Evidence map›Paper›PMID 30794945›Full record

Observational studyTransplant immunology2019

Prevalence of antibodies to lung self-antigens (Kα1 tubulin and collagen V) and donor specific antibodies to HLA in lung transplant recipients and implications for lung transplant outcomes: Single center experience.

Usha Rao, Monal Sharma, Thalachallour Mohanakumar, Chul Ahn, Ang Gao, Vaidehi Kaza

Open access · greenAbstract readObservational Study
In one paragraph

Observational study in Transplant immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 9% 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.

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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  5. Review
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  9. Immune processes in the pathogenesis of chronic lung allograft dysfunction: identifying the missing pieces of the puzzle.European respiratory review : an official journal of the European Respiratory Society · 2022
    Review
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  15. Three Is Better than One: An Improved Multiple-Hit Model of Primary Graft Dysfunction.American journal of respiratory cell and molecular biology · 2019
    Article
  16. 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

6 authors at 3 institutions in 1 country.

Usha RaoKaiser Permanente San Jose Medical Center, San Jose, CA, United States.
Monal SharmaSt. Joseph's Hospital and Medical Center, Phoenix, AZ, United States.
Thalachallour MohanakumarSt. Joseph's Hospital and Medical Center, Phoenix, AZ, United States.
Chul AhnDepartment of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Ang GaoDepartment of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, TX, United States.
Vaidehi KazaDivision of Pulmonary and Critical Care Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States. Electronic address: Vaidehi.kaza@utsouthwestern.edu.
The University of Texas Southwestern Medical Center · USSt. Joseph's Hospital and Medical Center · USKaiser Permanente San Jose Medical Center · US

Funding

IMMUNE MECHANISMS OF REJECTION IN HUMAN LUNG ALLOGRAFTSR01HL056643 · NHLBI · WASHINGTON UNIVERSITY · PI MOHANAKUMAR, THALACHALLOUR · 1996 to 2015
$6.5M
NHLBI NIH HHS R01 HL056643
6 · The paper itself

Abstract

purposeFor patients with end stage lung disease, lung transplantation (LT) remains the only definitive treatment option. Long term survival post LT is limited by acute and chronic allograft dysfunction. Antibodies to lung self-antigens Kα1Tubulin and collagen V (autoantibodies) have been implicated in adverse outcomes post LT. The aim of our study was to determine the prevalence of autoantibodies in pre- and post-transplant sera, evaluate the impact on post-transplant outcomes.

methodsIn a prospective observational cohort analysis, 44 patients were enrolled who received LT between 09/01/2014 and 10/31/2015. Pre- and post-transplant sera were analyzed using enzyme-linked immunosorbent assay (ELISA) for the presence of antibodies to collagen I, collagen V, and K-alpha 1 tubulin. The outcome variables are presence of primary graft dysfunction (PGD), cumulative acute cellular rejection (ACR), treatment with pulse steroids for clinical rejection, association with DSA, and onset of Bronchiolitis Obliterans Syndrome (BOS).

resultsIn our cohort, 33 patients (75%) tested positive for the presence of autoantibodies. Pre-transplant autoantibodies were present in 23 patients (70%). Only a small percentage (26%) cleared these antibodies with standard immunosuppression. Some developed de novo post-transplant (n = 10). PGD was observed in 34% of our cohort, however the presence of autoantibodies did not correlate with increase in the incidence or severity of PGD. The prevalence of donor specific antibodies (DSA) in the entire cohort was 73%, with an increased prevalence of DSA noted in the autoantibody positive group (78.7% vs. 54.5%) than in the autoantibody negative group. BOS was observed in 20% of the cohort, with a median time to onset of 291 days' post-transplant. Patients with pre-transplant autoantibodies had a statistically significant decrease in BOS-free survival (p = 0.029 by log-rank test).

conclusionsIn our cohort, we observed a high prevalence of autoantibodies and DSA in lung transplant recipients. Pre-transplant autoantibodies were associated with de novo development of DSA along with a decrease in BOS-free survival. Limitations to our study include the small sample size and single center enrollment, along with limited time for follow-up.

Indexed as

Lung TransplantationAcute DiseaseAdultAgedAutoantibodiesBronchiolitis ObliteransCohort StudiesCollagen Type ICollagen Type VFemaleGraft RejectionHLA AntigensHumansImmunity, HumoralIsoantibodiesLungAutoantibodiesCollagen Type ICollagen Type VHLA AntigensIsoantibodiesTUBA1A protein, humanTubulinAutoantibodiesBronchiolitis obliterans syndromeDonor specific antibodiesLung transplantPrimary graft dysfunction

Identifiers

PMID30794945
PMCPMC6513684
OpenAlexW2915780658

What OpenQuestion holds

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Registered trials

None linked

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.