Evidence map›Paper›PMID 38962936›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2024

Association of Autoantibody Concentrations and Trajectories With Lupus Nephritis Histologic Features and Treatment Response.

Andrea Fava, Catriona A Wagner, Carla J Guthridge, Joseph Kheir, Susan Macwana, Wade DeJager, Tim Gross, Peter Izmirly, H Michael Belmont, Betty Diamond and 9 more

Abstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Trial
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  10. Review
  11. Article
  12. Article
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  14. Observational
  15. Review
  16. Not So Benign: Revisiting Pure Membranous Lupus Nephritis.Journal of personalized medicine · 2025
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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

19 authors.

Andrea FavaJohns Hopkins University, Baltimore, Maryland.ORCID https://orcid.org/0000-0001-6738-4836
Catriona A WagnerOklahoma Medical Research Foundation, Oklahoma City.
Carla J GuthridgeOklahoma Medical Research Foundation, Oklahoma City.
Joseph KheirOklahoma Medical Research Foundation, Oklahoma City.
Susan MacwanaOklahoma Medical Research Foundation, Oklahoma City.
Wade DeJagerOklahoma Medical Research Foundation, Oklahoma City.
Tim GrossOklahoma Medical Research Foundation, Oklahoma City.
Peter IzmirlyNew York University School of Medicine, New York City.
H Michael BelmontNew York University Langone Health, New York City.ORCID https://orcid.org/0000-0003-3389-2976
Betty DiamondThe Feinstein Institutes for Medical Research, Manhasset, New York.
Anne DavidsonThe Feinstein Institutes for Medical Research, Manhasset, and Donald and Barbara Zucker School of Medicine, Northwell Health, Hempstead, New York.ORCID https://orcid.org/0000-0002-4081-6464
Paul J UtzStanford University School of Medicine, Stanford, California.
Michael H WeismanCedars-Sinai Medical Center, Los Angeles, California.
Laurence S MagderUniversity of Maryland, Baltimore.
Accelerating Medicines Partnership Rheumatoid Arthritis and Systemic Lupus Erythematosus (AMP RA/SLE) Network
Joel M GuthridgeOklahoma Medical Research Foundation, Oklahoma City.
Michelle PetriJohns Hopkins University, Baltimore, Maryland.ORCID https://orcid.org/0000-0003-1441-5373
Jill BuyonNew York University School of Medicine, New York City.ORCID https://orcid.org/0000-0002-3852-7129
Judith A JamesOklahoma Medical Research Foundation and University of Oklahoma Health Sciences Center, Oklahoma City.ORCID https://orcid.org/0000-0002-9574-7355

