Dysfunction of polymorphonuclear leukocytes in uremia: Role of parathyroid hormone

Abstract

Polymorphonuclear leukocytes (PMNLs) from uremic patients have elevated basal levels of cytosolic calcium ([Ca2+]i), reduced calcium signal after activation of Fcγ RIII receptor, and impaired phagocytosis. Chronic excess of parathyroid hormone (PTH) in uremia mediates its effect on PMNL's metabolism and function through the sustained elevation of their [Ca2+]i. Because calcium channel blockers interfere with this effect of PTH on PMNLs, treatment of patients on hemodialysis with verapamil, nifedipine, or amlodipine was associated with an improvement in metabolism and phagocytosis of PMNLs in humans. The therapy with calcium channel blockers should be continued in order to maintain its beneficial effects.