For Kaplan-Meier survival

analysis, patient status ( aliv

For Kaplan-Meier survival

analysis, patient status ( alive, dead, or lost to follow up) at December 2005 was used as the observational end point. Modality differences were analyzed using a Cox regression model. A total of 237 patients were evaluated: 139 on CAPD and 98 on APD. The median age was 62 years on CAPD and 59 years on APD (P < 0.031), and the percentage of diabetics was, respectively, 77 and 70% ( P = NS). The CAPD drop out causes were death (57%), transfer to HD (29%), and other causes (16%), whereas in APD, 62% were due to death, 24% to transfer to HD, and 14% to other causes. APD/CAPD patient survival for year 1, 2, and 3 was 82/62, 62/49, and selleck kinase inhibitor 56/42%, respectively. In conclusion, both therapies are considered good renal replacement therapy options in our hospital, but APD is the most attractive

one as demonstrated by the positive results presented here.”
“Leptin and adiponectin are adipokines with respective pro-atherogenic and anti-atherogenic properties, defining the plasma leptin/adiponectin ratio as a novel Volasertib cell line marker for atherosclerosis. In non-renal patients, both hyperleptinemia and hypoadiponectinemia are associated with cardiovascular complications. In peritoneal dialysis (PD) patients, the leptin/adiponectin ratio is markedly elevated, which is consistent with their increased cardiovascular risk. As glucose metabolism regulates adipokines, we hypothesized that glucose and/or other PD fluid components may affect adipokine production balance. This review summarizes the available data arising from research in this area. In 3T3-L1 adipocytes, glucose-based PD4 1.36% significantly increased leptin secretion vs amino-acid-based ( AA) and icodextrin (ICOD)-based PD fluids. In contrast, adiponectin secretion was significantly reduced by PD4 1.36% vs glucose-free dialysates.

Glucose concentration in PD fluids was shown to determine leptin secretion. Preliminary data from PD patients showed that a single 6-h dwell with PD4 3.86% glucose acutely increased plasma leptin vs AA (P<0.05). The reduction in glucose load in a standard PD regimen was associated with an improvement in the plasma leptin/adiponectin ratio at 6 months. pH-neutral PD fluids increased leptin secretion science in vitro vs acidic PD fluids, without effect on adiponectin. Whether this effect may have an impact on plasma leptin levels in PD patients is unknown. In conclusion, glucose-based PD fluids worsen the adipokine production balance in vitro while glucose-free solutions improve it. In PD patients, hypertonic glucose-based PD fluids may increase plasma leptin levels. Glucose-sparing PD regimens appear to improve the leptin/adiponectin ratio. However, their potential to reduce cardiovascular complications needs to be demonstrated.”
“Nitric oxide (NO) has emerged as an important endogenous inhibitor of apoptosis.

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