A Fast Decline of Residual Renal Function in the First Year is a Predictor for Early Withdrawal from Peritoneal Dialysis in Non-Diabetic Patients

Background/Aims: Little is known about the relationship between residual renal function (RRF) decline in early period and survival in non-diabetic peritoneal dialysis (PD) patients. Methods: A total of 567 non-diabetic patients who began PD from January 1, 2005 to June 30, 2013 was investigated. The rate of RRF decline was determined by the “slope of the trend equation” of serial RRFs. A composite end-point of all-cause mortality and conversion to hemodialysis (HD) was used, survival status was censored on June 30, 2016. Results: The median of “the slope of RRF decline equation” was 0.308 (0.001-2.111) ml/min/1.73 m2/ month. In the median follow-up period of 43 months (range 12 to 120 months), 65 (11.5%) patients died, 90 (15.9%) patients converted to HD and 171 (30.2%) patients received kidney transplantation. Multivariate linear regression showed male, high baseline RRF, high baseline peritoneal Kt/V urea, low serum albumin and low uric acid were independently associated with the rate of RRF decline in the first year of PD. Multivariate Cox models revealed that RRF decline in the first year remained a predictor for composite end-point (HR, 2.74, 95% CI, 1.53 to 4.90, P=0.001). The patients were divided into high RRF decline group (> 0.308ml/ min/1.73m2/month) and low RRF decline group (≤0.308 ml/min/1.73m2/month). In the first three years of PD, the rate of end-point events was higher in high RRF decline group (23.2%) than that in low RRF decline group (11.0%) (P< 0.001). There were 189 patients in low RRF decline group and 171 patients in high RRF decline group maintaining PD for more than 3 years, in a median follow-up of 54 months (range 37 to 120 months), the survival rate was 30.9% in high RRF decline group and 46.4% in low RRF decline group (P=0.883). In high RRF decline group, there were 92 patients reaching composited end-point and 112 patients maintaining PD; multivariate Cox model showed high peritoneal Kt/V urea after 1 year of PD and high albumin level were protective factors (HR, 0.29, 95% CI, 0.13 to 0.61, P= 0.001; HR, 0.94, 95% CI, 0.90-0.99, P=0.022, respectively), while fast RRF decline remained risk factor for composite end-point (HR, 3.28, 95% CI,1.48-7.31, P=0.004). Conclusion: A faster RRF decline in the first year was a predictor for all-cause mortality and conversion to HD in non-diabetic PD patients, mainly in the first three year. For patients with faster RRF decline, increasing PD dose was effective to improve survival

Association Between Comprehensive Nutritional Scoring System (CNSS) and Outcomes of Continuous Ambulatory Peritoneal Dialysis Patients

Background/Aims: The presence of protein–energy wasting (PEW) among dialysis patients is a crucial risk factor for outcomes. The complicated pathogenesis of PEW makes it difficult to assess and treat. This single-center retrospective study focuses on the association between nutritional markers and the outcomes of continuous ambulatory peritoneal dialysis(CAPD) patients, aiming to establish a practical comprehensive nutritional scoring system for CAPD patients. Methods: 924 patients who initiated peritoneal dialysis in our center from January 1st,2005 to December 31st,2015 were enrolled. Comprehensive nutritional scoring system(CNSS) was based on items including SGA, BMI, ALB, TC, MAC and TSF. We divide patients into 3 groups according to their CNSS score. Outcomes including mortality, hospitalization days and hospitalization frequency were compared between 3 grades. Results: The CNSS grade correlated significantly with hospitalization days (P<0.05). Both categorized CNSS grade (HR:0.56; 95% CI:0.41-0.78; P = 0.001) and continuous CNSS score (HR:0.87; 95% CI: 0.80-0.94; P = 0.001) independently protect PD patients from all-cause mortality. Conclusion: CNSS provides an integrated scoring system with significant associations with hospitalization and mortality in PD patients. The CNSS grade differentiates patients with malnutritional risk and independently predicts high risk of morbidity and mortality

