Abstract
Patients with chronic renal failure have impaired humoral immunity, inadequate B-cell proliferation and antibody production, and elevated basal levels of cytosolic calcium ([Ca2+]i) in their B cells. Multiple mechanisms can be involved in generation of these derangements. This article reviews data suggesting that high levels of parathyroid hormone (PTH) of uremia affect the 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 followed by improvement of B-cell function. Thus, therapy with calcium channel blockers has the potential to decrease the infectious complication of uremia.
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