Evidence of Impaired T Cell Function in Hemodialysis Patients: Potential Role for Secondary Hyperparathyroidism

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Abstract
Previous studies in our laboratory showed that the T cell is a target for parathyroid hormone (PTH) action. It is theoretically possible, therefore, that chronic exposure of the T cells to high blood levels of PTH in patients with chronic renal failure may adversely affect T cell function. We examined in both normal subjects and dialysis patients several aspects of T cell function, including (1) T cell proliferation in response to phytohemagglu-tinin (PHA) mitogen with and without PTH and with and without exogenous interleukin 2 (IL-2); (2) the IL-2 production induced by PHA with and without PTH, and (3) resting levels of cytosolic calcium – [Ca2+]i – and the increment in [Ca2+]; in response to anti-CD3 antibody. Although PHA significantly (p 2+]i in T cells from dialysis patients were significantly (p 2+]i in response to anti-CD3 antibody were significantly (p 2+]i and with a reduced calcium signal in response to anti-CD3 antibody, and these cellular derangements may interfere with the proper response of T cells to mitogens.

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