Abstract
In 1977 Pirson and his colleagues in Belgium reported that patients with renal failure who were found to have hepatitis B surface antigen (HBsAg) in their circulation before or after renal transplantation were subject to a fivefold increase in mortality due to hepatic failure.1 At that time, a very high proportion (about 40 to 50 per cent) of European patients with renal failure were HBsAg-positive. In contrast, the use of simple precautionary measures to prevent hepatitis B infection in our own hospital and in others in North America2 3 4 resulted in a low (<5 per cent) proportion of HBsAg carriers. Most . . .