The British Society of Gastroenterology in collaboration with British Association for the Study of the Liver has prepared this document. The aim of this guideline is to review and summarise the evidence that guides clinical diagnosis and management of ascites in patients with cirrhosis. Substantial advances have been made in this area since the publication of the last guideline in 2007. These guidelines are based on a comprehensive literature search and comprise systematic reviews in the key areas, including the diagnostic tests, diuretic use, therapeutic paracentesis, use of albumin, transjugular intrahepatic portosystemic stent shunt, spontaneous bacterial peritonitis and beta-blockers in patients with ascites. Where recent systematic reviews and meta-analysis are available, these have been updated with additional studies. In addition, the results of prospective and retrospective studies, evidence obtained from expert committee reports and, in some instances, reports from case series have been included. Where possible, judgement has been made on the quality of information used to generate the guidelines and the specific recommendations have been made according to the ‘Grading of Recommendations Assessment, Development and Evaluation (GRADE)’ system. These guidelines are intended to inform practising clinicians, and it is expected that these guidelines will be revised in 3 years’ time.

Current therapy for preventing the first variceal bleed includes beta-blocker and variceal band ligation (VBL). VBL has lower bleeding rates, with no differences in survival, whereas betablocker therapy can be limited by side effects. Carvedilol, a non-cardioselective vasodilating beta-blocker, is more effective in reducing portal pressure than propranolol; however, there have been no clinical studies assessing the efficacy of carvedilol in primary prophylaxis. The goal of this study was to compare carvedilol and VBL for the prevention of the first variceal bleed in a randomized controlled multicenter trial. One hundred fifty-two cirrhotic patients from five different centers with grade II or larger esophageal varices were randomized to either carvedilol 12.5 mg once daily or VBL performed every 2 weeks until eradication using a multibander device. T he most serious complication of portal hypertension is variceal hemorrhage. The annual incidence of esophageal varices in patients with cirrhosis is approximately 5%, 1 and a third of these will bleed. 2,3 Current therapy with propranolol results in a reduction in the first variceal bleed and mortality compared with placebo. 4,5 There have been two recent metaanalyses with 16 trials studied in total. 6,7 The one showed variceal band ligation (VBL) to be more effective than beta-blockers in primary prevention of variceal hemorrhage, although there was no difference in survival. 7 The other showed similar overall results, although when trials with unclear bias control and follow-up less than 20 months were excluded, the difference in bleeding was not present. 6 Carvedilol is a potent non-cardioselective betablocker, with weak vasodilating properties due to alpha-1 blockade. 8 A fall in both intrahepatic and portocollateral resistance contributes to the enhanced effects on portal pressure reduction through blockade of alpha-1 receptors as has been shown with prazosin. 9-11 A reduction in the hepatic venous pressure gradient (HVPG) of 8%-43% was observed with carvedilol in nine published hemodynamic studies involving 158 patients. [12][13][14][15][16][17][18][19][20] Carvedilol was also found to have a greater portal hypotensive effect than propranolol in randomized controlled hemodynamic studies. 15,17

Donation after cardiac death (DCD) liver transplantation is associated with an increased frequency of hepato-biliary complications. The implications for renal function have not been explored previously. The aims of this single-center study of 88 consecutive DCD liver transplant recipients were (1) to compare renal outcomes with propensity-risk-matched donation after brain death (DBD) patients and (2) in the DCD patients specifically to examine the risk factors for acute kidney injury (AKI; peak creatinine ≥2 times baseline) and chronic kidney disease (CKD; eGFR <60 mL/min/1.73 m 2 ). During the immediate postoperative period DCD liver transplantation was associated with an increased incidence of AKI (DCD, 53.4%; DBD 31.8%, p = 0.004). In DCD patients AKI was a risk factor for CKD (p = 0.035) and mortality (p = 0.017). The cumulative incidence of CKD by 3 years post-transplant was 53.7% and 42.1% for DCD and DBD patients, respectively (p = 0.774). Importantly, increasing peak perioperative aspartate aminotransferase, a surrogate marker of hepatic ischemia reperfusion injury, was the only consistent predictor of renal dysfunction after DCD transplantation (AKI, p < 0.001; CKD, p = 0.032). In conclusion, DCD liver transplantation is associated with an increased frequency of AKI. The findings suggest that hepatic ischemia reperfusion injury may play a critical role in the pathogenesis of post-transplant renal dysfunction.Key words: Acute kidney injury, chronic kidney disease, donation after cardiac death, ischemia reperfusion injury, transplantation Abbreviations: AKI, acute kidney injury; AST, aspartate aminotransferase; BMI, body mass index; CI, confidence interval. DBD, donation after brain death; DCD, donation after cardiac death; eGFR, estimated glomerular filtration rate; FFP, fresh frozen plasma; INR, international normalised ratio; IQR, inter-quartile range; MELD, model for end-stage liver disease; NASH, non-alcoholic steatohepatitis; OR, odds ratio; PRS, propensity risk score; RCC, red cell concentrate; SD, standard deviation; UKELD, UK score for patients with end-stage liver disease.