Spectrally and Time-Resolved Fluorescence Imaging of 22-NBD-Cholesterol in Human Peripheral Blood Mononuclear Cells in Chronic Kidney Disease Patients.

The interaction of the fluorescent probe 22-NBD-cholesterol with membranes of human peripheral blood mononuclear cells (PBMC) was tested by time- and spectrally resolved fluorescence imaging to monitor the disturbance of lipid metabolism in chronic kidney disease (CKD) and its treatment with statins. Blood samples from healthy volunteers (HV) and CKD patients, either treated or untreated with statins, were compared. Spectral imaging was done using confocal microscopy at 16 spectral channels in response to 458 nm excitation.

[Vitamin D3 supplementation and cellular calcium homeostasis in patients with chronic kidney disease].

Mini review summarizes the results of our studies focused on elucidation of the pathophysiological mechanisms of altered calcium homeostasis in nonexcitable cells from patients with early stages of chronic kidney disease (CKD), as well as on determining the effect of vitamin D3 supplementation on these mechanisms. The basic mechanisms of calcium entry to and removal of the cell are already changed in early stages of CKD. These disturbances cause an increased the concentration of cytosolic free calcium ([Ca2+]i), which may change a number of cellular processes, and the expression of various signaling molecules.

The Impact of Vitamin D3 Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease.

Intracellular calcium concentration in peripheral blood mononuclear cells (PBMCs) of patients with chronic kidney disease (CKD) is significantly increased, and the regulatory mechanisms maintaining cellular calcium homeostasis are impaired. The purpose of this study was to examine the effect of vitamin D3 on predominant regulatory mechanisms of cell calcium homeostasis. The study involved 16 CKD stages 2-3 patients with vitamin D deficiency treated with cholecalciferol 7000-14000 IU/week for 6 months.

Purinergic P2X7 receptors participate in disturbed intracellular calcium homeostasis in peripheral blood mononuclear cells of patients with chronic kidney disease.

Background: P2X(7) receptors intervene with lymphocyte activation and are responsible for multiple processes, including calcium influx. Here, we studied the participation of P2X(7) receptors in disturbed intracellular calcium homeostasis regulation in early-stage chronic kidney disease (CKD).

Methods: The study involved 20 healthy volunteers and 20 CKD stage 2-3 patients.

Intracellular calcium homeostasis in patients with early stages of chronic kidney disease: effects of vitamin D3 supplementation.

Background: Chronic renal failure 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)), intracellular calcium reserves and the capacitative calcium entry in peripheral blood mononuclear cells (PBMCs) of early-stage chronic kidney disease (CKD) patients, and to determine the effect of vitamin D(3) supplementation on these parameters.

Methods: The study involved 44 patients with CKD stages 2-3; 27 of them were treated with cholecalciferol (5000 IU/week) for 12 months.

Effects of long-term cholecalciferol supplementation on mineral metabolism and calciotropic hormones in chronic kidney disease.

Background: Data on the efficacy and safety of long-term vitamin D supplementation in chronic kidney disease (CKD) are scarce. We assessed the effects of the 12-month vitamin D(3) treatment on mineral metabolism and calciotropic hormones in patients with CKD stages 2-4.

Methods: Eighty-seven patients (mean age 66 years, men/women 33/54) were randomized to cholecalciferol treatment with either 5,000 or 20,000 IU/week.

Rapid effects of 1alpha,25(OH)2D3 in resting human peripheral blood mononuclear cells.

The steroid hormone 1alpha,25(OH)2D3 produces biological responses via both genomic and nongenomic mechanisms. Stimulation of rapid, nongenomic responses by 1alpha,25(OH)2D3 has been postulated to result from interaction of the ligand with cell membrane 1alpha,25(OH)2D3 receptors and to involve membrane receptors. We examined the rapid effects of 1alpha,25(OH)2D3 on calcium mobilization and calcium entry into resting human peripheral blood mononuclear cells isolated from healthy volunteers.

4-Aminopyridine activates calcium influx through modulation of the pore-forming purinergic receptor in human peripheral blood mononuclear cells.

We investigated whether 4-aminopyridine (4AP), a drug recently linked to calcium influx and apoptosis, also affected purinergic receptor channels that are known to play an important role in the activation of T lymphocytes. The application of 4AP induced a rise in [Ca2+]i that was sensitive to nickel. This action was also observed in cells in which calcium reserves were emptied using thapsigargin (Tg).