Abstract and Introduction
Background: Acute kidney injury (AKI) is a common complication after liver transplantation, which is associated with increased morbidity and mortality. Therefore, this study investigated mannitol as an oxygen-free radical scavenger and its role in the prevention of early AKI after living donor liver transplantation (LDLT).
Methods: A total of 84 adult patients who underwent LDLT were randomly assigned to two equal groups: the M group, where patients received 1 g/kg mannitol 20%, or the S group, where patients received an equal volume of saline. The primary outcome was the incidence of early AKI, defined as a 0.3 mg/dl increase in the serum creatinine 48 h postoperatively. Laboratory assessments of the graft and creatinine were recorded until 3 months after transplantation besides the post-reperfusion syndrome and the intraoperative hemodynamic measurements.
Results: The AKI incidence was comparable between groups (relative risk ratio of 1.285, 95% CI 0.598–2.759, P = 0.518). Moreover, AKI stages and serum creatinine 3 months after transplantation, P = 0.23 and P = 0.25, respectively. The incidence of the post-reperfusion syndrome was comparable in both groups, 29/39 (74.4%) and 31/41 (75.6%) in M and S groups, respectively, P = 0.897. The intraoperative hemodynamic parameters showed no significant difference between groups using the area under the curve.
Conclusion: The current LDLT recipient sample was insufficient to demonstrate that pre-reperfusion 1 g/kg mannitol infusion would reduce the risk of early AKI or post-reperfusion syndrome.
Clinical Trial Registration Number: Pan African Clinical Trials Registry (PACTR202203622900599); https://pactr.samrc.ac.za/TrialDisplay.aspx?TrialID=21511.
Liver transplantation became the standard treatment for end-stage liver disease and selected cases of liver neoplasms. The incidence of acute kidney injury (AKI) can reach up to 95% after the liver transplantation (LT) setting due to ischemia-reperfusion injury (IRI).
Degradation of adenosine triphosphate (ATP) molecules results in an accumulation of hypoxanthine during liver graft ischemia. Hypoxanthine produces toxic reactive oxygen species (ROSs) by xanthine oxidase after reperfusion and reoxygenation of the graft.[2,3] Those ROS produce cellular injury by lipid peroxidation of the cell membranes, leukocyte activation, chemotaxis, and leukocytes-endothelial adhesion.[2,3]
Mannitol, vitamin C, vitamin E, superoxide dismutase, N-acetyl cysteine, and allopurinol are common examples of antioxidants. Mannitol and ascorbic acid were effective in scavenging and inhibiting ROS after liver IRI on the histopathological and biochemical levels. Additionally, mannitol creates a hyperosmolar environment, which may blunt the IRI.
Mannitol drip within 15 min of cross-clamping enhances renal preservation during living donor kidney transplantation. While in LT, mannitol infusion during the anhepatic phase could ameliorate post-reperfusion syndrome (PRS), Whitta and colleagues found no protective effect of mannitol on kidney function during LT.
We hypothesized that using mannitol during the anhepatic phase in living donor liver transplantation (LDLT) would decrease the early AKI incidence. The aim of the study was to investigate the role of mannitol for prevention of AKI and PRS in LDLT.
BMC Anesthesiol. 2022;22(393) © 2022 BioMed Central, Ltd.