# Updates, Management, and Future of Diagnosing and Managing Chronic Lung Allograft Dysfunction

**Authors:** Emily Gosche, Joshua B. Smith

PMC · DOI: 10.3390/jcm15041543 · 2026-02-15

## TL;DR

This review discusses the diagnosis, management, and future research directions for chronic lung allograft dysfunction, a major issue in lung transplant patients.

## Contribution

The paper provides updated insights into diagnosing and managing CLAD and highlights future research opportunities.

## Key findings

- CLAD is the leading cause of death in lung transplant patients after the first year.
- Approximately 50% of lung transplant patients develop CLAD within five years.
- Recent guidelines have been published to help clinicians diagnose and characterize CLAD.

## Abstract

Lung transplantation provides a curative option for patients living with end-stage lung disease, with a goal of improving survival and quality of life. Chronic lung allograft dysfunction, or CLAD, represents a major cause of morbidity and mortality, particularly after the first year of transplant. Background/Objectives: The goal of this review is to outline the diagnosis and management of CLAD within the lung transplant population, as well as discuss future areas of potential research interest. Methods: A PubMed literature review of relevant publications regarding CLAD epidemiology, diagnosis, and management was performed to assess current understandings. Results: CLAD is the leading cause of death in lung transplant patients following the first year of transplant, and is common, with approximately 50% of patients exhibiting some degree of CLAD within five years of surgery. Well-established guidelines on diagnosis were recently published to aid clinicians in diagnosing and characterizing CLAD. Several medical and surgical interventions exist, although no therapy consistently and reliably stabilizes or reverses CLAD. Conclusions: CLAD management remains a priority within the lung transplant field as a leading cause of morbidity and mortality.

## Full-text entities

- **Genes:** MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, CD52 (CD52 molecule) [NCBI Gene 1043] {aka CDW52, EDDM5, HE5}, RHO (rhodopsin) [NCBI Gene 6010] {aka CSNBAD1, OPN2, RP4}, TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}, CD4 (CD4 molecule) [NCBI Gene 920] {aka CD4mut, IMD79, Leu-3, OKT4D, T4}
- **Diseases:** Dyslipidemia (MESH:D050171), death (MESH:D003643), AMR (MESH:D020274), airway neutrophilia (MESH:C563010), bronchiectasis (MESH:D001987), headaches (MESH:D006261), inflammation (MESH:D007249), injury to (MESH:D014947), GERD (MESH:D005764), end-stage lung disease (MESH:D058625), fibrosis (MESH:D005355), volume loss (MESH:D016388), toxicity (MESH:D064420), graft dysfunction (MESH:D055031), GvHD (MESH:D006086), thoracic cage injuries (MESH:D013898), decline of lung function (MESH:D055370), edema (MESH:D004487), Infection (MESH:D007239), IPF (MESH:D054990), endocrinopathies (MESH:C567425), neurotoxicity (MESH:D020258), cardiovascular disease (MESH:D002318), malignancy (MESH:D009369), lymphopenia (MESH:D008231), bone marrow suppression (MESH:D001855), pulmonary dysbiosis (MESH:D064806), damage to the lungs (MESH:D008171), COPD (MESH:D029424), dysfunction (MESH:D006331), pulmonary fibrosis (MESH:D011658), leukopenia (MESH:D007970), weight gain (MESH:D015430), pleural effusion (MESH:D010996), opacities (MESH:D003318), BOS (MESH:D000092122), cytomegalovirus (MESH:D003586), congestive heart failure (MESH:D006333), organ dysfunction (MESH:D009102), Serum sickness (MESH:D012713), infectious complications (MESH:D003141), bronchiolitis (MESH:D001988), ACR (MESH:D000208), neuromuscular disease (MESH:D009468), RAS (MESH:D002313)
- **Chemicals:** daclizumab (MESH:D000077561), tacrolimus (MESH:D016559), Montelukast (MESH:C093875), Everolimus (MESH:D000068338), Alemtuzumab (MESH:D000074323), cyclosporine (MESH:D016572), CLAD (-), MMF (MESH:D009173), Azithromycin (MESH:D017963), AZA (MESH:D001379), basiliximab (MESH:D000077552), Sirolimus (MESH:D020123), pirfenidone (MESH:C093844), leukotriene (MESH:D015289), 8-methoxypsoralen (MESH:D008730), macrolide (MESH:D018942), prednisone (MESH:D011241), Methotrexate (MESH:D008727), nintedanib (MESH:C530716), PFT (MESH:C006717)
- **Species:** Homo sapiens (human, species) [taxon 9606], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12941879/full.md

---
Source: https://tomesphere.com/paper/PMC12941879