![]() | Only 14 pages are availabe for public view |
Abstract The susceptibility of uremic patients to infectious diseases has been widely reported, but the host immune factors associated with the increased incidence of infection have not been clearly defined (Goldblum and Reed, 1980). Uremia is claimed to cause impaired immune responsiveness (Wilson et al., 1965 and Goldblum and Reed, 1980). The mechanism of this impairment is not fully understood. Unknown uremic toxin (Touraine et al., 197 5 and Raska et al., 1980) and reduction in cellular reactivity have been impHcated (Huber et al., 1969 and Alvey et al., 19 8l). There have been only a few detailed ;nvestigations concerned with the antibody response in uremic patients, and available data are controversial: some authors reported normal responses (Friedman et aL, 1980). While others found reduced antibody responses (Macy et al., 1991). Some investigators found a diminished responses to tetanus toxoid in chronic uremic patients. On the other hand, others found a normal secondary response to diphtheria toxoid m patients with uremia (Goldblum and Reed, 1980). The influence of dialysis membrane on immunoglobulin production was studied in vitro and it was concluded that the long tenn exposure of mononuclear cells to artificial surfaces during dialysis may contribute to the impaired humoral response observed in dialysis patients. This effect may be due to a decline in B-cell stimulation by monocytes (Paczek et aL, 1990). |