Supplementary Material for: Salt Intake and All-Cause Mortality in Hemodialysis Patients

<b><i>Background:</i></b> Although some clinical practice guidelines regarding hemodialysis recommend salt restriction, few studies have examined the association between salt intake and clinical outcomes in hemodialysis patients. This study aimed to clarify the association between salt intake and mortality in hemodialysis patients. <b><i>Methods:</i></b> This retrospective cohort study was based on the Japanese Society for Dialysis Therapy renal data registry database (2008) and included 88,115 adult patients who had received hemodialysis for at least 2 years. Estimated salt intake was the main predictor and was calculated from intra-dialytic weight loss and pre- and post-dialysis serum sodium levels. Nonlinear logistic regression was used to determine the association between salt intake and mortality, adjusting for potential confounders. The outcomes considered were all-cause mortality and cardiovascular death at 1 year. <b><i>Results:</i></b> The median (25–75th percentile) salt intake at baseline was 6.4 (4.6–8.3) g/day. At 1 year, all-cause mortality occurred in 1,845 (2.1%) patients, including 807 cardiovascular deaths. The low salt intake group (< 6 g/day) demonstrated the highest all-cause mortality and cardiovascular deaths. No association was observed between high salt intake, all-cause mortality and cardiovascular deaths. The lowest risk for all-cause mortality and cardiovascular death occurred among patients with an estimated salt intake of 9 g/day. <b><i>Conclusion:</i></b> Low salt intake, but not high salt intake, was associated with all-cause and cardiovascular mortality in Japanese hemodialysis patients. Further studies to justify including a lower limit of salt intake for hemodialysis patients are suggested

Supplementary Material for: Genome-wide analysis of DNA methylation in pseudomyxoma peritonei originated from appendiceal neoplasms

Introduction: Pseudomyxoma peritonei (PMP) is a disease characterized by progressive accumulation of intraperitoneal mucinous ascites produced by neoplasms in the abdominal cavity. Since the prognosis of patients with PMP remain unsatisfactory, the development of effective therapeutic drug(s) is a matter of pressing concern. Genetic analyses of PMP have clarified the frequent activation of GNAS and/or KRAS. However, the involvement of global epigenetic alterations in PMPs has not been reported. Methods: To clarify the genetic background of the 15 PMP tumors, we performed genetic analysis using AmpliSeq Cancer HotSpot Panel v2. We further investigated global DNA methylation in the 15 tumors and eight non-cancerous colonic epithelial cells using Methylation EPIC array BeadChip (Infinium 850k) containing a total of 865,918 probes. Results: This is the first report of comprehensive DNA methylation profiles of PMPs in the world. We clarified that the 15 PMPs could be classified into at least two epigenotypes, unique methylation epigenotype (UME) and normal-like methylation epigenotype (NLME), and that genes associated with neuronal development and synaptic signaling may be involved in the development of PMPs. In addition, we identified a set of hypermethylation marker genes such as HOXD1 and TSPYL5 in the 15 PMPs. Conclusions: These findings may help the understanding of the molecular mechanism(s) of PMP and contribute to the development of therapeutic strategies for this life-threatening disease