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This retrospective study of 70 liver transplant patients examined whether intraoperative alactic base excess (ABE), a measure of metabolic acid-base imbalance excluding lactate, could predict acute kidney injury (AKI) within 7 days after surgery. While patients who developed AKI had lower ABE values during surgery, after adjusting for other clinical factors, ABE was not independently associated with either overall AKI or severe AKI. The findings suggest that a single intraoperative ABE measurement has limited utility for predicting postoperative kidney injury in liver transplant recipients.
Why it matters
Identifying reliable intraoperative predictors of AKI after liver transplantation could enable earlier interventions and improved patient outcomes. This study suggests that clinicians should not rely on single ABE measurements alone for AKI risk assessment, though monitoring ABE trends throughout different surgical phases may still prove valuable.
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⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Background: Acute kidney injury (AKI) is a common complication after liver transplantation (LT). Alactic base excess (ABE) reflects the metabolic component of acid base disturbances not attributable to lactate and has been associated with kidney dysfunction in other clinical settings. We evaluated the association between intraoperative ABE and postoperative AKI after LT. Methods: We conducted a retrospective cohort study of adult patients undergoing LT. ABE was calculated from standard base excess and lactate obtained from the last intraoperative arterial blood gas analysis. The primary outcome was creatinine based AKI occurring within the first 7 postoperative days according to Kidney Disease: Improving Global Outcomes criteria. The association between ABE and AKI was estimated using modified Poisson regression with robust variance, adjusted for age, sex, body mass index, MELD score, cold ischemia time, and anhepatic phase duration. A post hoc exploratory analysis evaluated severe AKI, defined as KDIGO stages 2,3. Results: Seventy patients were included, of whom 32 (45.7%) developed AKI. ABE values were lower among patients who developed AKI than among those who did not (median, -1.15 vs 0.75 mmol/L; Hodges Lehmann location shift, -1.60 mmol/L; 95%CI, -2.80 to -0.20). After multivariable adjustment, ABE was not independently associated with AKI (aRR, 0.91; 95%CI, 0.82-1.01; p=0.07). Severe AKI occurred in 14 patients (20.0%), and ABE was not independently associated with severe AKI (aRR, 0.98; 95%CI, 0.78-1.23; p=0.87). Sensitivity analyses yielded consistent findings. Conclusions: A single intraoperative ABE measurement was not independently associated with postoperative AKI or severe AKI after LT. Serial measurements across different phases of transplantation may better characterize the potential relationship between ABE dynamics and postoperative kidney injury.