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BC are a common source of morbidity after pediatric LT. Knowledge about risk factors may help to reduce their incidence. Retrospective analysis of BC in 116 pediatric patients (123 LT) (single institution, 05/1990-12/2011, medium follow-up 7.9 yr). One-, five-, and 10-yr survival was 91.1%, no patient died of BC. Prevalence and risk factors for anastomotic and intrahepatic BC were examined. There were 29 BC in 123 LT (23.6%), with three main categories: 10 (8.1%) primary anastomotic strictures, eight (6.5%) anastomotic leaks, and three (2.4%) intrahepatic strictures. Significant risk factors for anastomotic leaks were total operation time (increase 1.26-fold) and early HAT (<30 days post-LT; increase 5.87-fold). Risk factor for primary anastomotic stricture was duct-to-duct choledochal anastomosis (increase 5.96-fold when compared to biliary-enteric anastomosis). Risk factors for intrahepatic strictures were donor age >48 yr (increase 1.09-fold) and MELD score >30 (increase 1.2-fold). To avoid morbidity from anastomotic BC in pediatric LT, the preferred biliary anastomosis appears to be biliary-enteric. Operation time should be kept to a minimum, and HAT must by all means be prevented. Children with a high MELD score or receiving livers from older donors are at increased risk for intrahepatic strictures.

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Background The hepatic Acute Phase Response(APR) is an organ-specific response to a diverse array of insults and is largely under transcriptional control. Liver-specific transcription factors, Hepatic Nuclear Factors(HNFs)-1α and 4α, play important roles in maintenance of liver phenotype and function and their binding activity changes early after injury. However, their role in modulation of the liver’s response over time is not defined. Materials and Methods C57/BL6 mice were anesthetized and exposed to 95°C water for 10sec to create a 15% body surface area full-thickness burn. At specific time points, the mice were sacrificed. An ELISA for IL-6 was performed on serum and hepatic mRNA levels for Fibrinogen-γ and Serum Amyloid A(SAA)-3 were obtained through PCR. Transcriptional factor binding activity was assessed with electrophoretic mobility shift assays. Results Serum IL-6 levels peaked at 3h and Fibrinogen-γ and SAA mRNA levels increased more than 6-fold at 12h before returning to control levels at 48h. The binding activity of HNF-4α and HNF-1α rapidly declined after injury(1.5h) but recovered to near control level at 24h and 6h, respectively. Conclusions Changes in HNF-4α and HNF-1α binding occurred before changes in acute phase protein mRNA levels and were preceded by the peak in IL-6 levels. The rapid suppression and reconstitution of liver-specific transcription factor binding after injury may represent a mechanism which allows the normal liver phenotype to change and an injury-response phenotype to prevail. The role in the liver’s adaptive response to injury suggests a central role for both HNF-4α and HNF-1α in transcriptional regulation of the hepatic APR.

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The demand for transplantable organs far outweighs the supply. Recently, efforts have been made to increase the donor pool by adopting extended criteria for livers, including those from hypernatremic donors. Currently, there is no clear evidence that the use of organs from hypernatremic donors has detrimental effects on pediatric liver transplantation (LT) recipients. Our aim was to use the Scientific Registry of Transplant Recipients database to evaluate the effects of donor hypernatremia on 30-day outcomes in pediatric LT recipients. We performed an analysis of 2325 children who underwent whole or partial LT between 2005 and 2010. First, we sought to determine a donor sodium threshold for increased mortality following pediatric LT. Second, we examined rates of mortality and graft failure at 30 days after LT in patients receiving grafts from hypernatremic donors compared to patients receiving grafts from normonatremic donors. Hypernatremia was defined as a donor sodium level of 160 mmol/L. The primary outcome measure was mortality at 30 days after transplant. The secondary outcome measure was graft failure at 30 days after transplant. There was no threshold sodium level for increased 30-day mortality following pediatric LT. Mean recipient ages/weights, Pediatric End-Stage Liver Disease/Model for End-Stage Liver Disease scores, and mean cold and warm ischemia times were similar between the 2 study groups. There were no significant differences in mortality rates (3.9% versus 4.5%; P 5 0.87) and graft failure rates (2.2% versus 1.9%; P 5 1.00) in patients receiving grafts from hypernatremic donors compared to patients receiving grafts from normonatremic donors at 30 days after LT. In conclusion, donor hypernatremia just before procurement does not appear to have negative effects on mortality and graft failure rates at 30 days following pediatric LT. Liver Transpl 21:1076-1081, 2015. V C 2015 AASLD.Received December 11, 2014; accepted April 1, 2015.Organ shortage remains a significant problem in the field of solid organ transplantation. The demand for organs far outweighs the supply. In order to expand the donor pool, many institutions have adopted extended donor criteria (EDC), including donor hypernatremia, which has led to the acceptance of organs previously deemed too risky. At the present time, there is conflicting evidence regarding the effects of donor hypernatremia on outcomes following liver transplantation (LT). 1 Some studies in adult recipients suggest higher graft Additional supporting information may be found in the online version of this article.