Patients with chronic renal failure have impaired humoral immunity, inadequ
ate B-cell proliferation and antibody production, and elevated basal levels
of cytosolic calcium ([Ca2+]i) in their B cells. Multiple mechanisms can b
e involved in generation of these derangements. This article reviews data s
uggesting that high levels of parathyroid hormone (PTH) of uremia affect th
e metabolism and function of B cells. We also review studies on the role of
normalization of [Ca2+]i in these abnormalities. Small but well-documented
studies suggest that treatment of dialysis patients with calcium channels
blockers can reverse the elevation of [Ca2+]i in B cells, which was followe
d by improvement of B-cell function. Thus, therapy with calcium channel blo
ckers has the potential to decrease the infectious complication of uremia.