4.6 Article

A Focused Review on Primary Graft Dysfunction after Clinical Lung Transplantation: A Multilevel Syndrome

期刊

CELLS
卷 11, 期 4, 页码 -

出版社

MDPI
DOI: 10.3390/cells11040745

关键词

acute lung injury; histology; ischemia-reperfusion injury; lung transplantation; pathophysiology; primary graft dysfunction; radiology; review

资金

  1. Broere Foundation
  2. Research Foundation Flanders (FWO) [12G8715N, 1198920N]
  3. UZ Leuven research grant [STG15/023]
  4. KU Leuven [C24/18/073, C16/19/005]
  5. KU Leuven University Chair - Medtronic
  6. University Hospitals Leuven (KOOR-UZ Leuven)
  7. Research Foundation Flanders project (FWO) [G090922N]

向作者/读者索取更多资源

Primary graft dysfunction (PGD) is the clinical syndrome of acute lung injury after lung transplantation, involving various levels including clinical, physiological, radiological, histological, and cellular. Understanding these aspects of PGD can provide insights into acute lung failure after transplantation and contribute to the development of novel therapies.
Primary graft dysfunction (PGD) is the clinical syndrome of acute lung injury after lung transplantation (LTx). However, PGD is an umbrella term that encompasses the ongoing pathophysiological and -biological mechanisms occurring in the lung grafts. Therefore, we aim to provide a focused review on the clinical, physiological, radiological, histological and cellular level of PGD. PGD is graded based on hypoxemia and chest X-ray (CXR) infiltrates. High-grade PGD is associated with inferior outcome after LTx. Lung edema is the main characteristic of PGD and alters pulmonary compliance, gas exchange and circulation. A conventional CXR provides a rough estimate of lung edema, while a chest computed tomography (CT) results in a more in-depth analysis. Macroscopically, interstitial and alveolar edema can be distinguished below the visceral lung surface. On the histological level, PGD correlates to a pattern of diffuse alveolar damage (DAD). At the cellular level, ischemia-reperfusion injury (IRI) is the main trigger for the disruption of the endothelial-epithelial alveolar barrier and inflammatory cascade. The multilevel approach integrating all PGD-related aspects results in a better understanding of acute lung failure after LTx, providing novel insights for future therapies.

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