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Association between low fasting glucose of the living donor and risk of graft loss in the recipient after liver transplantation

Authors
 Hwa-Hee Koh  ;  Minyoung Lee  ;  Minyu Kang  ;  Seung Hyuk Yim  ;  Mun Chae Choi  ;  Eun-Ki Min  ;  Jae Geun Lee  ;  Dong Jin Joo  ;  Myoung Soo Kim  ;  Jae Seung Lee  ;  Deok-Gie Kim 
Citation
 SCIENTIFIC REPORTS, Vol.15 : 951, 2025-01 
Journal Title
SCIENTIFIC REPORTS
Issue Date
2025-01
MeSH
Adult ; Blood Glucose* / metabolism ; Fasting* / blood ; Female ; Graft Rejection ; Graft Survival* ; Humans ; Liver Transplantation* / adverse effects ; Living Donors* ; Male ; Middle Aged ; Retrospective Studies ; Risk Factors ; Transplant Recipients
Keywords
Donor fasting glucose ; Graft survival ; Living donor liver transplantation ; Recipient outcomes
Abstract
Several donor-specific factors influence the functional recovery and long-term outcomes of liver grafts. This study investigated the association between donor fasting glucose (DFG) and recipient outcomes after living donor liver transplantation (LDLT) in 950 cases at a single center. Patients were divided into two groups: low-DFG (< 85 mg/dL, n = 120) and control (≥ 85 mg/dL, n = 830). The five-year graft survival rate was significantly lower in the low-DFG group (71.5%) compared to the control group (80.0%) (P = 0.02). Multivariable Cox regression analysis showed that low DFG was independently associated with graft loss (hazard ratio 1.72, 95% CI 1.15-2.56, P = 0.008). In propensity score-matched groups, the low-DFG group also had lower survival rates (71% vs. 83.1%, P = 0.004). The presence of additional risk factors, such as low graft-to-recipient weight ratio, older donor age, and longer cold ischemic time, further reduced graft survival in the low-DFG group. A DFG level < 85 mg/dL is associated with higher risk of graft failure after LDLT, especially when combined with other risk factors. Low DFG should be considered a prognostic marker in LDLT planning, with potential to improve patient outcomes as further research clarifies the underlying pathophysiological mechanisms.
Files in This Item:
T202500770.pdf Download
DOI
10.1038/s41598-024-80604-x
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Deok Gie(김덕기)
Kim, Myoung Soo(김명수) ORCID logo https://orcid.org/0000-0002-8975-8381
Lee, Jae Geun(이재근) ORCID logo https://orcid.org/0000-0002-6722-0257
Lee, Jae Seung(이재승) ORCID logo https://orcid.org/0000-0002-2371-0967
Yim, Seung Hyuk(임승혁) ORCID logo https://orcid.org/0000-0003-2146-3592
Joo, Dong Jin(주동진) ORCID logo https://orcid.org/0000-0001-8405-1531
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/204381
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