W. Grotz et al., OCCURRENCE AND MANAGEMENT OF HEPATITIS-B VIRUS REACTIVATION FOLLOWINGKIDNEY-TRANSPLANTATION, Clinical nephrology, 49(6), 1998, pp. 385-388
A 28-year-old woman was kidney transplanted. She had an inapparent hep
atitis B virus (HBV) infection 2 years previously. At the time of tran
splantation she was hepatitis B surface antigen (HBsAg) negative, anti
-HBs, anti-HBc, anti-HBe and anti-HCV antibody positive and her transa
minase activities were within the normal range. The donor of the kidne
y allograft was HBV negative. Twelve weeks after transplantation a Lif
e-threatening liver failure occurred with a rapid rise of alanine amin
otransferase (ALT) to 1427 U/l and a decrease of the prothrombin time
to 25% of normal value. Anti-HBs had become negative, anti-HBc and ant
i-HBe titers had decreased. HBsAg became positive, associated with a H
BV DNA of 3 x 10(8) genome equivalents/ml. Azathioprine and prednisone
were withdrawn and foscarnet therapy was started. This therapy led to
a decrease of ALT activity associated with an elimination of HBsAg an
d HBV DNA. Eight months after transplantation liver function tests wer
e within the normal range. Graft rejection did not occur despite low o
r intermittent cessation of immunosuppressive therapy.