No abstract

Background/Aim: Increased apoptosis along with enhanced inflammation has been reported in hemodialysis and pre-dialysis patients. However, there is limited information at which stage during the progression of chronic kidney disease (CKD) the balance between pro- and anti-apoptotic mechanisms is disturbed and inflammatory response is activated. The aim of this study was to investigate possible alterations in apoptotic and inflammatory markers during CKD (stages 1–4) progression and the probable interactions between them. Methods: In a cross-sectional study, 152 steady-state CKD outpatients (83 males, 55%) with mean estimated glomerular filtration rate 46 (29–76) ml/min/1.73 m² were studied. Apoptosis was assessed in peripheral blood mononuclear cells by estimating Bcl-2 expression, annexin V-propidium iodine staining and serum soluble Fas (sFas) and Fas-ligand. Serum levels of C-reactive protein, tumor necrosis factor-α (TNF-α), interleukin-6 and plasma levels of fibrinogen were measured as markers of inflammation. Results: Bcl-2 expression was found to decrease significantly in both lymphocytes and monocytes from CKD stage 1 to 4. In contrast, the activity of sFas increased significantly and so did the levels of TNF-α and fibrinogen. The majority of these alterations occurred as soon as patients entered stage 3 of CKD. A multivariate regression analysis demonstrated that CKD remained a significant predictor of the aggregate of the assessed markers. Conclusions: Apoptosis appeared to increase across CKD stages 1–4, and this was associated with increased proinflammatory activity.

We carried out this retrospective study to examine the magnesium status of our chronic ambulatory peritoneal dialysis (CAPD) patients dialyzed with 0.75 mmol/L (group I) or 0.50 mmol/L (group II) magnesium peritoneal dialysis solution. A total of 34 anuric patients on CAPD (age:31-72 years; duration of CAPD:7-74 months) were studied. None of them received magnesium-containing phosphate binders or vitamin D. Biochemical parameters including magnesium, calcium, phosphate, parathormone, and albumin were measured in all patients. The corrected for hypoalbuminemia serum magnesium concentration in group I was significantly higher compared to that found in group II. However, there were no significant differences in the other measured parameters between the two groups of CAPD patients, though iPTH levels were somewhat increased in group II patients. Serum magnesium levels were weakly correlated with serum prealbumin levels in both groups of CAPD patients (r=0.16, P=0.08 and r=0.17, P=0.07). The incidence of hypermagnesemia was significantly higher in group I patients versus those in group II (13/19 68.4%] vs. 2/15 13.3%], P<0.01). On the other hand, no patient developed hypomagnesemia (corrected total magnesium <0.65 mmol/L), despite the trend toward decreased magnesium levels in group II patients. Our results point out that serum iPTH levels and nutritional parameters, such as prealbumin levels, should be taken into account in the choice of the magnesium concentration of the peritoneal dialysis fluid.

Dialyzer membrane and the type of heparin used can influence lipid parameters. However, there are limited and debatable data concerning lipid alterations during a single hemodialysis session. Moreover, the role of hemoconcentration after every hemodialysis session confuses the real effect of the heparin on lipid profile. We investigated the acute effect of heparin administration on lipids in hemodialysis patients, but on an off-hemodialysis day in order to eliminate any effect of ultrafiltration. We studied six patients on hemodialysis, six patients on peritoneal dialysis, and six healthy persons. The study was performed in two phases (1 week apart). In phase A, we used unfractionated heparin (5000 IU, intravenous), whereas in phase B, low-molecular-weight heparin (3500 anti-FXa, intravenous) was used. Total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and Lp(a) were estimated before and 1, 2, 3, and 4 hours after heparin administration. We observed a reduction only in triglycerides (at the first, second, and third hour) in both phases in all groups. The other lipid parameters were not affected. In conclusion, acute administration of both types of heparin seems to affect only triglyceride levels in patients on renal replacement therapy.

Background/Aim: We investigated the potential role of the membrane type on phosphate kinetics. Methods: Six patients on dialysis (HD) were studied using modified cellulose (Hemophan), ethylene-vinyl alcohol (EVAL) and polyacrylonitrile (PAN). Total (TPR), extracellular (EPR) and intracellular (IPR) phosphate removal and effective dialyzer phosphate clearance (K_d) were determined by the DDQ method. The intercompartment transfer coefficient (K_C) was calculated using a mathematical model. Erythrocyte phosphate (P_ERY) and 2,3-biphosphoglycerate (2,3-BPG) concentrations were determined before and after HD. Results: TPR was 1.2 ± 0.4, 1.10 ± 0.4 and 1.09 ± 0.4 g with Hemophan, EVAL and PAN, respectively (p = n.s.). EPR and IPR were independent of membrane type. There was no difference in K_C between membranes (321 ± 70, 338 ± 92 and 341 ± 83 ml/min, respectively). The P_ERY and 2,3-BPG remained statistically insignificant for all membranes. Conclusion: Our results show that the type of membrane does not influence the kinetics of phosphate during dialysis, neither in the transfer from plasma to dialysate nor from the intra- to the extracellular compartment.