Summary Background There have been encouraging reports on transjugular intrahepatic portosystemic stent‐shunt (TIPSS) for Budd–Chiari syndrome (BCS). Long‐term data are lacking. Aim To assess long‐term outcomes and validate prognostic scores following TIPSS for BCS. Methods A single centre retrospective study. Patients underwent TIPSS using bare or polytertrafluoroethane (PTFE)‐covered stents. Results Sixty‐seven patients received successful TIPSS between 1996 and 2012 using covered (n = 40) or bare (n = 27) stents. Patients included had a Male: Female ratio of 21:46, and were characterised (mean ± s.d.) by age 39.9 ± 14.3 years, Model of end stage liver disease (MELD) 16.1 ± 7.0 and Child's score 8.8 ± 2.0. Seventy‐eight percent had haematological risk factors. Presenting symptoms were ascites (n = 61) and variceal bleeding (n = 6). Nine patients underwent hepatic vein dilatation or stenting prior to TIPSS. Mean follow‐up was 82 months (range 0.5–184 months). Fifteen percent had post‐TIPSS encephalopathy. Two have been transplanted. Primary patency rates (76% vs. 27%, P < 0.001) and shunt re‐interventions (22% vs. 100%, P < 0.001) significantly favoured covered stents. Secondary patency was 99%. Six‐, 12‐, 24‐, 60‐ and 120‐month survival was 97%, 92%, 87%, 80% and 72% respectively. Six patients had liver related deaths. Two patients developed hepatocellular carcinoma. The BCS TIPS PI independently predicted mortality in the whole cohort, but no prognostic score was a significant predictor of mortality after subgroup validation. Conclusions Long‐term outcomes following TIPSS for Budd–Chiari syndrome are very good. PTFE‐covered stents have significantly better primary patency. The value of prognostic scores is controversial. TIPSS should be considered as first line therapy in symptomatic patients in whom hepatic vein patency cannot be restored.

SummaryDonation after cardiac death liver transplant recipients have an increased frequency of acute kidney injury (AKI). This suggests that hepatic ischemiareperfusion injury may play a critical role in the pathogenesis of AKI after liver transplantation. The aim of this single-center study was to determine if hepatic ischemia-reperfusion injury, estimated by peak peri-operative serum aminotransferase (AST), is associated with AKI following donation after brain death (DBD) liver transplantation. A total of 296 patients received 298 DBD liver transplants from January 2007 to June 2011. The incidence of AKI was 35.9%. AKI was a risk factor for chronic kidney disease (P = 0.037) and mortality (P = 0.002). On univariate analysis, peak AST correlated with peak creatinine (P < 0.001) and peak change in creatinine from baseline (P < 0.001). Peak AST was higher in AKI patients (P < 0.001). The incidence of AKI in patients with a peak AST of <1500, 1500-2999 and ≥3000 U/l was 26.1%, 39.8% and 71.2%, respectively (P < 0.001). On multiple logistic regression analysis, peak AST was independently associated with the development of AKI (P < 0.001). In conclusion, hepatic ischemiareperfusion injury demonstrates a strong relationship with peri-operative AKI in DBD liver transplant recipients.

Small series have suggested that split liver transplantation (SLT) has an increased frequency of peri-operative acute kidney injury (AKI). However, the optimal donor selection in this setting could have a favourable impact on renal outcomes. This was a retrospective single-centre study of 76 adults who underwent SLT (right extended lobe) and 301 adults who underwent elective full-size donation after brain death liver transplantation (FSLT). SLT recipients were less likely than unmatched FSLT recipients to develop AKI (≥stage 1 KDIGO criteria) (40.3% vs. 56.1%, P = 0.016) and had a reduced frequency of renal replacement therapy (11.8% vs. 21.9%, P = 0.049). In 72 pairs of SLT patients and propensity risk score-matched FSLT controls the incidence of AKI was not significantly different (40.3% vs. 47.2%, P = 0.473). However, SLT patients were less likely to require renal replacement therapy (11.1% vs. 23.6%, P = 0.078; adjusted OR 0.32; 95% CI 0.11-0.87, P = 0.026). There was no association between SLT and the development of chronic kidney disease (eGFR<60 ml/min/1.73 m(2) , log rank P = 0.534). In conclusion, SLT is not associated with an increased frequency of AKI. These observations support the postulation that the optimal donor status of SLT may result in less graft injury with renal sparing effects.

No abstract

No abstract