Low response to HBsAg vaccine in chronic renal failure patients is not due to intrinsic defect of B cells.

OBJECTIVE

The aim of this study was to investigate whether the inability of chronic renal failure patients to mount an adequate antibody response following hepatitis B vaccination was due to an inherent defect in the antibody producing capacity of their B cells.

MATERIAL AND METHODS

Peripheral blood mononuclear cells of end stage renal disease (ESRD) patients, who were not on maintenance hemodialysis (CRF) and those undergoing long-term hemodialysis (HD) were stimulated in vitro with pokeweed mitogen, a B cell mitogen or hepatitis B surface antigen. The total immunoglobulin (IgG, IgM and IgA) levels and anti-HBs specific IgM and IgG were quantitiated by sandwich ELISA and levels between patients who had a good antibody response in vivo and those who failed to mount an antibody response were compared.

RESULTS

Spontaneous IgG production was significantly higher than normals in CRF and HD group; PWM induced IgM, IgG and IgA production was comparable to normals in both groups of patients. The spontaneous IgG and PWM stimulated IgM and IgG production was significantly higher in HD patients as compared to CRF. The in vitro Ig levels in the vaccine responders and non-responders was comparable except for the spontaneous IgG which was highest in the responders. The in vitro anti-HBs production was comparable in HB vaccine responders and non-responders; the in vivo and in vitro anti-HBs titers showed a significant correlation coefficient thereby indicating that the in vitro assay reflects the in vivo functional status of B cells.

CONCLUSION

Our results demonstrate that the B cells in ESRD patients are functionally normal and cannot be the cause of the compromised vaccine response in these patients.