Panel reactive antibodies in predicting hepatitis C virus treatment outcome in kidney transplant candidates.

OBJECTIVES

Chronic hepatitis C virus infection compromises hemodialysis patients and increases liver-related mortality. Interferon treatment is associated with improved sustained virological response rates and increased risk of graft loss after kidney transplant. This may be related to the development of antihuman leukocyte antigen antibodies, which may be a surrogate marker of potent immune response. We evaluated panel reactive antibody 1 and 2 levels for prediction of sustained viral response in patients with kidney transplant.

MATERIALS AND METHODS

In this retrospective cohort study, we reviewed data from hepatitis C virusinfected hemodialysis patients who received interferon treatment before kidney transplant. Panel reactive antibody > 20% was considered positive. Sustained viral response rates for interferon treatment were obtained and compared with panel reactive antibody 1 and 2 values.

RESULTS

There were 40 patients (16 female and 24 male patients; mean age, 41.5 y; range, 18-65 y). Sustained viral response rate was 18/40 (45%). Panel reactive antibody 1 was negative in 31 patients and positive in 9 patients. Sustained viral response ratio was not correlated with panel reactive antibody 1 positivity. Panel reactive antibody 2 was negative in 31 patients (sustained viral response: present, 11 patients; absent, 20 patients) and positive in 9 patients (sustained viral response: present, 7 patients; absent, 2 patients). Sustained viral response ratio was significantly correlated with panel reactive antibody 2 positivity.

CONCLUSIONS

We showed a correlation between panel reactive antibody 2 positivity and sustained viral response rates that may be a predictive tool for hepatitis C virus treatment response. In patients with other complications that compromise hepatitis C virus treatment, panel reactive antibody 2 may be a surrogate marker for sustained viral response prediction. The induction of cellular immunity may cause clearance of hepatitis C virus infection and formation of high panel reactive antibody 2 levels.