Evidence map›Paper›PMID 23429890›Full record

ArticleChest2013

Latent class analysis identifies distinct phenotypes of primary graft dysfunction after lung transplantation.

Rupal J Shah, Joshua M Diamond, Edward Cantu, James C Lee, David J Lederer, Vibha N Lama, Jonathan Orens, Ann Weinacker, David S Wilkes, Sangeeta Bhorade and 9 more

Open access · bronzeAbstract readMulticenter Study
In one paragraph

Article in Chest, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Primary graft dysfunction: what we know.Journal of thoracic disease · 2021
    Review
  15. Use of donor-derived-cell-free DNA as a marker of early allograft injury in primary graft dysfunction (PGD) to predict the risk of chronic lung allograft dysfunction (CLAD).The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2021
    Observational
  16. Adipose tissue quantification and primary graft dysfunction after lung transplantation: The Lung Transplant Body Composition study.The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation · 2019
    Article
  17. Review
  18. Lung transplantation for pulmonary sarcoidosis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2019
    Review
  19. Early Graft Dysfunction after Lung Transplantation.Current pulmonology reports · 2018
    Article
  20. Peripheral Blood Gene Expression Changes Associated With Primary Graft Dysfunction After Lung Transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 11 institutions in 1 country.

Rupal J ShahPulmonary, Allergy, and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia, PA; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA. Electronic address: rupal.shah@uphs.upenn.edu.
Joshua M DiamondPulmonary, Allergy, and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia, PA; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA.
Edward CantuDivision of Cardiovascular Surgery, University of Pennsylvania School of Medicine, Philadelphia, PA.
James C LeePulmonary, Allergy, and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia, PA.
David J LedererDivision of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NY.
Vibha N LamaDivision of Pulmonary, Allergy, and Critical Care Medicine, University of Michigan, Ann Arbor, MI.
Jonathan OrensDivision of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Johns Hopkins University Hospital, Baltimore, MD.
Ann WeinackerDepartment of Pulmonary and Critical Care, Stanford University, Palo Alto, CA.
David S WilkesDivision of Pulmonary, Allergy, and Critical Care Medicine, Indiana University School of Medicine, Indianapolis, IN.
Sangeeta BhoradeDivision of Pulmonary and Critical Care Medicine, University of Chicago, Chicago, IL.
Keith M WilleDivision of Pulmonary and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL.
Lorraine B WareDivision of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN.
Scott M PalmerDivision of Pulmonary, Allergy, and Critical Care Medicine, Duke University, Raleigh-Durham, NC.
Maria CrespoDivision of Pulmonary, Allergy, and Critical Care, University of Pittsburgh, Pittsburgh, PA.
A Russell LocalioCenter for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA.
Ejigayehu DemissieCenter for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA.
Steven M KawutPulmonary, Allergy, and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia, PA; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA.
Scarlett L BellamyCenter for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA.
Jason D ChristiePulmonary, Allergy, and Critical Care Division, University of Pennsylvania School of Medicine, Philadelphia, PA; Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, PA.
University of Pennsylvania · USColumbia University · USDuke University · USIndiana University – Purdue University Indianapolis · USJohns Hopkins University · USStanford University · USUniversity of Alabama at Birmingham · USUniversity of Chicago · USUniversity of Michigan–Ann Arbor · USUniversity of Pittsburgh · USVanderbilt University Medical Center · US

Funding

Clinical Risk Factors for Primary Graft DysfunctionR01HL087115 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CHRISTIE, JASON D · 2007 to 2017
$7.1M
Treatment of Pulmonary Edema in Organ DonorsR01HL088263 · NHLBI · VANDERBILT UNIVERSITY · PI WARE, LORRAINE B · 2008 to 2012
$2.3M
Midcareer Investigator Award in Patient-Oriented Research in Acute Lung InjuryK24HL103836 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI WARE, LORRAINE B · 2010 to 2020
$1.6M
Mentored Patient Oriented Research in Lung TransplantationK24HL115354 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CHRISTIE, JASON D · 2012 to 2021
$1.2M
Lung Transplant donor: prediction, evaluation, and mechanismK23HL116656 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI CANTU, EDWARD · 2013 to 2017
$872k
NHLBI NIH HHS HL088263NHLBI NIH HHS K23 HL116656NHLBI NIH HHS K24 HL103836NHLBI NIH HHS K24 HL115354NHLBI NIH HHS R01 HL087115NHLBI NIH HHS R01-HL087115NHLBI NIH HHS R01 HL088263
6 · The paper itself

Abstract

backgroundThere is significant heterogeneity within the primary graft dysfunction (PGD) syndrome. We aimed to identify distinct grade 3 PGD phenotypes based on severity of lung dysfunction and patterns of resolution.

methodsSubjects from the Lung Transplant Outcomes Group (LTOG) cohort study with grade 3 PGD within 72 h after transplantation were included. Latent class analysis (LCA) was used to statistically identify classes based on changes in PGD International Society for Heart & Lung Transplantation grade over time. Construct validity of the classes was assessed by testing for divergence of recipient, donor, and operative characteristics between classes. Predictive validity was assessed using time to death.

resultsOf 1,255 subjects, 361 had grade 3 PGD within the first 72 h after transplantation. LCA identified three distinct phenotypes: (1) severe persistent dysfunction (class 1), (2) complete resolution of dysfunction within 72 h (class 2), and (3) attenuation, without complete resolution within 72 h (class 3). Increased use of cardiopulmonary bypass, greater RBC transfusion, and higher mean pulmonary artery pressure were associated with persistent PGD (class 1). Subjects in class 1 also had the greatest risk of death (hazard ratio, 2.39; 95% CI, 1.57-3.63; P < .001).

conclusionsThere are distinct phenotypes of resolution of dysfunction within the severe PGD syndrome. Subjects with early resolution may represent a different mechanism of lung pathology, such as resolving pulmonary edema, whereas those with persistent PGD may represent a more severe phenotype. Future studies aimed at PGD mechanism or treatment may focus on phenotypes based on resolution of graft dysfunction.

Indexed as

Lung TransplantationPrimary Graft DysfunctionAdultFemaleHumansMaleMiddle AgedPhenotypeProspective StudiesRisk AssessmentRisk FactorsSeverity of Illness Index

Identifiers

PMID23429890
PMCPMC3734891
OpenAlexW2171922445

What OpenQuestion holds

Textmetadata
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Registered trials

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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.