BACKGROUND: Uremia displays increased cytosolic free calcium ([Ca2+]i) in many different cell types, supporting the hypothesis of an altered Ca2+ transport modifying the functional activity of calcium signaling pathway. METHODS: Thirty-five hemodialyzed patients and 20 age-matched subjects were studied. Erythrocyte resting [Ca2+]i and Ca2+ influx were measured by the fluorescent Ca2+-sensitive dye fura-2. RESULTS: We found an increase of resting [Ca2+]i in erythrocytes from uremic hemodialyzed patients compared with matched healthy controls (103 +/- 2.5 nM, N = 20, vs. 90 +/- 4, N = 20, P < 0.01). Moreover, we found an altered voltage-dependent Ca2+ influx showing a reduced transport rate (0.42 +/- 0.03 nM/second vs. 0.74 +/- 0.08, P < 0.01). High levels of plasma parathyroid hormone (PTH) were related to augmented Ca2+ entry (r = 0.511, P < 0.05), contributing to maintain a high level of [Ca2+]i. Hemodialysis had no effect on cell calcium level and Ca2+ influx indices. The therapy with Ca2+ antagonists did not modify the values of resting [Ca2+]i or Ca2+ influx indices, but the correlation between PTH and influx indices was lost. CONCLUSIONS: In conclusion, we found evidence for an alteration of erythrocyte Ca2+ influx caused by uremic toxicity that could be related to some organ disorders in uremia. The chronic increase of cellular calcium may contribute to influx derangement.
BACKGROUND:Uremia displays increased cytosolic free calcium ([Ca2+]i) in many different cell types, supporting the hypothesis of an altered Ca2+ transport modifying the functional activity of calcium signaling pathway. METHODS: Thirty-five hemodialyzed patients and 20 age-matched subjects were studied. Erythrocyte resting [Ca2+]i and Ca2+ influx were measured by the fluorescent Ca2+-sensitive dye fura-2. RESULTS: We found an increase of resting [Ca2+]i in erythrocytes from uremic hemodialyzedpatients compared with matched healthy controls (103 +/- 2.5 nM, N = 20, vs. 90 +/- 4, N = 20, P < 0.01). Moreover, we found an altered voltage-dependent Ca2+ influx showing a reduced transport rate (0.42 +/- 0.03 nM/second vs. 0.74 +/- 0.08, P < 0.01). High levels of plasma parathyroid hormone (PTH) were related to augmented Ca2+ entry (r = 0.511, P < 0.05), contributing to maintain a high level of [Ca2+]i. Hemodialysis had no effect on cell calcium level and Ca2+ influx indices. The therapy with Ca2+ antagonists did not modify the values of resting [Ca2+]i or Ca2+ influx indices, but the correlation between PTH and influx indices was lost. CONCLUSIONS: In conclusion, we found evidence for an alteration of erythrocyte Ca2+ influx caused by uremic toxicity that could be related to some organ disorders in uremia. The chronic increase of cellular calcium may contribute to influx derangement.
Authors: Maria Pietrzak-Nowacka; Krzysztof Safranow; Joanna Bober; Maria Olszewska; Bożena Birkenfeld; Monika Nowosiad; Kazimierz Ciechanowski Journal: Arch Med Sci Date: 2012-10-16 Impact factor: 3.318