Evidence map›Paper›PMID 37385828›Full record

ArticleNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2023

Using imlifidase to elucidate the characteristics and importance of anti-GBM antibodies produced after start of treatment.

Linnéa Tyrberg, Fanny Andersson, Fredrik Uhlin, Thomas Hellmark, Mårten Segelmark

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03157037 (Open-Label Phase II Study in Anti-GBM Disease), which is not on this map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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.

NCT03157037 phase2completednot on this map

Open-Label Phase II Study in Anti-GBM Disease (Goodpasture's Disease) With Adverse Renal Prognosis to Evaluate the Efficacy and Safety of IdeS - GOOD-IDES

TypeinterventionalSponsorMårten SegelmarkRan2017 to 2020Enrolled15ConditionsAnti-Glomerular Basement Membrane Antibody DiseaseArmsImlifidase
3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Guideline
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Immunomodulating Enzymes fromMicroorganisms · 2024
    Review
  9. Article
  10. Article
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

5 authors at 2 institutions in 2 countries.

Linnéa TyrbergDepartment of Clinical Sciences Lund, Lund University, Lund, Sweden.
Fanny AnderssonDepartment of Clinical Sciences Lund, Lund University, Lund, Sweden.
Fredrik UhlinDepartment of Nephrology and Department of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden.
Thomas HellmarkDepartment of Clinical Sciences Lund, Lund University, Lund, Sweden.
Mårten SegelmarkDepartment of Clinical Sciences Lund, Lund University, Lund, Sweden.ORCID 0000-0002-1221-0772
Lund University · SELinköping University · SE

Funding

Hansa Biopharma IMH-2016-00286Inga-Britt and Arne Lundberg Foundation LU-2021Ingrid Asp Foundation 991 602Region Östergötland LIO-755 381Region Skåne 2020-O000028Skane University Hospital Research FoundationsSwedish Research CouncilThelma Zoéga's Fund for Medical Research 91 282
6 · The paper itself

Abstract

backgroundAutoantibodies are common in glomerulonephritis, but the clinical benefit of rapid elimination has not been determined, even in anti-glomerular basement membrane (GBM) disease. Even less is known about the importance of autoantibody characteristics, including epitope specificity and immunoglobulin G (IgG) subclass distribution. We aimed to address this by characterizing the autoantibody profile in anti-GBM patients: we utilized samples from the GOOD-IDES-01 (treating GOODpasture's disease with Imunoglobulin G Degrading Enzyme of Streptococcus pyogenous) (ClinicalTrials.gov identifier: NCT03157037) trial , where imlifidase, which cleaves all IgG in vivo within hours, was given to 15 anti-GBM patients.

methodsIn the GOOD-IDES-01 trial, plasmapheresis was (re)started if anti-GBM antibodies rebounded. Serum samples were collected prospectively for 6 months and analyzed for anti-GBM epitope specificity using recombinant constructs of the EA and EB epitopes, IgG subclass using monoclonal antibodies, and anti-neutrophil cytoplasmic antibodies (ANCA). The results were correlated with clinical data.

resultsPatients with a rebound (n = 10) tended to have lower eGFR at 6 months (11 vs 34 mL/min/1.73 m2, P = .055), and patients with dialysis at 6 months had a higher EB/EA ratio at rebound (0.8 vs 0.5, P = .047). Moreover, two patients demonstrated increasing epitope restriction and several patients displayed a shift in subclass distribution at rebound. Six patients were double positive for ANCA. ANCA rebound was seen in 50% of patients; only one patient remained ANCA positive at 6 months.

conclusionsIn this study, rebound of anti-GBM antibodies, especially if directed against the EB epitope, was associated with a worse outcome. This supports the notion that all means should be used to eliminate anti-GBM antibodies. In this study ANCA was removed early and long-term by imlifidase and cyclophosphamide.

Indexed as

Antibodies, Antineutrophil CytoplasmicAnti-Glomerular Basement Membrane DiseaseAutoantibodiesEpitopesHumansImmunoglobulin GImmunosuppressive AgentsRenal DialysisAntibodies, Antineutrophil Cytoplasmicantiglomerular basement membrane antibodyAutoantibodiesEpitopesImmunoglobulin GImmunosuppressive Agentsanti-GBM diseaseautoantibody-mediated renal diseasedouble positivityepitope specificitysubclass distribution

Identifiers

PMID37385828
PMCPMC10730795
OpenAlexW4382515254

What OpenQuestion holds

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LicenceCC BY-NC
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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.