Acute Kidney Injury After Liver Transplantation Is Set in Motion Early After Reperfusion of the Liver Graft: A Prospective Cohort Study.
1Abdominal Transplant Surgery, University Hospitals Leuven, Leuven, Belgium
2Abdominal Transplant Surgery, University of Liège, Academic Hospital, Liège, Belgium.
Meeting: 2016 American Transplant Congress
Abstract number: 79
Keywords: Liver transplantation, Post-operative complications, Renal injury, Risk factors
Session Information
Session Name: Concurrent Session: The Kidney in Liver Transplantation
Session Type: Concurrent Session
Date: Sunday, June 12, 2016
Session Time: 2:30pm-4:00pm
Presentation Time: 3:06pm-3:18pm
Location: Room 302
Objective: Determine creatinine changes during liver transplantation and risk factors for acute kidney injury (AKI) in a prospective cohort study (NCT01333319).
Background Data: AKI, a major risk factor for poorer outcome after liver transplantation, is usually attributed to posttransplant events and drug toxicity. In rodents, liver ischemia-reperfusion injury (IRI) has been shown to cause AKI. There are no prospective studies investigating liver transplantation and IRI as cause of AKI.
Methods: In 80 adult liver-only recipients (no hepatorenal syndrome or dialysis) AKI was assessed by RIFLE-criteria based on creatinine changes from baseline to hepatectomy, reperfusion, postreperfusion [0.5h, 1h, 6h, 12h, postoperative day (POD) 1-5]. Kidney injury markers [urinary kidney-injury-molecule-1, plasma heart-type-fatty-acid-binding-protein (H-FABP)] at baseline, 6h, 12h postreperfusion were compared between Injury/Failure and matched cohort without AKI. Multivariate logistic regression determined AKI risk factors. Data: median (IQR).
Results: 21 patients (26%) developed AKI at 12h (6h-POD1) postreperfusion; 10 progressed from Risk to Injury; 5 to Failure. Cold ischemia time was longer in AKI-patients [7.9h (6.9-9.0) vs 5.7h (4.8-7.8), p=0.004). AKI-patients had higher peak AST [2430U/L (718-4645) vs 944U/L (675-1347), p<0.001], more early allograft dysfunction (62% vs 17%, p<0.001), and longer ICU/hospital stay vs to those without AKI. Creatinine changes during liver transplantation and follow-up were larger in AKI-patients vs those without AKI, despite similar tacrolimus trough levels. In AKI-patients creatinine increased during liver transplantation and was higher vs baseline at 6h-POD4; perop creatinine remained stable in those without AKI. H-FABP at 12h was higher in Injury/Failure. Peak AST (6h) was the only risk factor for AKI [adjusted odds ratio 2.42 (1.24-4.91), p<0.001]. Patient survival at 1y was 90% for AKI-patients vs 98% for those without AKI (p=0.17).
Conclusion: AKI is initiated during liver transplantation and its association with peak AST suggests liver IRI as determinant. Identifying operating mechanisms and early intervention might avoid AKI associated morbidity.
CITATION INFORMATION: Jochmans I, Meurisse N, Monbaliu D, Pirenne J. Acute Kidney Injury After Liver Transplantation Is Set in Motion Early After Reperfusion of the Liver Graft: A Prospective Cohort Study. Am J Transplant. 2016;16 (suppl 3).
To cite this abstract in AMA style:
Jochmans I, Meurisse N, Monbaliu D, Pirenne J. Acute Kidney Injury After Liver Transplantation Is Set in Motion Early After Reperfusion of the Liver Graft: A Prospective Cohort Study. [abstract]. Am J Transplant. 2016; 16 (suppl 3). https://atcmeetingabstracts.com/abstract/acute-kidney-injury-after-liver-transplantation-is-set-in-motion-early-after-reperfusion-of-the-liver-graft-a-prospective-cohort-study/. Accessed May 9, 2025.« Back to 2016 American Transplant Congress