Background Lean body mass (LBM) represents the “fat-free” muscle mass in hemodialysis (HD) patients and is an important nutritional measure. Previous studies have found that both higher LBM and body mass index (BMI) were related to greater survival in HD patients. Additional studies have shown differences in survival across racial-ethnic groups of HD patients. However, the association of LBM and mortality across racial-ethnic subgroups has not been examined. Objective We hypothesize that racial differences in LBM affect the mortality in HD patients. Setting and Participants chronic HD patients from a large dialysis organization in the US Predictors estimated LBM (eLBM), self-identified racial subgroups Outcome variable 5 year survival Study Design We examined the association between baseline eLBM and survival using Cox proportional hazard models adjusted for demographics, comorbidities and laboratory measures. Associations were examined across subgroups of race-ethnicity (Non-Hispanic white, African American, and Hispanic) and BMI. Results The final cohort included 117,683 HD patients, who were 62±15 (mean ± SD) years old, 43% women and 59% with diabetes mellitus. Higher eLBM was linearly associated with lower mortality. Compared to the reference group (48.4–<50.5 kg), patients with the lowest eLBM (<41.3 kg) had a 1.4-fold higher risk of mortality (HR: 1.37, 95%CI: 1.30–1.44) in the fully adjusted model. A similar linear association was seen among patients with BMI <35 kg/m2 and in non-Hispanic whites and African American subgroups. However, higher eLBM was not associated with improved survival in Hispanic patients or patients with BMI ≥35 kg/m2. Limitation Potential Residual Confounding. Conclusions Higher eLBM is associated with a lower mortality risk in HD patients, especially among non-Hispanic white and African American groups. Hispanic patients do not demonstrate a similar inverse relationship. The association between LBM and mortality among different racial groups of HD patients deserves additional study.

Bladder cancer (BC) is a potentially life-threatening malignancy. Due to a high recurrence rate, frequent surveillance strategies and intravesical drug therapies, BC is considered one of the most expensive tumors to treat. As a fundamental evolutionary catabolic process, autophagy plays an important role in the maintenance of cellular environmental homeostasis by degrading and recycling damaged cytoplasmic components, including macromolecules and organelles. Scientific studies in the last two decades have shown that autophagy acts as a double-edged sword with regard to the treatment of cancer. On one hand, autophagy inhibition is able to increase the sensitivity of cancer cells to treatment, a process known as protective autophagy. On the other hand, autophagy overactivation may lead to cell death, referred to as autophagic cell death, similar to apoptosis. Therefore, it is essential to identify the role of autophagy in cancer cells in order to develop novel therapeutic agents. In addition, autophagy may potentially become a novel therapeutic target in human diseases. In this review, the current knowledge on autophagy modulation in BC development and treatment is summarized.

Background: Abnormalities in mineral and bone disorder (MBD) markers are common in patients with chronic kidney disease. However, previous studies have not accounted for their changes over time, and it is unclear whether these changes are associated with survival. Methods: We examined the association of change in MBD markers (serum phosphorus (Phos), albumin-corrected calcium (Ca_Alb), intact parathyroid hormone (iPTH) and alkaline phosphatase (ALP)) during the first 6 months of hemodialysis (HD) with all-cause mortality across baseline MBD strata using survival models adjusted for clinical characteristics and laboratory measurements in 102,754 incident HD patients treated in a large dialysis organization between 2007 and 2011. Results: Across all MBD markers (Phos, Ca_Alb, iPTH and ALP), among patients whose baseline MBD levels were higher than the reference range, increase in MBD levels was associated with higher mortality (reference group: MBD level within reference range at baseline and no change at 6 months follow-up). Conversely, decrease in Phos and iPTH, among baseline Phos and iPTH levels lower than the reference range, respectively, were associated with higher mortality. An increase in ALP was associated with higher mortality across baseline strata of ALP ≥80 U/l. However, patients with baseline ALP <80 U/l trended towards a lower risk of mortality irrespective of the direction of change at 6 months follow-up. Conclusions: There is a differential association between changes in MBD markers with mortality across varying baseline levels in HD patients. Further study is needed to determine if consideration of both baseline and longitudinal changes in the management of MBD derangements improves outcomes in this population.

Results from this study demonstrate that TGF-beta signalling is essential in protection against acute peritoneal inflammation induced by bacterial infection.