Impaired in vivo antibody production in CRF rats: Role of secondary hyperparathyroidism

Impaired in vivo antibody production in CRF rats: Role of secondary hyperparathyroidism. Antibody responses to antigens are impaired in humans and animals with chronic renal failure (CRF), and parathyroid hormone (PTH) inhibits Staphylococcus aureus Cowan I (SAC) or pokeweed mitogen (PWM)-induced antibody production by B cells from normal subjects. Since CRF is associated with secondary hyperparathyroidism and elevated blood levels of PTH, it is possible that impaired humoral immunity in CRF is due to chronic excess of PTH. To test this hypothesis we examined in vivo antibody production in response to sheep red blood cells (SRBC), BSA and influenza vaccine in normal rats, CRF rats and parathyroidectomized CRF rats maintained normocalcemic (CRF-PTX). The blood levels of PTH in CRF rats were elevated and significantly (P < 0.01) higher than those in normal and CRF-PTX rats. The latter groups of animals did not have elevated blood levels of PTH. The antibody response to all three antigens in CRF rats were significantly (P < 0.01) and markedly lower than in normal or CRF-PTX rats. The antibody response to SRBC, the IgG anti-BSA and the IgG and IgM anti-influenza vaccine in CRF-PTX rats were not different from normal, while the IgM anti-BSA was lower than in normal rats but higher than in CRF rats. The data demonstrate that the state of secondary hyperparathyroidism of CRF plays a paramount role in the genesis of impaired humoral immunity in CRF