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Association between Gut Colonization of Vancomycin-resistant Enterococci and Liver Transplant Outcomes
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- Author / Creator
- Chiang Jurado, Diana Alejandra
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Background: Vancomycin-resistant Enterococci (VRE) colonization is common in liver
transplant candidates. In addition to the risk of invasive enterococcal infections, dominance of
VRE colonization in the gut may contribute to low microbiota diversity playing a role in the
transplant outcomes. The purpose of this study is to evaluate the association between VRE
colonization and liver transplant on 6-month post-transplant complications and mortality at 2-
years.
Methods: We performed a retrospective cohort analysis of all adult patients (≥18 years old) who
underwent liver transplantation for chronic liver disease between 1st September 2014 and 31st
December 2017 at the University of Alberta Hospital in Edmonton, Alberta, Canada. Health
clinical outcome included patient and graft survival status, follow-up, and causes of death. The
primary cause of death was used to calculate Kaplan-Meier survival analysis. Multivariate
Analyses was performed to identify independent variables associated with outcome using Coxregression
Hazard Model. We calculated the hazard ratio at 95% confidence intervals of
mortality and acute kidney injury at 30 days. Patient mortality was the primary endpoint. Acute
rejection, clinically significant infections, ischemia reperfusion injury and acute kidney injury
were secondary endpoints.
Results: Of the included 343 liver transplants, 67% were males with a median age of 56.5. The
prevalence of VRE colonization pre-liver transplant was 19.8 % (68/343). VRE colonized patients
had higher MELD scores pre-transplant than non-colonized patients (median MELD 24 vs 17;
p<0.001), but other variables were similar between both groups. The association of VRE
colonization with pre-defined endpoints was: acute kidney injury at 30 days (66% vs 54%,
p=0.066), clinically significant bacterial/fungal infection (31% vs 21%, p=0.074), acute rejection
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(12% vs 11%, p=0.779) and death (15% vs 11%, p=0.435). Eight patients had VRE infection: 3
VRE colonized and 5 non-colonized pre-transplantation. 27 patients without VRE colonization at
baseline acquired VRE post-transplant (27/275, 9.8%). Probability of survival at baseline between
the VRE colonized and the non-VRE colonized was p=0.215. Percentage-free of acute kidney
injury at baseline was log rank test p=0.009 at 30 days. Of the 68 VRE colonized patients at
baseline, there were 45 (66.2%) presenting AKI versus 144 (52.4%) non-AKI. VRE colonized had
a higher hazard ratio (1.610, 95% CI: 1.127-2.299; p=0.009) for acute kidney injury at 30 days
post-transplantation. Of the 95 VRE colonized patients at baseline death 12 (12.6%) versus 248
alive 17 (6.9%), the VRE colonized showed a trend towards high risk of mortality at 2-years after
transplantation (1.974, 95% CI: 0.890-4.378; p=0.094).
Conclusion: VRE colonization pre-transplant was associated with the development of acute
kidney injury and a trend towards high risk of mortality. VRE colonization is an independent
predictor of complication in the liver transplant than MELD. These results suggest optimizing
the management of these patients in the peri-transplant period, including renal-protective
strategies in VRE positive patients. Further efforts are needed to decolonize patients before liver
transplantation. -
- Graduation date
- Spring 2020
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- Type of Item
- Thesis
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- Degree
- Master of Science
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- License
- Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.