Funding

Accelerating Medicines Partnership-Autoimmune and Immunologic Disease Tissue Research Core Admin Supplement: Preclinical Studies in Sjogren'sUC2AR081032 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI Joel Marvin Guthridge, JUDITH A JAMES · 2022 to 2026
$30.7M
PEARL: Pathway Exploration and Analysis in Renal LupusUH2AR067688 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI DIAMOND, BETTY, WOFSY, DAVID · 2014 to 2020
$9.0M
Oklahoma Rheumatic Disease Research Cores Center (Overall Application)P30AR073750 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JUDITH A JAMES · 2018 to 2026
$8.5M
Tissue Acquisition Research GroupUM2AR067678 · NIAMS · STANFORD UNIVERSITY · PI HOLERS, VERNON MICHAEL, UTZ, PAUL JOSEPH · 2014 to 2020
$8.2M
Multi-Ethnic Translational Research Optimization (METRO) Lupus ConsortiumUH2AR067689 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BUYON, JILL P, PUTTERMAN, CHAIM · 2014 to 2020
$6.3M
Lupus Omics Cutaneous Kidney Investigative Team (LOCKIT) - Pain SupplementUC2AR081039 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Jill P Buyon, MICHELLE A PETRI · 2022 to 2026
$6.3M
Evolving Adaptive and Effector Mechanisms from Pre-RA Through Established DiseaseUH2AR067681 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI HOLERS, VERNON MICHAEL · 2014 to 2020
$5.5M
Molecular and Cellular Dissection of Early Rheumatoid ArthritisUH2AR067694 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI BRENNER, MICHAEL B., GREGERSEN, PETER K. · 2014 to 2020
$5.4M
Autoimmune Drivers and Protectors Team Science (ADAPTS)U01AI176244 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JUDITH A JAMES, Jeffrey C Rathmell · 2023 to 2026
$5.1M
RA-SLE Molecular Deconstruction Leadership CenterUH2AR067677 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI BRENNER, MICHAEL B., RAYCHAUDHURI, SOUMYA · 2014 to 2020
$4.3M
Oklahoma ACE: Molecular Destruction of Autoimmune Disease to Aid Clinical Trail SuccessUM1AI144292 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI JUDITH A JAMES · 2019 to 2026
$3.3M
Cellular Dynamics at the Synovium-Bone interface in RAUH2AR067690 · NIAMS · UNIVERSITY OF ROCHESTER · PI ANOLIK, JENNIFER HOWITT · 2014 to 2020
$3.0M
NHLBI NIH HHS UM1-AI144292NIAID NIH HHS UM1 AI144292NIAMS NIH HHS P30 AR073750NIAMS NIH HHS P30-AR073750NIAMS NIH HHS UC2 AR081032NIAMS NIH HHS UC2-AR081032NIAMS NIH HHS UC2 AR081039NIAMS NIH HHS UC2-AR081039NIAMS NIH HHS UH2 AR067676NIAMS NIH HHS UH2-AR067676NIAMS NIH HHS UH2 AR067677NIAMS NIH HHS UH2-AR067677NIAMS NIH HHS UH2 AR067679NIAMS NIH HHS UH2-AR067679NIAMS NIH HHS UH2 AR067681NIAMS NIH HHS UH2-AR067681NIAMS NIH HHS UH2 AR067685NIAMS NIH HHS UH2-AR067685NIAMS NIH HHS UH2 AR067688NIAMS NIH HHS UH2- AR067688NIAMS NIH HHS UH2 AR067689NIAMS NIH HHS UH2-AR067689NIAMS NIH HHS UH2 AR067690NIAMS NIH HHS UH2-AR067690NIAMS NIH HHS UH2 AR067691NIAMS NIH HHS UH2-AR067691NIAMS NIH HHS UH2 AR067694NIAMS NIH HHS UH2-AR067694NIAMS NIH HHS UM2 AR067678NIAMS NIH HHS UM2-AR067678NIDDK NIH HHS R01 DK134625NIDDK NIH HHS R01-DK134625
6 · The paper itself

Abstract

objectiveAutoantibodies are a hallmark of lupus nephritis (LN), but their association with LN classes and treatment response are not adequately known. In this study, we quantified circulating autoantibodies in the Accelerating Medicines Partnership LN longitudinal cohort to identify serological biomarkers of LN histologic classification and treatment response and how these biomarkers change over time based on treatment response.

methodsPeripheral blood samples were collected from 279 patients with systemic lupus erythematosus undergoing diagnostic kidney biopsy based on proteinuria. Of these, 268 were diagnosed with LN. Thirteen autoantibody specificities were measured by bead-based assays (Bio-Rad Bioplex 2200) and anti-C1q by enzyme-linked immunosorbent assay at the time of biopsy (baseline) and at 3, 6, and 12 months after biopsy. Clinical response was determined at 12 months.

resultsProliferative LN (International Society of Nephrology/Renal Pathology Society class III/IV±V, n = 160) was associated with higher concentrations of anti-C1q, anti-chromatin, anti-double-stranded DNA (dsDNA), and anti-ribosomal P autoantibodies compared to nonproliferative LN (classes I/II/V/VI, n = 108). Anti-C1q and-dsDNA were independently associated with proliferative LN. In proliferative LN, higher baseline anti-C1q levels predicted complete response (area under the curve [AUC] 0.72; P = 0.002) better than baseline proteinuria (AUC 0.59; P = 0.21). Furthermore, all autoantibody levels except for anti-La/SSB decreased over 12 months in patients with proliferative, but not membranous, LN with a complete response.

conclusionBaseline levels of anti-C1q and anti-dsDNA may serve as noninvasive biomarkers of proliferative LN, and anti-C1q may predict complete response at the time of kidney biopsy. In addition, tracking autoantibodies over time may provide further insights into treatment response and pathogenic mechanisms in patients with proliferative LN.

Indexed as

AutoantibodiesComplement C1qLupus NephritisAdultAntibodies, AntinuclearBiomarkersBiopsyChromatinFemaleHumansKidneyLongitudinal StudiesMaleMiddle AgedRibosomal ProteinsTreatment OutcomeAntibodies, Antinuclearanti-dsDNA autoantibodyAutoantibodiesBiomarkersChromatinComplement C1qRibosomal Proteins

Identifiers

PMID38962936
PMCPMC11521769

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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.