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BACKGROUND Reduced soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) levels follow declining renal function, are strongly associated with endothelial dysfunction and predict cardiovascular events in nondialyzed chronic kidney disease patients. In contrast, elevated levels of sTWEAK predict poor survival in hemodialysis (HD) patients. Recent evidence suggests a role for sTWEAK in the pathophysiology of vascular calcification. The aim of the study was to investigate plausible links between sTWEAK, atherosclerosis, arterial stiffness and vascular calcification in HD patients. METHODS Coronary artery calcification score (CACs) determined by multislice computed tomography, arterial stiffness by pulse wave velocity (PWV) and carotid artery intima-media thickness (CA-IMT) by carotid Doppler ultrasonography were assessed in 131 long-term prevalent HD patients. sTWEAK levels were measured by ELISA (Bender MedSystems, Vienna, Austria). RESULTS Mean serum sTWEAK level was 237.0 ± 147.5 pg/mL (range 78-937). sTWEAK level was inversely correlated with CA-IMT at a borderline significance (r=-0.168, p=0.05). Neither carotid-radial PWV nor carotid-femoral PWV values correlated with sTWEAK. sTWEAK level was higher in patients with severe vascular calcification (CACs ≥400) compared to patients with CACs

Background: High glycosylated hemoglobin (HbA 1c ) levels are recognized as a risk factor for cardiovas- cular disease in the diabetic dialysis population. However, it is not known whether this also applies to nondiabetic dialysis patients. We prospectively inves- tigated the association between HbA 1c levels and new cardiovascular events in nondiabetic patients treated with peritoneal dialysis. Methods: Eighty nondiabetic patients who had been on peritoneal dialysis treatment were prospectively followed for 5 years. HbA 1c levels were measured at baseline and every 3 months. Fatal and nonfatal cardiovascular events were assessed during the fol- low-up. Results: Mean age was 48.5 ± 15.2 years; 51% were male. Baseline HbA 1c level was 5.46% ± 0.41% (range 4.6%-6.3%). Mean HbA 1c was 5.44% ± 0.31% (range 4.8%-6.3%) during the study, and positively correlated with age and high-sensitivity C-reactive protein. Twen- ty fatal and nonfatal cardiovascular events were ob- served during a mean 41.8 ± 7.1 months of follow-up. Event-free survival was better in patients with HbA 1c levels

Objective Peritoneal fibrosis (PF) is one of the most serious causes of failure in continuous ambulatory peritoneal dialysis (PD). Although the underlying mechanism responsible for the genesis of PF is still unknown, transforming growth factor p (TGFβ1) has been shown to be associated with PF. Angiotensin converting enzyme inhibitors have been shown to prevent the stimulating effect of growth factors. The aim of the present study was to investigate the effect of enalapril on peritoneal function and morphology in a rat model of experimental PF. Methods Twenty-one albino Wistar rats were divided into three groups: ( 1 ) the control group (C) received 10 mL isotonic saline intraperitoneally (IP), ( 2 ) the dextrose (Dx) group 10 mL 3.86% dextrose PD solution IP, and ( 3 ) the enalapril-treated group (ENA) 10 cc 3.86% dextrose PD solution IP plus 100 mg/L enalapril in drinking water. After 4 weeks, a 1-hour peritoneal equilibration test was performed with 20 mL 2.27% dextrose PD solution. Dialysate-to-plasma urea ratio (D/P urea), glucose reabsorption (D1/D0 glucose), ultrafiltration (UF) volume, and levels of dialysate protein, TGFβ1, and cancer antigen 125 (CA125) were determined. The parietal peritoneum was evaluated histologically by light microscopy. Results Administration of enalapril resulted in preserved UF (-0.2 ± 0.7 mL vs 1.7 ± 0.3 mL, p < 0.05), protein loss (2.3 ± 0.5 g/L vs 1.6 ± 0.2 g/L, p > 0.05), and peritoneal thickness (77 ± 7 μ vs 38 ± 5 μ, p < 0.001). D/P urea increased significantly in the Dx group ( p < 0.05). Both higher levels of TGFβ1 (undetectable vs 298 ± 43 pg/mL, p < 0.001) and lower levels of CA125 in dialysate effluent (0.94 ± 0.5 U/L vs 0.11 ± 0.1 U/L, p > 0.05) were determined in the Dx group. Conclusion These findings show that peritoneal morphology and function tests were dramatically deranged in the Dx group. The same properties were partially preserved in the ENA group. The production of TGFβ1 was significantly reduced but peritoneal thickness was not completely inhibited. In conclusion, by inhibiting the production of TGFβ1, enalapril can preserve peritoneal histology, peritoneal function, and remodeling of mesothelial cells.

Background One of the origins of cardiovascular disease in dialysis patients is arterial stiffness. The aim of our study was to assess the relationship between the calcium content of peritoneal dialysis (PD) solution and arterial stiffness. Patients and Methods We enrolled into the study 49 PD patients who had been treated with the same PD solution for the preceding 6 months. The calcium content of the PD solution was 1.25 mmol/L in 34 patients (low-Ca group) and 1.75 mmol/L in 15 patients (high-Ca group). Study patients were followed for 6 months on the same PD prescription. Arterial stiffness was assessed by measurement of augmentation index (AI) and brachial pulse wave velocity (PWV) at baseline and at month 6 (SphygmoCor: Atcor Medical, West Ryde, NSW, Australia). Demographic data were recorded from patient charts. Results Mean age of the whole group was 51 ± 11 years, prevalence of diabetes was 14%, duration of PD was 43 ± 30 months, percentage of women was 45%, and percentage of patients using a cycler was 33%. We observed no differences between groups with regard to those variables or creatinine clearance, residual renal function, Ca, phosphorus, parathormone, C-reactive protein, lipid parameters, and use of phosphate binder with or without Ca content. Mean arterial pressure was higher in the high-Ca group, but the difference was not statistically significant (100 ± 22 mmHg vs 88 ± 18 mmHg, p = 0.06). At baseline, AI was significantly higher in the high-Ca group than in the low-Ca group (27% ± 10% vs 21% ± 9%, p < 0.05). Measurements of PWV were not different between the groups (8.4 ± 1.1 m/s vs 8.5 ± 1.7 m/s). Measurement of arterial stiffness parameters at month 6 revealed that PWV had increased in the high-Ca group (to 9.6 ± 2.3 m/s from 8.4 ± 1.1 m/s, p < 0.05), but had not changed in the low-Ca group (to 8.2 ± 1.9 m/s from 8.5 ± 1.7 m/s). The AI did not change in either group. Conclusions These data suggest that Ca exposure through PD solution plays a role in the progression of arterial stiffness, which may be related to increased vascular calcification.