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Background Evidence regarding volume-outcome effects on peritoneal dialysis (PD) catheter implantation is limited. This study aimed to investigate associations between hospital volume (annual caseload of catheter implantation) and perioperative outcomes. Methods Clinical data for patients who underwent PD catheter implantation from 2007 to 2012 were extracted from the Japanese nationwide Diagnosis Procedure Combination database. Hospital volume was divided into tertiles: low-volume (1 – 6 cases/year), medium-volume (7 – 13 cases/year), and high-volume (≥ 14 cases/year). Multivariate logistic regression analysis for the occurrence of any adverse events and blood transfusion, and gamma-distributed log-linked linear regression analysis for postoperative length of stay were conducted with explanatory variables of hospital volume, age, sex, Charlson comorbidity index, history of hemodialysis, type of anesthesia, and type of hospital. Results Among 906, 855, and 744 cases in the low-volume, medium-volume, and high-volume groups, overall adverse events were 10.0%, 7.6%, and 6.0%, transfusion rates were 1.3%, 1.1%, and 0.9%, and median postoperative stays were 12, 10, and 9 days, respectively. In multivariate analyses, compared with the low-volume group, medium-volume and high-volume groups were associated with a lower incidence of overall adverse events (odds ratio [OR] = 0.71, p = 0.058, and OR = 0.59, p = 0.013, respectively) and shorter postoperative stay (% difference = -10.5%, p = 0.023, and % difference = -18.5%, p = 0.001, respectively), while no significant association was detected for transfusion. Conclusions Less frequent adverse events and shorter stays were observed in higher-volume centers. Inverse volume-outcome relationships in PD catheter implantation were confirmed.

Long-term peritoneal dialysis using glucose-based dialysates is associated with peritoneal fibrosis. The object of this study was to investigate the hypothesis that endothelin (ET)-1, which is known to play an important role in various fibrotic diseases, may also be involved in peritoneal fibrosis using human peritoneal mesothelial cells (HPMC).HPMC were cultured with 4% D- or L-glucose, or loaded with 10 nmol/L ET-1. In some experiments, the ETA receptor antagonist BQ-123, the ETB receptor antagonist BQ-788, and antioxidants 4-hydroxy-2,2,6,6-tetramethyl-piperidine 1-oxyl (TEMPOL) and diphenyleneiodium chloride (DPI) were used. mRNA expression of ET-1, ETA receptor, ETB receptor, and fibronectin (FN) was analyzed by real-time polymerase chain reaction (real-time PCR). The protein levels for FN and ET-1 were measured by ELISA. CM-H2DCFDA-sensitive reactive oxygen species (ROS) were evaluated by flow cytometry.D-Glucose significantly induced mRNA expression of ET-1 and the ETB receptor but not the ETA receptor. FN production under high glucose conditions was inhibited by BQ-788. ET-1 directly stimulated H PMC to increase mRNA expression of FN and CM-H2DCFDA-sensitive ROS production. BQ-788, TEMPOL, and DPI inhibited mRNA expression of FN induced by ET-1.The present study suggests that high-glucose-induced FN synthesis is mediated by the ET-1/ETB receptor pathway and, therefore, an ETB receptor antagonist may be usefulin preventing FN production in HPMC.

It is known that peritoneal mesothelial cells (PMCs) are denuded in patients undergoing long-term continuous ambulatory peritoneal dialysis (CAPD); the mechanism of damage is not well known. A high quantity of glucose loaded onto PMCs in these patients may generate toxic radicals during the mitochondrial metabolism, leading to mitochondrial DNA damage that accumulates due to the incomplete repair system of this DNA.To study damage to the PMCs of long-term CAPD patients, and to examine whether glucose overload accelerates this damage in vitro.Descriptive clinical and in vitro study.Stable CAPD patients and nonuremic patients undergoing elective abdominal surgery.(1) Clinical Samples: 13 peritoneal tissue samples from CAPD patients and 5 omental tissue samples from patients with normal renal function were investigated. PMCs in dialysate effluent were collected from another 13 stable CAPD patients. (2) In Vitro Samples: Primary PMCs were incubated for up to 144 hours in medium containing one of the following: 5.6 mmol/L glucose (control), 56 mmol/L glucose (G), 222 mmol/L glucose (high G), or 222 mmol/L mannitol (high M; osmolar control for high G). The tissues and cells of clinical and in vitro samples were stained for light and immunoelectron microscopy with anti-8-hydroxy-2'-deoxyguanosine (anti-8-OH-dG) antibody, a marker of oxidative DNA damage. In vitro cells were also studied using transmission electron microscopy. Cellular ATP content, mitochondrial membrane potential, and intracellular generation of reactive oxygen species (ROS) were analyzed by luciferase-luciferin system, or by flow cytometry using rhodamine 123 and 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA).Biopsy specimens showed strong cytoplasmic staining with 8-OH-dG in patients on long-term CAPD, but only faint staining in patients with end-stage renal disease before the initiation of CAPD, and no staining in patients with normal renal function. Dialysate effluent showed strong granular staining with 8-OH-dG in most PMCs in all long-term CAPD patients, but only faint and focal staining in patients at the start and after 3-5 months of CAPD. In vitro experiments also showed strong granular staining by 8-OH-dG in most PMCs cultured in high G, weak staining in G and high M, and no staining in the control. Immunoelectron microscopy revealed the localization of 8-OH-dG to mitochondria. Transmission electron microscopy showed swelling of mitochondria, with decreased cristae, in PMCs cultured in high G. However, only partial expansion of mitochondria was seen in G and high M, and no changes were seen in the control. Cellular ATP content and mitochondrial membrane potential were reduced early, followed by an increase when cultured in high G. Intracellular ROS production was also increased in PMCs cultured in high G and high M.These data suggest that high-glucose peritoneal dialysate may promote oxidative mitochondrial DNA damage in PMCs in CAPD patients.