Perioperative kidney injury in liver transplantation: a prospective study with renal histology and measured glomerular filtration rates

Abstract

Background

Acute kidney injury (AKI) is frequent after liver transplantation (LT), with impact on graft function, morbidity and mortality. Although multifactorial, the pathophysiology of perioperative kidney injury remains unclear. Our aims were to analyze the frequency, evolution and risk factors for kidney impairment during the peri- and early post-operative period.

Methods

In a prospective, single-center study of 27 adult patients undergoing first single-organ LT, we analyzed measured glomerular filtration rate (mGFR) pre-transplant, at post-operative day (POD) 10, and at 1, 3, 12 and 36 months. Kidney and liver graft biopsies were performed during LT.

Results

A median mGFR decline of 45% was detected from pre-transplant to POD 10, correlating strongly with the mGFR evolution from baseline to 12 months (rs = 0.80, p<.001) and baseline to 36 months (rs = 0.82, p<.001). AKI occurred in 59% of recipients within 48 h of LT, notably before the introduction of calcineurin inhibitors on POD 3. AKI was strongly associated with mGFR at 12 and 36 months. Kidney and liver graft biopsies showed only minor histological changes. Donor and recipient body mass index, recipient age, model of end-stage liver disease score, diagnosis of hepatitis C, donor cause of death, as well as bleeding, transfusions and duration of the anhepatic phase correlated with early kidney dysfunction.

Conclusion

The greatest decline in mGFR was evident within 10 days and AKI within hours of LT, irrespective of baseline mGFR and before introduction of calcineurin inhibitors. Very early post-LT kidney injury has substantial consequences for long-term kidney function.

Keywords:

• Liver transplantation
• acute kidney injury
• chronic kidney disease
• measured glomerular filtration rate
• kidney histopathology
• hepatic ischemia reperfusion injury

Disclosure statement

No potential conflict of interest was reported by the author(s).

Author contributions

ÅN: the primary author, participated in study design and planning, data collection, statistical analysis, interpretation of results and writing of the first draft; FÅ: participated in statistical analysis, interpretation of results, revised and provided critical comments to the manuscript; JM: participated in study design, assessment and interpretation of biopsies, writing of the first draft and revision of the manuscript; WB: participated in revision of and provided constructive comments to the manuscript; SF: participated in study design and planning, interpretation of results and provided critical comments to the manuscript; GH: participated in study design and planning, interpretation of results, revised and provided critical comments to the manuscript.

Data availability statement

The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

Additional information

Funding

ÅN received research grants from Stiftelsen för Transplantations- och Cancerforskning, Stiftelsen Professor Lars-Erik Gelins Minnesfond, and Stiftelsen för Njursjuka.