Impaired cellular host defense and chronic inflammatory abnormalities in end-stage renal disease

Infectious complications are the second most frequent single cause of death (1). Viral infections include hepatitis B, hepatitis C or influenza. The secondary immune defect of end-stage renal disease (ESRD) patients (2) results in low antibody titers, short duration of protection, and nonresponsiveness to standard vaccination protocols (3–5). Nonresponse to hepatitis B vaccine is accompanied by an impaired activation of T lymphocytesin vitro and a reduced secretion of interleukin 2 (IL-2) (6). The costimulatory system of B7 molecules on antigenpresenting cells is responsible for this defect, since supplementation of B7 signalsin vitro led to a normalization of T-cell function (7). Response rates of vaccination with hepatitis B surface antigen (HbsAg) in the initial studies among dialysis patients ranged from 50% to 60% (3, 8, 9). Even in recent studies more than 30–40% of patients could not be protected against hepatitis B by means of active vaccination (10–12).