Glycocalyx kinetics and injury during liver procurement and transplantation as predictors of early graft dysfunction

Ischemia-reperfusion injury causes endothelial damage, partly through degradation of the glycocalyx. This study aimed to evaluate glycocalyx degradation from graft procurement to reperfusion and assess its potential as a biomarker of early graft function (early allograft dysfunction, EAD).

This single-center observational prospective study was conducted at Paul Brousse Hospital from April 2022 to April 2023. All primary liver transplantation (LT) recipients were included. Glycocalyx degradation was assessed at procurement, at the end of cold ischemia, and during LT in liver graft caval effluent and correlated with liver histological injury. The primary endpoint was EAD, defined as a Model for Early Allograft Function score ≥9. We quantified glycocalyx components [Syndecan-1 (Synd-1), heparan sulfate, angiopoietin-1, and angiopoietin-2], inflammation (TNF-alpha), and cell death markers.

Thirty-one patients were included; 12 (39%) developed EAD. Synd-1 plasma levels at procurement (donor Synd-1 level = d-Synd-1) were significantly higher in patients with EAD [12,173 pg/mL (10,538-17,570) vs. 6,282 pg/mL (4,604-10,002), p = 0.004]. A plasma d-Synd-1 cutoff of 9,419.7 pg/mL predicted EAD [AUC = 0.81, 95% confidence interval (95% CI) (0.65-0.97); sensitivity 83%; specificity 74%, positive predictive value = 67%, negative predictive value = 88%, p < 0.05]. d-Synd-1 ≥9,419.7 pg/mL was associated with severe post-LT complications (p = 0.007).

d-Synd-1 levels in graft effluent during procurement may serve as a predictor of early allograft dysfunction. Strategies aimed at protecting the endothelial during procurement could improve graft outcomes.