Background <p>Combined liver–kidney transplantation (CLKT) is associated with substantial intraoperative hemodynamic instability and metabolic stress. The role of modifiable intraoperative perfusion-related exposures in early allograft dysfunction (EAD) remains incompletely defined.</p> Methods <p>In this retrospective cohort study, adult and pediatric CLKT recipients (2016–2025) were evaluated. Intraoperative exposures included cumulative duration of mean arterial pressure (MAP) below 65 and 55 mmHg, norepinephrine area under the curve, and serial serum lactate measurements. EAD was defined using established criteria. Discriminatory performance was assessed using receiver operating characteristic analysis, and associations were explored using logistic regression.</p> Results <p>Among 25 recipients, EAD occurred in 8 (32%). Patients with EAD had significantly longer cumulative durations of MAP &lt; 65 mmHg and higher end-of-surgery serum lactate levels. The cumulative duration of MAP &lt; 65 mmHg demonstrated strong discriminatory performance for EAD (AUC 0.85; 95% CI 0.60–1.00), and end-of-surgery serum lactate also showed robust discrimination (AUC 0.82). Vasopressor exposure did not differ between groups. In multivariable analysis, cumulative MAP &lt; 65 mmHg exposure showed a borderline association with EAD. Thirty-day and 90-day mortality were markedly higher in the EAD group (50% and 62.5%, respectively) compared with 0% in the non-EAD group; however, given the small number of events and complete separation between groups, these findings should be regarded as exploratory.</p> Conclusions <p>EAD after CLKT is associated with sustained moderate hypotension and impaired metabolic recovery. These hypothesis-generating findings suggest that intraoperative perfusion adequacy may represent a potentially modifiable determinant of early graft function, warranting prospective validation in larger, multicenter cohorts.</p>

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Intraoperative hemodynamic instability and metabolic recovery are associated with early allograft dysfunction after combined liver–kidney transplantation: a single-center cohort study

  • Taylan Sahin,
  • Ali Sait Kavakli,
  • Alaaddin Aydin,
  • Cansu Altuntas,
  • Eryigit Eren,
  • Mehmet Tasdemir,
  • Hakan Parlak,
  • Mehmet Tokac,
  • Fatih Ensaroglu,
  • Ali Kocyigit,
  • Ayhan Dinckan

摘要

Background

Combined liver–kidney transplantation (CLKT) is associated with substantial intraoperative hemodynamic instability and metabolic stress. The role of modifiable intraoperative perfusion-related exposures in early allograft dysfunction (EAD) remains incompletely defined.

Methods

In this retrospective cohort study, adult and pediatric CLKT recipients (2016–2025) were evaluated. Intraoperative exposures included cumulative duration of mean arterial pressure (MAP) below 65 and 55 mmHg, norepinephrine area under the curve, and serial serum lactate measurements. EAD was defined using established criteria. Discriminatory performance was assessed using receiver operating characteristic analysis, and associations were explored using logistic regression.

Results

Among 25 recipients, EAD occurred in 8 (32%). Patients with EAD had significantly longer cumulative durations of MAP < 65 mmHg and higher end-of-surgery serum lactate levels. The cumulative duration of MAP < 65 mmHg demonstrated strong discriminatory performance for EAD (AUC 0.85; 95% CI 0.60–1.00), and end-of-surgery serum lactate also showed robust discrimination (AUC 0.82). Vasopressor exposure did not differ between groups. In multivariable analysis, cumulative MAP < 65 mmHg exposure showed a borderline association with EAD. Thirty-day and 90-day mortality were markedly higher in the EAD group (50% and 62.5%, respectively) compared with 0% in the non-EAD group; however, given the small number of events and complete separation between groups, these findings should be regarded as exploratory.

Conclusions

EAD after CLKT is associated with sustained moderate hypotension and impaired metabolic recovery. These hypothesis-generating findings suggest that intraoperative perfusion adequacy may represent a potentially modifiable determinant of early graft function, warranting prospective validation in larger, multicenter cohorts.