Introduction. Chronic kidney disease (CKD) has been referred to as a state of cellular calcium toxicity. The aim of this study was to investigate the status of free cytosolic calcium ([Ca 2+ ] i ) and intracellular calcium reserves and the capacitative calcium entry in peripheral blood mononuclear cells (PBMCs) of CKD patients, and to determine the effect of vitamin D3 supplementation on these parameters. Methods. The study involved 44 patients with CKD sta- ges 2-3 and 70 healthy volunteers. 27 were treated with cholecalciferol (5000 IU/week) for 12 months. [Ca 2+ ] i was measured using Fluo-3 AM fluorimetry. Intracellular calci- um reserves were emptied by the application of thapsigar- gin (Tg), a specific inhibitor of endoplasmic reticulum Ca 2+ - ATPase. 2-Aminoethyl-diphenyl borate (2APB) was used to examine the capacitative calcium entry. Results. [Ca 2+ ] i of CKD patients was substantially higher in comparison with healthy subjects: 123 (115-127) vs 102 (98-103) nmol/l; p<0.001. The calcium concentration of Tg-sensitive stores and the capacitative calcium entry were also significantly increased in CKD patients. After the 12- month vitamin D3 supplementation, there was a marked decrease in [Ca 2+ ] i [105 (103-112) nmol/l; p<0.001 vs. baseline], independently of the increase in 25(OH)D 3 or the decrease in PTH levels. No significant changes in intracel- lular calcium reserves and the capacitative calcium entry were found. Conclusions. Our results demonstrate that: (1) [Ca 2+ ] i , intracellular calcium stores and the capacitative calcium entry were significantly increased already in early stages of CKD; (2) long-term vitamin D3 supplementation normalized [Ca 2+ ] i without any effect on intracellular calcium reserves or the capacitative calcium entry.

Slovak Medical University Department of Clinical and Experimental Pharmacotherapy Bratislava

9. mezinárodní nefrologické sympozium "Metabolické změny při chronickém selhání ledvin", Tatranská Lomnica, 21.10.2009