Anil J. Trindade, Ciara M. Shaver, Caitlin T. Demarest, David Erasmus, Brian C. Keller, Nathaniel B. Langer, Jasleen Kukreja, Steven Hays, Lara Schaheen, Jose Luis Campo- Canaveral de la Cruz, Rodrigo Alonso-Moralejo, Silvana Crowley Carrasco, Rosalia Laporta Hernandez, Hamir Akbarshahi, Sandra Lindstedt, Stephanie Chang, Luis F. Angel, Alberto Benazzo, Péter Jaksch, Aman Sidhu, Marcelo Cypel, Matthew Bacchetta, Konrad Hoetzenecker
Primary graft dysfunction (PGD) is a proinflammatory syndrome occurring within the first days following lung transplantation. It is initiated by ischemia-reperfusion injury and perpetuated by donor and recipient immunologic factors, resulting in alveolar damage and progressive hypoxemic respiratory failure. PGD is a known risk factor for both early allograft failure and chronic lung allograft dysfunction (CLAD). Incidence of severe PGD remains high at 10% to 25%, though it is variable; risk factors for PGD include center experience, underlying recipient disease type, size matching, donor lung storage conditions, operative time, and post-operative management. Strategies to prevent PGD or mitigate the long-term consequences after it develops are sorely needed. However, lack of specificity of the current PGD definition may hamper further progress in the field, especially as it pertains to the development of robust and relevant clinical trials. We propose that future modifications of the PGD definition incorporate more objective surrogates of allograft injury and subsequent diffuse alveolar damage, which may improve our ability to accurately study disease pathogenesis and improve outcomes.