J. P. Davis1, C. A. Kubal1, B. Ekser1, J. A. Fridell1, K. A. Thatch1, R. S. Mangus1 1Indiana University School Of Medicine,Indianapolis, IN, USA
Introduction:
Deceased donor liver transplant allografts with steatosis have an increased risk of post-transplant primary non-function and early allograft dysfunction. The degree of allograft steatosis which results in these negative outcomes is not clearly defined, largely because there is significant variability in grading graft steatosis. This study reviews a large number of liver transplants at a single center. The percent of total graft steatosis from the permanent reperfusion biopsy is recorded. Early clinical outcomes are then measured with increasing severity of steatosis.
Methods:
The records of all liver transplants (LTs) performed over a 15-year period were reviewed. Reperfusion biopsy reports were reviewed and recorded in the transplant center research database. All biopsies were read by experienced liver pathologists, from permanent sections taken at transplant. Total steatosis included both micro- and macrovesicular and was categorized into four study groups, (1) none (0%), (2) mild (1-10%), (3) moderate (11-20%) and (4) severe (>20%). Outcomes included early allograft dysfunction (EAD) and graft loss, peak alanine aminotransferase (ALT) and total bilirubin (TB) values, length of hospital stay, and change in renal function.
Results:
Data were available for 1864 adult LT recipients, 40% of whom had some liver allograft steatosis. Donor factors associated with increasing graft steatosis included White race, older age, and chronic alcohol abuse. Pre-procurement donor peak ALT and TB levels were no different for livers with or without steatosis. Recipient post-transplant peak ALT levels were similar to non-steatotic livers when there was <10% steatosis. However, above 10% steatosis, there was an incremental increase (p<0.001). Peak TB did not differ among the groups. EAD was similarly seen only in livers with > 10% steatosis, reaching 42% in the 11-20% steatosis group and 54% in the >20% steatosis group (p<0.001). There was a significant risk of graft loss, but this was only seen in grafts with >20% steatosis (p<0.01 at 7 days and p=0.02 at 30 days). Steatosis >20% was associated with an acute decrease in glomerular filtration rate (>20%) which persisted through day 30.
Conclusion:
Initial liver function is delayed in grafts with more than 10% steatosis, being demonstrated by high peak ALT and a 40-50% risk of early allograft dysfunction. There is a significant risk of graft loss when total steatosis is greater than 20%. Severe steatosis is also associated with acute kidney dysfunction early post transplant. The early graft losses seen in livers with > 20% steatosis lead to a 10% reduction in survival at 10-years compared to non-steatotic grafts.
