Evidence map›Paper›PMID 40301559›Full record

Trial reportNature medicine2025

Effect of felzartamab on the molecular phenotype of antibody-mediated rejection in kidney transplant biopsies.

Matthias Diebold, Patrick T Gauthier, Katharina A Mayer, Martina Mackova, Christian Hinze, Jessica Chang, Uptal D Patel, Ekkehard Schütz, Bernd Jilma, Eva Schrezenmeier and 3 more

Registry-linked trialAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Nature medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01299168 (Multi-centric Observational Study to Analyse the Diagnostic Molecular Features in the Clinical Setting of Kidney Allograft Biopsies), which is not on this map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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.

NCT01299168 recruitingnot on this map

Multi-centric Observational Study to Analyse the Diagnostic Molecular Features in the Clinical Setting of Kidney Allograft Biopsies

TypeobservationalSponsorUniversity of AlbertaRan2011 to 2028Enrolled500ConditionsValidation Study of Molecular Diagnostic System, Development of Reporting System for Molecular Diagnosis, Incorporate Molecular Diagnosis Into Diagnostic Standards
3 · Its place in the literature

Who cites it

19 citing papers in PubMed.

  1. Review
  2. Article
  3. Biologics in Kidney Transplantation: Why and How Should We Personalize Their Dosage?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Sensitization in Transplantation Assessment of Risk 2025 innate working group: The potential role of innate allorecognition in kidney allograft damage.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Review
  15. Article
  16. Article
  17. [Innovations in transplantation medicine].Innere Medizin (Heidelberg, Germany) · 2025
    Review
  18. Antibody-mediated rejection-treatment standard.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
  19. Targeting CD38 in Antibody-Mediated Rejection.Transplant international : official journal of the European Society for Organ Transplantation · 2025
    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

13 authors.

Matthias Diebold *Division of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0002-6914-9132
Patrick T Gauthier *Alberta Transplant Applied Genomics Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Katharina A MayerDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria.ORCID http://orcid.org/0000-0003-2495-790X
Martina MackovaAlberta Transplant Applied Genomics Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.
Christian HinzeDepartment of Nephrology and Hypertension, Hannover Medical School, Hannover, Germany.
Jessica ChangAlberta Transplant Applied Genomics Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada.ORCID http://orcid.org/0000-0001-5039-2186
Uptal D PatelHuman Immunology Biosciences, South San Francisco, CA, USA.ORCID http://orcid.org/0000-0002-6905-6649
Ekkehard SchützChronix Biomedical GmbH, Göttingen, Germany.
Bernd JilmaDepartment of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria.
Eva SchrezenmeierDepartment of Nephrology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Klemens BuddeDepartment of Nephrology, Charité Universitätsmedizin Berlin, Berlin, Germany.ORCID http://orcid.org/0000-0002-7929-5942
Georg A BöhmigDivision of Nephrology and Dialysis, Department of Medicine III, Medical University of Vienna, Vienna, Austria. georg.boehmig@meduniwien.ac.at.ORCID http://orcid.org/0000-0002-7600-912X
Philip F HalloranAlberta Transplant Applied Genomics Centre, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, Canada. phallora@ualberta.ca.ORCID http://orcid.org/0000-0003-1371-1947

Funding

Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) P500PM_214237
6 · The paper itself

Abstract

A recent randomized controlled trial demonstrated that treatment with anti-CD38 monoclonal antibody felzartamab suppressed antibody-mediated rejection (ABMR) in kidney transplant patients but with recurrence after treatment in some patients. Here we examined the molecular effects of 6 months of felzartamab treatment on biopsies from the trial using genome-wide microarray analysis, comparing pretreatment, end-of-treatment (week 24) and posttreatment (week 52) biopsies from ten patients treated with felzartamab and ten patients in the placebo group. Felzartamab reduced molecular ABMR activity scores in all nine patients with baseline ABMR activity, selectively suppressing interferon gamma-inducible and natural killer cell transcripts, with minimal effect on ABMR stage-related endothelial transcripts. Suppression was often incomplete when ABMR activity was intense, and molecular recurrence was nearly universal by week 52. However, we also found that felzartamab had parenchymal benefits at week 52, slowing the trajectories of molecular injury scores beyond the treatment period, suggesting that suppression of ABMR activity could potentially slow future progression to kidney failure. These data provide preliminary molecular insights into the effects of CD38-directed treatment for ABMR, which have the potential to inform future therapeutic strategies.

Indexed as

Antibodies, MonoclonalAntibodies, Monoclonal, HumanizedGraft RejectionKidney TransplantationADP-ribosyl Cyclase 1AdultBiopsyFemaleHumansKidneyKiller Cells, NaturalMaleMiddle AgedPhenotypeADP-ribosyl Cyclase 1Antibodies, MonoclonalAntibodies, Monoclonal, Humanized

Identifiers

PMID40301559
PMCPMC12092283

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.