Evidence map›Paper›PMID 40581272›Full record

ArticleThe Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation2025

Impact of donor specific antibodies on longitudinal lung function and baseline lung allograft dysfunction.

Muhtadi Alnababteh, Junfeng Sun, Rohan Meda, Lucia Ponor, Pali Shah, Joby Mathew, Hyesik Kong, Ananth Charya, R N Helen Luikart, Shambhu Aryal and 6 more

Registry-linked trialAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07516379 (GRAfT 2.0. A Multimodal Prospective Approach to Define the Mechanisms and Clinical Features of Acute and Chronic Rejection in Lung Transplantation), which is not on this map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–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.

NCT07516379 recruitingnot on this mapstarted 2026, after this paper: background citation

GRAfT 2.0. A Multimodal Prospective Approach to Define the Mechanisms and Clinical Features of Acute and Chronic Rejection in Lung Transplantation

TypeobservationalSponsorNational Heart, Lung, and Blood Institute (NHLBI)Ran2026 to 2032Enrolled100ConditionsLung Transplant, End Stage Lung Disease, Rejection
3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. International Society for Heart and Lung Transplantation Scientific Statement on pulmonary antibody-mediated rejection and proposed graft, antibody, and pathology (GAP) definition.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2026
    Guideline
  2. Article
  3. Review
  4. Article
  5. 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

16 authors.

Muhtadi AlnababtehLaborarory of Applied Precision Omics (APO), National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD.
Junfeng SunCritical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD.
Rohan MedaLaboratory of Transplantation Genomics, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD.
Lucia PonorGenomic Research Alliance for Transplantation (GRAfT); Division of Hospital Medicine, Johns Hopkins Bayview Medical Center, Baltimore, MD.
Pali ShahGenomic Research Alliance for Transplantation (GRAfT); Pulmonary and Critical Care Medicine, Johns Hopkins Hospital, Baltimore MD.
Joby MathewGenomic Research Alliance for Transplantation (GRAfT); Pulmonary and Critical Care Medicine, Johns Hopkins Hospital, Baltimore MD.
Hyesik KongLaborarory of Applied Precision Omics (APO), National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Laboratory of Transplantation Genomics, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Genomic Research Alliance for Transplantation (GRAfT).
Ananth CharyaDivision of Pulmonary and Critical Care Medicine, University of Maryland Medical Center, Baltimore MD.
R N Helen LuikartGenome Transplant Genomics (GTD); Division of Cardiovascular Medicine and Stanford University School of Medicine, Palo Alto, CA; Department of Pathology, Stanford University School of Medicine, Palo Alto, CA.
Shambhu AryalGenomic Research Alliance for Transplantation (GRAfT); Inova Fairfax Hospital, Falls Church, VA.
Steven D NathanGenomic Research Alliance for Transplantation (GRAfT); Inova Fairfax Hospital, Falls Church, VA.
Jonathan B OrensGenomic Research Alliance for Transplantation (GRAfT); Pulmonary and Critical Care Medicine, Johns Hopkins Hospital, Baltimore MD.
Kiran K KhushGenome Transplant Genomics (GTD); Division of Cardiovascular Medicine and Stanford University School of Medicine, Palo Alto, CA.
Moon JangLaborarory of Applied Precision Omics (APO), National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Laboratory of Transplantation Genomics, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Genomic Research Alliance for Transplantation (GRAfT).
Sean Agbor-EnohLaborarory of Applied Precision Omics (APO), National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Laboratory of Transplantation Genomics, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Genomic Research Alliance for Transplantation (GRAfT); Pulmonary and Critical Care Medicine, Johns Hopkins Hospital, Baltimore MD.
Michael B KellerLaborarory of Applied Precision Omics (APO), National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Laboratory of Transplantation Genomics, National Heart, Lung and Blood Institute (NHLBI), National Institutes of Health, Bethesda, MD; Genomic Research Alliance for Transplantation (GRAfT); Critical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD; Division of Pulmonary and Critical Care Medicine, University of Maryland Medical Center, Baltimore MD. Electronic address: mkeller1@som.umaryland.edu.

Funding

Use of donor-derived cell-free DNA for risk stratification and post-treatment monitoring of lung transplant patients at risk for chronic lung allograft dysfunctionK22HL166368 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI Michael Keller · 2025 to 2026
$498k
NHLBI NIH HHS K22 HL166368
6 · The paper itself

Abstract

backgroundLung transplantation offers life-saving benefits for patients with end-stage lung disease, however, long-term outcomes remain poor, with a median survival of 6.5 years. Identifying patients at risk for poor post-transplant lung function is crucial for improving outcomes. While peri-operative and demographic factors have previously been studied, the impact of donor-specific antibodies (DSA) on longitudinal post-transplant lung function remains unclear. This study examines the effects of DSA on post-transplant lung function and the risk of baseline lung allograft dysfunction (BLAD). RESEARCH QUESTION: Is DSA development linked to worse longitudinal lung function, higher BLAD rates, and poorer survival compared to DSA-negative patients regardless of the development of clinical AMR?

methodsThis study included lung transplant recipients from two prospective cohort studies, comparing DSA+ and DSA- patients. All participants underwent serial surveillance and clinically-indicated bronchoscopy, pulmonary function tests, and DSA testing. Statistical analysis included linear mixed models for longitudinal lung function data, multivariable logistic regression for BLAD, and survival analysis using Cox Proportional Hazard models.

resultsWe analyzed 213 patients with a median follow-up of 48.1 months. Among them, 50.7% developed DSA. DSA+ patients showed significantly lower rates of post-transplant spirometric improvement compared to DSA- patients (p=0.008 for %FVC; p=0.02 for %FEV1). After DSA detection, there was a significant decrease in the slopes of %FVC and %FEV1 (p=0.0008 and p=0.0006, respectively). DSA+ patients had a higher risk of developing BLAD (OR 2.14, 95% CI [1.45, 3.17], p=0.0001). Additionally, DSA+ patients had a higher risk of death (HR 2.98, 95% CI [1.79, 4.99], p<0.0001). These findings were consistent even when excluding patients with clinical antibody-mediated rejection (AMR).

interpretationOur study demonstrates that DSA development significantly impairs post-transplant lung function and increases the risk of BLAD even in the absence of clinical AMR. These findings suggest that DSA may serve as a biomarker of BLAD, and could potentially aid in risk stratification following lung transplantation.

Indexed as

Graft RejectionIsoantibodiesLungLung TransplantationTissue DonorsAdultAllograftsFemaleFollow-Up StudiesHumansMaleMiddle AgedProspective StudiesRespiratory Function TestsIsoantibodiesBLADDSALung Transplant

Identifiers

PMID40581272
PMCPMC13251798

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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.