We present the case of a 62-year-old French man who received a kidney transplant in November 1996. Before transplantation, antibodies to hepatitis B surface (anti-HBs) antigen (Ag) and core antigen (anti-HBc) were positive; HBsAg and HBV DNA were negative. HBsAg, anti-HBc, anti-HBs, and HB virus (HBV) DNA were negative in the donor. The immunosuppressive regimen (antithymocyte globulin, cyclosporine, azathioprine, and steroids) was progressively decreased in the absence of allograft acute rejection. The HBV serological profile was the same until December 1999 when anti-HBs became undetectable after having progressively decreased. In October 2001, the patient was surgically treated for pulmonary carcinoma and received a blood transfusion. HBsAg and anti-HBc from the two blood donors were persistently negative. Serum aminotransferases and gamma glutamyl transferase (GGT) increased moderately in December 2001. In February 2002, anti-HBs increased to >1000 IU/L without vaccination, and surprisingly, HBsAg was positive. The HBV DNA level was 7.2 Log(copies/milliliter). Phylogenetic analysis of HBV surface gene retrieved genotype D. Four mutations were observed in the major hydrophilic region: P120L, P142L, D144E, and G145R (Fig. 1). In November 2003, biological markers predicted strong hepatic fibrosis and strong viral activity. Thus, lamivudine and adefovir treatment was begun. Now, the patient is well, and only GGT remains moderately increased. Concomitant anti-HBs and HBsAg persist. HBV DNA decreased to 3.3 Log(copies/milliliter). Serum creatinine is 150 μmol/L with cyclosporine, azathioprine, and steroids.FIGURE 1.: Amino acid changes in the major hydrophilic region of HBsAg from our patient. Substitutions form wild-type to mutated amino acid (arrow). More than one amino acid (dotted line); disulphide bridges (punctured line).This is the first report of HBsAg and anti-HBs coexistence in a renal transplant patient who previously recovered from HBV infection. Hence, simultaneous detection of HBsAg, anti-HBs, and anti-HBc should be performed in such a context, even if the patient has recovered from HBV infection. The HBV surface mutants and, particularly, the G145R mutants occur in endemic regions with large HBV vaccination programs (vaccine escape mutants) (1). Therapy with HBV immune globulins can also select these mutants after liver transplantation (immune escape mutants) (2). The P120L mutant was associated with marked decrease in binding of antibodies mapped to amino acid 139–147 (3), and the P142L prevents the full display of HBV antigenicity (4). In our patient, it is difficult to clearly establish if HBV infection occurred through selection of HBV mutants after reactivation or de novo, yet risk factors for the latter hypothesis were not evidenced. Surface mutations are clinically important in HBV prevention because they can make the epitope unlikely to bind to anti-HBs generated against wild-type HBsAg, thus leading to the emergence of escape mutants. Detection failure with HBsAg assays has also been reported (5). We outline here the public health significance of the surface mutants in patients with end-stage renal disease as a new hepatitis B nosocomial risk. Indeed, we have diagnosed a second case since. Also, after 8 years, half of renal transplants are unsuccessful, and patients are dialyzed again (6). Hepatitis B incidence in hemodialysis units decreased, thanks to routine vaccination and use of erythropoietin. Emergence of surface mutants sets the problem of the efficiency of vaccines against these viruses in other patients and family contacts. Moreover, it confirms the importance of strictly respecting standard precautions against contamination by blood in hemodialysis units. Valérie Moal Henri Vacher-Coponat Elisabeth Botelho Yvon Berland Service de Néphrologie et d'Hémodialyse Hôpital La Conception Marseille Cedex, France Philippe Colson Catherine Tamalet Mireille Henry Laboratoire de Virologie Hôpital Timone Marseille Cedex, France