Defects in B-cell function and metabolism in uremia: Role of parathyroid hormone

• Published in: Kidney international Vol. 59; no. S78; pp. S186 - S189
• Main Authors: Smogorzewski, Miroslaw, Massry, Shaul G.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2001; Elsevier Limited
• Subjects: Animals; Antibody Formation; B-Lymphocytes - drug effects; B-Lymphocytes - immunology; B-Lymphocytes - metabolism; Calcium - metabolism; calcium channel blockers; Calcium Channel Blockers - pharmacology; Cell Division; Cyclic AMP - biosynthesis; cytosolic calcium; dialysis; Humans; immune system; In Vitro Techniques; Lymphocyte Activation; Nifedipine - pharmacology; Parathyroid Hormone - metabolism; Parathyroid Hormone - pharmacology; Uremia - drug therapy; Uremia - immunology; Uremia - metabolism; uremic toxin; dialysis; immune system; uremic toxin; calcium channel blockers; cytosolic calcium
• ISSN: 0085-2538; 0098-6577; 1523-1755
• DOI: 10.1046/j.1523-1755.2001.59780186.x

Defects in B-cell function and metabolism in uremia: Role of parathyroid hormone. 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.