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Background and Aims Infections and thrombosis of central venous catheter (CVC) in hemodialysis patients are the major causes of catheter loss resulting in hospitalization and increased costs. Interdyalitic catheter lock solutions, usually heparin, avoid these complications. Among the many, sodium bicarbonate has been proved as effective and safe catheter lock solution due to its antimicrobial and antithrombotic properties. The aim of this study was to compare the efficacy of two different CVC lock solution: sodium heparin versus sodium bicarbonate, to prevent catheter–related thrombosis and infection in hemodialysis patients Method They were enrolled, in a 12 months case-control study, 17 hemodialysis patients with tunneled hig-flux CVC (femoral or internal jugular). Each patient was evaluated in its common treatment for CVC dysfunction (Qb, CVC that works in reverse branches during the hemodialysis session, use of urokinase or extra lock with sodium heparin or 4% citrate) and infection (WBC count, C reactive protein -CRP, bloodstream culture, exit-site infection -ESI) during standard sodium heparin CVC lock solution (hep-lock), for the first 6 months, and then, during sodium bicarbonate lock solution (10 mEq/10 ml, bic-lock) for following 6 months. aPTT, PLT, Hct and albumin are also montly evaluated. Type and anticoagulant dose during hemodialysis sessions were unchanged over the study as well as any antiplatelet/anticogulant home therapy. Results Fifteen patients on 17 completed the study and the main results are reported in table 1. There were no significant differences between patients on demographics and number of catheter days treatments for both study periods. The blood flow was similar in either study phases and stable during the hemodialysis sessions (Qb 225±13 ml/m’ at 2-hours vs 225±15 ml/min at start of dialysis), even the use of reverse branches was similar. Hep-lock showed a lower usage of extra lock drug in comparison with Bic-lock (0,4% vs 3,1%, p Conclusion There is no CVC ideal lock solution and although sodium bicarbonate is inexpensive and readily avalaible our data shows better CVC performances with sodium heparin.

Background and Aims The High-Flux (HF) dialyzer in standard hemodialysis (HD) allow the removal of a wider spectrum of uremic toxin. However, the HD can remove mostly low molecular weight solutes while the HDF can remove solutes around 15kDa, so-called Middle Molecules (MM), improving morbidity and mortality by exchange volumes >23L per session. The new medium cut-off (MCO) filter Theranova® is designed to expand the removal of toxins up to 45kDa in HD compared to HF membranes (HemoDialysis eXpanded, HDx) even with conventional blood flows and without exchange fluid infusion. The aim of this study is to evaluate the performance of HDx and its impact on anemia and quality of life (QoL) in haemodialysis patients. Method 11 stable HDs patients were enrolled (M/F 8/3, age 70.8±9) with Qb ≤300 ml/min in a 12 months observational case-control study. Each patient was evaluated first with HF filter (T0) and then in HDx for 12 months (T12). At T0-T6-T12 were evaluated: urea, phosphate (P), beta2-microglobulin (B2m), myoglobin (Myo), free light-chains k and λ (FLC- K and FLC- λ), C-Reactive Protein (CRP), hemoglobin (Hb) and albumin as well. Furthermore Kt/V, dose of EPO, ERI and SF-36 questionnaire were evaluated at the beginning and end of observation. We treat HD patients accordingly to the KDIGO Guideline for Anemia in CKD. The values have been reported as mean ±SD. Results HDx (Qb = 275 ± 41 ml/min, TT 215 ± 21 m) shows a significant increase in KT/V (T0 1,33 ± 0,19; T12 1,57 ± 0,16; p = 0.001) with relevant RR of: Urea 73.5%; P 58.4%; B2m 66,1 % (p< 0.05); Myo 55,1% (p< 0.05); FLC-k 64.1 % (p< 0.05); FLC-λ 59.9% (p< 0.05). There is a significant reduction at 12months for PCR (Tab.1). HDx reduced ERI [T0 10.1 ± 11.2; T6 4.1 ± 5.3 (p Conclusion HDx effectively removes uremic toxins up to 45kDa, even with Qb

Although statins are lipid-lowering drugs that block cholesterol biosynthesis, they exert immunomodulatory, anti-inflammatory, anti-angiogenic and anti-proliferative functions by reducing the isoprenylation of proteins involved in cell signal transduction such as Ras and RhoA. In this study, we provide evidence that several natural (lovastatin, simvastatin and pravastatin) and synthetic (cerivastatin and atorvastatin) statins exert a cytotoxic effect on human T, B and myeloma tumor cells by promoting their apoptosis. Dissimilar susceptibility to apoptosis has been detected in these lines, presumably in relation to the altered expression of proteins involved in the regulation of cellular signals. Cerivastatin promptly activated the cell death even in doxorubicin resistant cell lines such as MCC-2, whereas pravastatin, a hydrophilic compound, failed to induce any effect on either proliferation or apoptosis. The statin-induced apoptotic pathway in these cell lines was presumably regulated by altered prenylation of either Ras or RhoA, as measured by the defective membrane localization of these small GTPases. In addition the cell proliferation was rescued by both farnesylpyrophosphate (FPP) and geranyl-geranylpyrophosphate (GGPP), whereas no effect was obtained with squalene, a direct precursor of cholesterol. Statins primed apoptosis through its intrinsic pathway involving the mitochondria. In fact, we observed the reduction of mitochondrial membrane potential and the cytosolic release of the second mitochondria-derived activator of caspases (Smac/DIABLO). The apoptotic pathway was caspase-dependent since caspases 9, 3 and 8 were efficiently activated. These results support the potential use of statins in association with conventional treatment as apoptosis-triggering agents in these tumors.