000917: Inflammation afterlife: how donor immune signals shape transplant futures

Published Date: 23rd November 2025

Publication Authors: Tridente. A

Introduction
Systemic hyper-inflammation is an established cause of organ dysfunction, evidenced by the multi-organ failure observed in sepsis [1]. Similarly, the process of death invokes a complex set of events leading to profound hyper-inflammation [2]. It is reasonable that in deceased organ donors, death-induced hyperinflammation could have significant consequences for organs being offered for transplant (Tx), hence current donor management guidelines advocating the administration of steroids early in the donor management process (DMP) to modulate donor inflammation and maximise organ utilisation [3]. Notably, disparities in graft quality and Tx success have been identified in organs received from deceased versus living donors [4-5]. It is hypothesised that donor death mechanisms and ensuing inflammation likely contribute to pre-Tx organ quality variations, with lasting effects on graft function.

Objective(s)
We performed a systematic review which aimed to 1) clarify what is currently known about the sources of inflammation following death, and 2) systematically evaluate the current body of evidence reporting higher levels of inflammation in deceased donors versus living donors and linking donor inflammation with kidney Tx outcome.

Method(s)
The review was conducted in agreement with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) reporting guidelines 8. We searched Medline, Web of Science, Scopus and CINHAL databases from January 2000 to March 2023 for articles relating donor inflammation with kidney Tx outcomes. National Institute of Health 'Quality Assessment Tool for Observational Cohort and Cross-Sectional Studies' was used to assess validity of studies.

Result(s)
From 530 articles screened, 21 studies were analysed, which included a total of 3397 donors and 4596 recipients. There was a very high degree of heterogeneity between studies in terms of the inflammatory markers assessed and the measured Tx outcomes, yet collective evidence showed higher inflammation, complement activation, and tissue injury in deceased donors compared with living donors and strongly suggested associations with less favourable short- and longterm Tx outcomes.

Conclusion(s)
To improve organ viability and Tx outcomes, a paradigm shift toward precision donor therapies is critical. Future efforts should prioritise disrupting specific drivers of inflammation and graft dysfunction, particularly dysregulated complement pathways, rather than relying on nonspecific immunosuppression. This targeted approach may suppress donor-derived inflammation more effectively, preserving organ function and also may expand the pool of transplantable grafts.

Tridente, A et al. (2025). 000917: Inflammation afterlife: how donor immune signals shape transplant futures. Intensive Care Medicine Experimental. 13(Suppl 1), p.476. [Online]. Available at: https://link.springer.com/article/10.1186/s40635-025-00797-x [Accessed 8 January 2026]