Erythrocyte voltage-dependent calcium influx is reduced in hemodialyzed patients

Background. Uremia displays increased cytosolic free calcium ([Ca2+](i)) in many different cell types, supporting the hypothesis of an altered Ca2+ tr ansport 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 th e fluorescent Ca2+-sensitive dye fura-2. Results. We found an increase of resting [Ca2+](i) in erythrocytes from ure mic 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 alter ed voltage-dependent Ca2+ influx showing a reduced transport rate (0.42 +/- 0.03 nM/second vs. 0.74 +/- 0.08, r < 0.01). High levels of plasma parathy roid hormone (PTH) were related to augmented Ca2+ entry (r = 0.511, P < 0.0 5), 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 erythroc yte Ca2+ influx caused by uremic toxicity that could be related to some org an disorders in uremia. The chronic increase of cellular calcium may contri bute to influx derangement.