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Hepatitis B virus (HBV) infection remains a major issue among dialysis patients. It is associated with a high risk of hepatic complication. The liver disease runs a unique clinical course in dialysis patients, as it can progress with modest hepatic inflammation and prominent fibrosis. The conventional cut-off level of serum alanine aminotransferase (ALT) for commencing antiviral therapy may prove too high and inappropriate for dialysis patients, and liver biopsy appears to be the only definitive means to establish the activity of liver disease in dialysis patients. Liver biopsy should be considered in patients with a serum ALT level that is persistently greater than 30 IU/L, or 0.75-fold the upper limit of the normal level, and/or other clinical and laboratory findings that suggest active liver disease. For antiviral treatment, preliminary reports have shown that lamivudine is effective and well tolerated in dialysis patients. However, the long-term efficacy of lamivudine and its optimal effective dose in dialysis patients remain unknown. The prevention of nosocomial transmission among dialysis patients is also important. Universal precaution measures should be strictly observed and the segregation of hepatitis B surface antigen-positive hemodialysis patients should be considered. For HBV non-immune patients, the importance of HBV vaccination should not be overemphasized. Until a new generation of highly immunogenic vaccines that are proven to be safe and effective in patients with end-stage renal disease becomes available, early vaccination before the development of end-stage renal failure remains the best way to secure immunological protection against HBV infection in dialysis patients.

Background: All patients with liver cirrhosis are recommended for evaluation of oesophagogastric varices (EGV) regularly. This prospective study was designed to develop a predictive model for EGV in cirrhotic patients. Methods: Ninety-two patients were recruited. From all patients studied, the size of palpable spleen, liver chemistry value, platelet count, prothrombin time, diameter of main portal vein and splenic length as assessed by ultrasonography were determined. Upper endoscopy was performed. Oesophageal varices (EV) and gastric varices (GV) were graded (EV, grade 1-4; GV, grade 1-3). In the predictive model, the EGV was classified into two grades (low, grade 1-2 EV or grade 1 GV; high, grade 3-4 EV or grade 2-3 GV). Results: There were 53 patients with EGV and 39 patients without EGV as determined by endoscopy. Patients with EGV had a significantly higher degree of ascites and hepatic encephalopathy, lower platelet count and longer splenic length than those without EGV. Low platelet count and presence of ascites were the significant independent predictors for high-grade EGV (concordance rate 0.83). The optimal critical value for the platelet count was 150 x 10 9 /L. Of patients without thrombocytopenia and ascites, 37% had low-grade EGV but none had high-grade EGV, whereas 38 and 35% of patients with thrombocytopenia or ascites had low and high-grade EGV, respectively. Therefore, this predictive model for high-grade varices had a positive and negative predictive value of 35 and 100%, respectively. Conclusion: Endoscopic screening for EGV was not necessary until thrombocytopenia or ascites occurred.