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Objectives There is a lack of consensus on the risk factors for hernia formation, and the impact on peritoneal dialysis (PD) survival has seldom been studied. Methods This was a population-based study and all collected data were retrieved from the National Health Insurance Research Database of Taiwan. Patients who commenced PD between January 1998 and December 2006 were screened for inclusion. Multiple logistic regression and Cox proportional hazards models were applied to estimate the predictors for hernia formation and determine the predictors of PD withdrawal. Results A total of 6,928 PD patients were enrolled and followed until December 2009, with 631 hernia events and 391 hernioplasties being registered in 530 patients (7.7%). The incidence rate was 0.04 hernias/patient/year. Longer PD duration (per 1 month increase, hazard ratio (HR) 1.019) and history of mitral valve prolapse (MVP) (HR 1.584) were independent risk factors for hernia formation during PD, and female gender (HR 0.617) was a protective factor. On the other hand, there were 4,468 PD withdrawals, with cumulative incidence rates of 41% at 1 year, 66% at 3 years, and 82% at 5 years. Independent determinants for cumulative PD withdrawal included hernia formation during PD (HR 1.154), age (per 1 year increase, HR 1.014), larger dialysate volume (per 1 liter increase, HR 0.496), female gender (HR 0.763), heart failure (HR 1.092), hypertension (HR 1.207), myocardial infarction (HR 1.292), chronic obstructive pulmonary disease (COPD) (HR 1.227), cerebrovascular accident (CVA) (HR 1.364), and history of MVP (HR 0.712) Conclusions Prolonged PD duration was a risk factor for hernia formation, and female gender was protective. Hernia formation during PD therapy may increase the risk of PD withdrawal.

Background: Polycystic kidney disease (PCKD) is one of the most common inherited disorders in end-stage renal disease patients. It is generally thought that the survival of PCKD patients undergoing dialysis sur- passes that of general dialysis patients, but the cause of this improved survival is not clear. Methods: Using Taiwan's national health insurance claims data, we performed a longitudinal cohort study to investigate the survival and impact of comorbidi- ties on mortality in dialysis patients with and without PCKD. We excluded patients without diabetes mellitus (DM) in a further analysis. A Cox proportional hazards model was used to identify the risk factors for all- cause mortality. The Kaplan-Meier method was used to describe overall patient survival. Results: Five hundred and one (2.25%) of 22,298 non- diabetic incident dialysis patients had PCKD. We found no significant difference in survival rates be- tween those with and without PCKD. Being male, being over 65 years old and having congestive heart failure or cerebrovascular accident were each found to be independent predictors of mortality in the PCKD dialysis patients. Conclusions: Taiwan has a lower incidence rate of PCKD than Western countries. In Taiwan, there is little difference in the long-term survival between dialysis patients with and without PCKD.

Objective To investigate the induction of nitric oxide synthase type II (iNOS) in human peritoneal mesothelial cells (HPMC) using cytokines and bacterial lipopolysaccharide (LPS). Design Confluent monolayers of HPMC were exposed to cytokines [tumor necrosis factor alpha (TNFα), interleukin-1 beta (IL-1β), interferon gamma (IFNγ)] or LPS, individually or in various double and triple combinations, for 24 – 72 hours. Concentrations of nitrate and nitrite in the media were quantified using the Griess reaction and used as indirect indices of nitric oxide (NO) production. The expression of iNOS was assessed using reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot. Results Neither single cytokines nor LPS was able to induce iNOS mRNA or NO production. Both double combinations of TNFα+ IFNγ and IL-1β + IFNγ were able to induce iNOS mRNA expression, but only TNFα + IFNγ induced significant NO production. The triple combination of TNFα + IFNγ + IL-1β induced even more NO production than TNFα + IFNγ. There was no constitutive NO synthase type III (eNOS) expression in HPMC. Conclusions Certain combinations of cytokines could stimulate cultured HPMC to produce NO, and HPMC might be a source of intraperitoneal NO production during peritonitis.

Objective To investigate the prevalence of nodular goiter and thyroid dysfunction in uremic patients undergoing hemodialysis (HD) and peritoneal dialysis. Design Cross-sectional study. Setting Single dialysis unit and outpatient clinic. Patients The study included 221 patients [143 HD and 78 continuous ambulatory peritoneal dialysis (CAPD) patients] along with 135 consecutively selected outpatients as controls. Main Outcome Measures Ultrasonography was used to detect patients’ thyroid function and nodular goiter. Results Nodular goiter was detected in 54.8% of the uremic patients and in 21.5% of the controls. Uremic patients had higher prevalence of thyroid dysfunction, which included reduced serum concentration of total T3, total T4, and free T4, and increased serum level of TSH. Hypothyroidism was also observed more frequently in uremic patients than in the control group (5.4% vs 0.7%, p < 0.05). Nodular goiter was more frequently found in females than in males (63.5% vs 48%, p < 0.05). Moreover, the prevalence of nodular goiter increased with age (p < 0.02) in uremic patients. Hemodialysis patients had a higher frequency of reduced total T3 level (46.9% vs 29.5%, p < 0.02). However, CAPD patients had lower T4 levels (6.23 ± 1.82μg/dL vs 7.15± 1.99μg/dL, p < 0.05). Conclusion Because of the high incidence of hypothyroidism and nodular goiter in uremic patients, screening of thyroid function and goiter detection with ultrasound should be considered in evaluation of end-stage renal disease patients.

ObjectiveTo investigate the modulation of superoxide dismutase, glutathione peroxidase, and catalase by cytokines and endotoxin in human peritoneal mesothelial cells.DesignCultured human peritoneal mesothelial cells were treated with various concentrations of interleu kin-1 α, tumor necrosis factor-α(TNFα), interleukin-6, interleukin-8, transforming growth factor-β (TGFβ), and lipopolysaccharide. Cell morphology was observed and the activities of superoxide dismutase, catalase, and glutathione peroxidase were assayed. The antioxidant enzyme activities of human peritoneal mesothelial cells were also compared with those of human liver and kidney tissues.ResultsInterleukin-1α, TNFα, TGFβ, and lipopolysaccharide caused dose-dependent cytotoxicities in mesothelial cells. The activities of these three antioxidant enzymes did not change after treatment with cytokines and endotoxin. The total superoxide dismutase activity of confluent human peritoneal mesothelial cells was found to be greater than that of human liver and kidney tissues and was composed mostly of manganese superoxide dismutase activity. Furthermore, glutathione peroxidase and catalase activities of human peritoneal mesothelial cells were lower than those of human liver and kidney tissues.ConclusionIn human peritoneal mesothelial cells, lack of induction of antioxidant enzymes by inflammatory cytokines, as well as high superoxide dismutase activity accompanied by insufficient glutathione peroxidase and catalase activities may both contribute to the susceptibility of these cells to oxidative damage. Therefore, appropriate management to decrease oxidative injury to the peritoneum should be taken into consideration when treating long-term continuous ambulatory peritoneal dialysis patients.