Fabrications of High-Capacity Alpha-Ni(OH)2

Three different methods were used to produce α-Ni(OH)2 with higher discharge capacities than the conventional β-Ni(OH)2, specifically a batch process of co-precipitation, a continuous process of co-precipitation with a phase transformation step (initial cycling), and an overcharge at low temperature. All three methods can produce α-Ni(OH)2 or α/β mixed-Ni(OH)2 with capacities higher than that of conventional β-Ni(OH)2 and a stable cycle performance. The second method produces a special core–shell β-Ni(OH)2/α-Ni(OH)2 structure with an excellent cycle stability in the flooded half-cell configuration, is innovative and also already mass-production ready. The core–shell structure has been investigated by both scanning and transmission electron microscopies. The shell portion of the particle is composed of α-Ni(OH)2 nano-crystals embedded in a β-Ni(OH)2 matrix, which helps to reduce the stress originating from the lattice expansion in the β-α transformation. A review on the research regarding α-Ni(OH)2 is also included in the paper

Association of very Low-density Lipoprotein Cholesterol with All-cause and Cardiovascular Mortality in Peritoneal Dialysis

Background/Aims: Cardiovascular disease (CVD) is the leading cause of death in dialysis patients. Little is known about the relationship between very low-density lipoprotein cholesterol (VLDL-C) and cardiovascular mortality in these patients. Methods: A total of 1324 incident patients who began continuous ambulatory peritoneal dialysis (CAPD) therapy at our hospital between January 1, 2005, and September 30, 2014, with baseline serum VLDL-C values were investigated. The associations of the VLDL-C levels with all-cause and cardiovascular mortality were assessed. Results: The mean age of the cohort was 50.2 ± 14.8 years, and the mean VLDL-C level was 33.6 ± 18.0 mg/dl. One hundred sixty-five (12.5%) patients died during the study period. Multivariable models revealed that the high VLDL-C group was associated with significantly higher all-cause (HR, 2.08, 95% CI, 1.13 to 3.29, P = 0.002) and cardiovascular mortality (HR, 1.92, 95% CI, 1.18 to 4.29, P = 0.013) compared with the low VLDL-C group even after adjusting for various covariates. Using the VLDL-C level as a continuous variable, the hazard ratios (HRs) of all-cause and cardiovascular mortality associated with a 10-mg/dl increase in VLDL-C level were 1.12 (95% CI, 1.02 to 1.26, P = 0.025) and 1.11 (95% CI, 1.02 to 1.22, P = 0.029), respectively. VLDL-C was associated more strongly to all-cause (e.g., Akaike information criteria of 1990.205 vs. 1994.451) and cardiovascular (e.g., Akaike information criteria of 984.146 vs. 985.634) mortality than triglyceride (TG) levels. Conclusions: An elevated VLDL-C level is an independent risk factor for all-cause and cardiovascular mortality in peritoneal dialysis (PD) patients

The adiponectin‐derived peptide ALY688 protects against the development of metabolic dysfunction‐associated steatohepatitis

Abstract Metabolic dysfunction‐associated steatohepatitis (MASH) is the severe form of non‐alcoholic fatty liver disease which has a high potential to progress to cirrhosis and hepatocellular carcinoma, yet adequate effective therapies are lacking. Hypoadiponectinemia is causally involved in the pathogenesis of MASH. This study investigated the pharmacological effects of adiponectin replacement therapy with the adiponectin‐derived peptide ALY688 (ALY688‐SR) in a mouse model of MASH. Human induced pluripotent stem (iPS) cell‐derived hepatocytes were used to test cytotoxicity and signaling of unmodified ALY688 in vitro. High‐fat diet with low methionine and no added choline (CDAHF) was used to induce MASH and test the effects of ALY688‐SR in vivo. Histological MASH activity score (NAS) and fibrosis score were determined to assess the effect of ALY688‐SR. Transcriptional characterization of mice through RNA sequencing was performed to indicate potential molecular mechanisms involved. In cultured hepatocytes, ALY688 efficiently induced adiponectin‐like signaling, including the AMP‐activated protein kinase and p38 mitogen‐activated protein kinase pathways, and did not elicit cytotoxicity. Administration of ALY688‐SR in mice did not influence body weight but significantly ameliorated CDAHF‐induced hepatic steatosis, inflammation, and fibrosis, therefore effectively preventing the development and progression of MASH. Mechanistically, ALY688‐SR treatment markedly induced hepatic expression of genes involved in fatty acid oxidation, whereas it significantly suppressed the expression of pro‐inflammatory and pro‐fibrotic genes as demonstrated by transcriptomic analysis. ALY688‐SR may represent an effective approach in MASH treatment. Its mode of action involves inhibition of hepatic steatosis, inflammation, and fibrosis, possibly via canonical adiponectin‐mediated signaling