Abstract
BackgroundAcute kidney injury (AKI) occurs frequently after liver transplantation and is associated with the development of chronic kidney disease and increased mortality. There is a lack of data on renal blood flow (RBF), oxygen consumption, glomerular filtration rate (GFR) and renal oxygenation, i.e. the renal oxygen supply/demand relationship, early after liver transplantation. Increased insight into the renal pathophysiology after liver transplantation is needed to improve the prevention and treatment of postoperative AKI. We have therefore studied renal hemodynamics, function and oxygenation early after liver transplantation in humans.MethodsSystemic hemodynamic and renal variables were measured during two 30-min periods in liver transplant recipients (n = 12) and post-cardiac surgery patients (controls, n = 73). RBF and GFR were measured by the renal vein retrograde thermodilution technique and by renal extraction of Cr-EDTA (= filtration fraction), respectively. Renal oxygenation was estimated from the renal oxygen extraction.ResultsIn the liver transplant group, GFR decreased by 40% (p < 0.05), compared to the preoperative value. Cardiac index and systemic vascular resistance index were 65% higher (p < 0.001) and 36% lower (p < 0.001), respectively, in the liver transplant recipients compared to the control group. GFR was 27% (p < 0.05) and filtration fraction 40% (p < 0.01) lower in the liver transplant group. Renal vascular resistance was 15% lower (p < 0.05) and RBF was 18% higher (p < 0.05) in liver transplant recipients, but the ratio between RBF and cardiac index was 27% lower (p < 0.001) among the liver-transplanted patients compared to the control group. Renal oxygen consumption and extraction were both higher in the liver transplants, 44% (p < 0.01) and 24% (p < 0.05) respectively.ConclusionsDespite the hyperdynamic systemic circulation and renal vasodilation, there is a severe decline in renal function directly after liver transplantation. This decline is accompanied by an impaired renal oxygenation, as the pronounced elevation of renal oxygen consumption is not met by a proportional increase in renal oxygen delivery. This information may provide new insights into renal pathophysiology as a basis for future strategies to prevent/treat AKI after liver transplantation.Trial registrationClinicalTrials.gov, NCT02455115. Registered on 23 April 2015.
Highlights
Acute kidney injury (AKI) occurs frequently after liver transplantation and is associated with the development of chronic kidney disease and increased mortality
Liver transplant recipients In the liver-transplanted group, informed consent was obtained from 14 patients
The renal oxygen supply/demand relationship was impaired in liver transplant recipients, as the increase in renal oxygen consumption was not met by a proportional increase in renal oxygen delivery, despite the hyperdynamic circulation seen in this group
Summary
Acute kidney injury (AKI) occurs frequently after liver transplantation and is associated with the development of chronic kidney disease and increased mortality. In patients with HRS, a splanchnic vasodilatation is seen This vasodilation is accompanied by an activation of the renin-angiotensin and of the sympathetic nervous system, resulting in increased renal vascular resistance. Blood flow will be distributed away from the kidneys and the kidneys will receive a decreased oxygen delivery [7, 8]. This could be considered as a potential mechanism causing AKI after liver transplantation
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