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Clinical predictors for restrictive allograft syndrome: A nested case-control study.

Hanne Beeckmans1, Pieterjan Kerckhof2, Nilufer Acet Öztürk3

  • 1Laboratory of Respiratory Diseases and Thoracic Surgery (BREATHE), Department of CHROMETA, KU Leuven, Leuven, Belgium; Department of Respiratory Diseases, University Hospitals Leuven, Leuven, Belgium.

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|February 1, 2025
PubMed
Summary

Identifying risk factors for restrictive allograft syndrome (RAS) after lung transplantation is crucial. Higher eosinophils, specific infections, and anti-HLA antibodies are linked to RAS development, aiding early detection and management.

Keywords:
HLA antibodiesantibody-mediated rejectionchest CT opacitieschronic lung allograft dysfunctioninfectionlung transplantationrestrictive allograft syndrometreatable traits

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Area of Science:

  • Transplantation immunology
  • Pulmonology
  • Allograft dysfunction

Background:

  • Restrictive allograft syndrome (RAS) is a severe form of chronic lung allograft dysfunction (CLAD) post-lung transplant.
  • Risk factors for RAS are not well-established, hindering proactive management.

Purpose of the Study:

  • To identify clinical risk factors associated with the development of RAS after lung transplantation.
  • To find early indicators of RAS for improved patient outcomes.

Main Methods:

  • Retrospective nested case-control study involving 69 RAS patients and 69 matched non-CLAD controls.
  • Analysis of clinical data, including blood/bronchoalveolar cell counts, infection history, antibody profiles, and histopathology.

Main Results:

  • RAS patients had higher blood and bronchoalveolar eosinophils and lymphocytes.
  • Increased incidence of Pseudomonas, fungal (Aspergillus), SARS-CoV-2, and CMV infections observed in RAS group.
  • Strong association between persistent donor-specific anti-HLA antibodies (targeting HLA-DQ/DR) and antibody-mediated rejection with RAS.
  • Histopathologic lung injury and persistent CT opacities were early RAS indicators.

Conclusions:

  • Elevated eosinophils, specific infections, anti-HLA antibodies, and specific histopathologic findings are key risk factors for RAS.
  • Proactive identification and management of these factors may reduce allograft dysfunction and RAS progression.
  • Further research into early treatment strategies targeting modifiable risk factors is warranted to improve long-term lung transplant outcomes.