circulating Antibodies Against Glomerular Neo-autoantigens as a Surrogate Biomarker of the Development of Lupus Nephritis), which is not on this map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
9.4field-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.

NCT02403115 unknown statusnot on this map

Validation of the Assay of Circulating Antibodies Against Glomerular Neo-autoantigens as a Surrogate Biomarker of the Development of Lupus Nephritis

TypeobservationalSponsorIstituto Giannina GasliniRan2014 to 2022Enrolled800ConditionsSystemic Lupus ErythematosusArmsSerum collection
3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Molecular and Cellular Mediators of Renal Fibrosis in Lupus Nephritis.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Efferocytosis in Homeostasis.Advances in experimental medicine and biology · 2025
    Review
  8. Lupus Nephritis Biomarkers: A Critical Review.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. [Relationship between anti-ENO1 antibody and systemic lupus erythematosus patients with retinopathy].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2022
    Article
  15. Article
  16. Review
  17. Review
  18. Inhibition of NETosis for treatment purposes: friend or foe?Molecular and cellular biochemistry · 2022
    Review
  19. Article
  20. Review

1 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

29 authors at 13 institutions in 3 countries.

Maurizio BruschiLaboratory on Pathophysiology of Uremia.
Renato Alberto SinicoDivision of Nephrology and Section of Clinical Immunology, San Carlo Hospital, Milan, Italy;
Gabriella MoroniDivision of Nephrology and Dialysis, Scientific Institute for Research and Health Care (IRCCS) Fondazione Ospedale Maggiore, Mangiagalli, Regina Elena, Milan, Italy;
Federico PratesiClinical Immunology Unit, Department of Internal Medicine, University of Pisa, Pisa, Italy;
Paola MiglioriniClinical Immunology Unit, Department of Internal Medicine, University of Pisa, Pisa, Italy;
Maricla GalettiDepartments of Clinical and Experimental Medicine, Italian Workers' Compensation Authority (INAIL) Research Center, University of Parma, Parma, Italy;
Corrado MurtasDivisions of Nephrology, Dialysis, and Transplantation, and.
Angela TincaniRheumatology and Clinical Immunology, Spedali Civili and University of Brescia, Brescia, Italy;
Michael MadaioDepartment of Medicine, Georgia Health Sciences University, Augusta, Georgia;
Antonella RadiceDivision of Nephrology and Section of Clinical Immunology, San Carlo Hospital, Milan, Italy;
Franco FranceschiniRheumatology and Clinical Immunology, Spedali Civili and University of Brescia, Brescia, Italy;
Barbara TrezziDivision of Nephrology and Section of Clinical Immunology, San Carlo Hospital, Milan, Italy;
Laura BianchiDivision of Nephrology and Section of Clinical Immunology, San Carlo Hospital, Milan, Italy;
Agata GiallongoInstitute of Biomedicine and Molecular Immunology, CNR, Palermo, Italy;
Rita GattiBiomedical, Biotechnological and Translational Sciences, and.
Regina TardanicoService of Pathological Anatomy, Division of Nephrology, Spedali Civili di Brescia, Brescia, Italy;
Andrea ScaloniCNR, Institute for Animal Production System in Mediterranean Environment (ISPAAM), Naples, Italy;
Chiara D'AmbrosioCNR, Institute for Animal Production System in Mediterranean Environment (ISPAAM), Naples, Italy;
Maria Luisa CarnevaliDepartments of Clinical and Experimental Medicine.
Piergiorgio MessaDivision of Nephrology and Dialysis, Scientific Institute for Research and Health Care (IRCCS) Fondazione Ospedale Maggiore, Mangiagalli, Regina Elena, Milan, Italy;
Pietro RavaniDivision of Nephrology, University of Calgary, Calgary, Alberta, Canada; and.
Giancarlo BarbanoDivisions of Nephrology, Dialysis, and Transplantation, and.
Beatrice BiancoDepartments of Clinical and Experimental Medicine.
Alice BonanniDivisions of Nephrology, Dialysis, and Transplantation, and.
Francesco ScolariDivision of Nephrology, University of Brescia, Montichiari Hospital, Brescia, Italy.
Alberto MartiniPaediatric Rheumatology, Istituto Giannina Gaslini, Genoa, Italy;
Giovanni CandianoLaboratory on Pathophysiology of Uremia.
Landino AllegriDepartments of Clinical and Experimental Medicine.
Gian Marco GhiggeriDivisions of Nephrology, Dialysis, and Transplantation, and GMarcoGhiggeri@ospedale-gaslini.ge.it.
Carlo Forlanini Hospital · ITUniversity of Pisa · ITAzienda Socio Sanitaria Territoriale degli Spedali Civili di Brescia · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITIstituto di Biomedicina e di Immunologia Molecolare Alberto Monroy · ITIstituto Giannina Gaslini · ITIstituto Nazionale per l'Assicurazione Contro gli Infortuni sul Lavoro · ITIstituto per il Sistema Produzione Animale in Ambiente Mediterraneo · ITOspedale Maggiore · ITOspedale San Carlo · ITUniversity of Brescia · ITUniversity of Calgary · CAUniversity of Parma · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal targets of autoimmunity in human lupus nephritis (LN) are unknown. We sought to identify autoantibodies and glomerular target antigens in renal biopsy samples from patients with LN and determine whether the same autoantibodies can be detected in circulation. Glomeruli were microdissected from biopsy samples of 20 patients with LN and characterized by proteomic techniques. Serum samples from large cohorts of patients with systemic lupus erythematosus (SLE) with and without LN and other glomerulonephritides were tested. Glomerular IgGs recognized 11 podocyte antigens, with reactivity varying by LN pathology. Notably, IgG2 autoantibodies against α-enolase and annexin AI were detected in 11 and 10 of the biopsy samples, respectively, and predominated over other autoantibodies. Immunohistochemistry revealed colocalization of α-enolase or annexin AI with IgG2 in glomeruli. High levels of serum anti-α-enolase (>15 mg/L) IgG2 and/or anti-annexin AI (>2.7 mg/L) IgG2 were detected in most patients with LN but not patients with other glomerulonephritides, and they identified two cohorts: patients with high anti-α-enolase/low anti-annexin AI IgG2 and patients with low anti-α-enolase/high anti-annexin AI IgG2. Serum levels of both autoantibodies decreased significantly after 12 months of therapy for LN. Anti-α-enolase IgG2 recognized specific epitopes of α-enolase and did not cross-react with dsDNA. Furthermore, nephritogenic monoclonal IgG2 (clone H147) derived from lupus-prone MRL-lpr/lpr mice recognized human α-enolase, suggesting homology between animal models and human LN. These data show a multiantibody composition in LN, where IgG2 autoantibodies against α-enolase and annexin AI predominate in the glomerulus and can be detected in serum.

Indexed as

AdolescentAdultAnimalsAnnexin A1AutoantibodiesBiomarkers, TumorBiopsyDNA-Binding ProteinsFemaleHumansImmunoglobulin GKidney GlomerulusLupus NephritisMaleMice, Inbred BALB CMice, Inbred MRL lprAnnexin A1annexin A1, mouseAutoantibodiesBiomarkers, TumorDNA-Binding ProteinsENO1 protein, humanEno1 protein, mouseImmunoglobulin GPhosphopyruvate HydrataseTumor Suppressor ProteinsGNimmunology and pathologylupus nephritis

Identifiers

PMID24790181
PMCPMC4214525
OpenAlexW2151204164

What OpenQuestion holds

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Registered trials

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.