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2022 ◽  
Vol 21 ◽  
pp. 100712
N. Hala ◽  
M. Ariba ◽  
S. Sarush Ahmed ◽  
S. Fahad Hassan

Saviola Alessia ◽  
Schipilliti Francesca Matilde ◽  
Isca Chrystel ◽  
Salati Massimiliano ◽  
Dini Daniele ◽  

2022 ◽  
Vol 8 ◽  
Momoko Matsuyama ◽  
Keiji Hirai ◽  
Hiroaki Nonaka ◽  
Moeka Ueda ◽  
Junki Morino ◽  

Objective:The aim of this study was to investigate the effects of elobixibat on constipation and lipid metabolism; and determine the factors associated with the effect of elobixibat on constipation in patients with moderate to end-stage chronic kidney disease (CKD).Methods:Stool frequency and serum lipid parameters were retrospectively analyzed before and after 4 weeks of elobixibat administration in 42 patients (CKD stage G3, 6; stage G4, 9; stage G5, 9; stage G5D, 18). Relationships between the change in stool frequency after initiation of elobixibat and various clinical parameters were analyzed by using linear regression analysis.Results:Elobixibat increased stool frequency from 0.5 ± 0.4 per day to 1.1 ± 0.6 per day (p < 0.001) regardless of whether patients were undergoing dialysis, on concomitant laxatives, or were administered elobixibat before or after breakfast. Elobixibat reduced low-density lipoprotein cholesterol concentration (from 90.9 ± 37.2 mg/dL to 77.5 ± 34.8 mg/dL, p < 0.05) and increased high-density lipoprotein cholesterol concentration (from 44.9 ± 14.3 mg/dL to 57.0 ± 25.8 mg/dL, p < 0.05), but did not change triglyceride concentration. Adverse effects were observed in two patients (nausea and diarrhea). Only phosphate concentration was correlated with the change in stool frequency after initiation of elobixibat (standard coefficient = 0.321, p = 0.043).Conclusions:Elobixibat improved constipation and lipid metabolism in patients with moderate to end-stage CKD, without serious adverse events.

2022 ◽  
Vol 12 ◽  
Chunhong Wang ◽  
Jiafeng Liu ◽  
Xiaoyao Zhang ◽  
Qiyan Chen ◽  
Xiaoyan Bai ◽  

Podocyte injury and proteinuria are the most common features of glomerular disease, which is the leading cause of end-stage renal failure. Hyperactivated Wnt/β-catenin signaling is closely associated with podocyte injury, but the underlying mechanisms are incompletely understood. Here we show that miRNA-671-5p (miR-671-5p) plays a crucial role in mediating β-catenin-triggered podocyte injury by targeting Wilms tumor 1 (WT1). Microarray-based expression profiling revealed that miR-671-5p was the most upregulated miRNA in podocytes after β-catenin activation. MiR-671-5p was colocalized with β-catenin in the glomeruli of proteinuric CKD in vivo. Bioinformatics analyses and luciferase reporter assays confirmed that miR-671-5p targeted WT1 mRNA. Overexpression of miR-671-5p mimics inhibited WT1 and impaired podocyte integrity, whereas miR-671-5p antagomir preserved the expression of WT1 and other podocyte-specific proteins under basal conditions or after β-catenin activation. In mouse remnant kidney model, overexpression of miR-671-5p aggravated podocyte injury, worsened kidney dysfunction and exacerbated renal fibrosis after 5/6 nephrectomy. In contrast, miR-671-5p antagomir alleviated podocyte injury and attenuated proteinuria and renal fibrotic lesions after glomerular injury in vivo. These studies underscore a pivotal role of miR-671-5p in mediating WT1 depletion and podocyte injury induced by β-catenin. Targeting miR-671-5p may serve as a new approach to prevent podocyte injury and proteinuria in proteinuric CKD.

2022 ◽  
pp. 112972982110676
Catherine Fielding ◽  
Louise Bramley ◽  
Carol Stalker ◽  
Sarah Brand ◽  
Suzanne Toft ◽  

Introduction: Cannulation is an essential part of haemodialysis with arteriovenous access. Patients’ experiences of cannulation for haemodialysis are problematic but poorly understood. This review aims to synthesise findings related to patients’ experiences of cannulation for haemodialysis from qualitative studies, providing a fuller description of this phenomenon. Methods: Eligibility criteria defined the inclusion of studies with a population of patients with end-stage kidney disease on haemodialysis. The phenomena of interest was findings related to patients’ experiences of cannulation for haemodialysis and the context was both in-centre and home haemodialysis. MedLine, CINAHL, EMBASE, EMCARE, BNI, PsycInfo and PubMed were last searched between 20/05/2019 and 23/05/2019. The quality of studies was assessed using the using Joanna Briggs Critical Appraisal Checklist for Qualitative Research. Meta-aggregation was used to synthesise findings and CERQual to assess the strength of accumulated findings. Results: This review included 26 studies. The subject of included studies covered cannulation, pain, experiences of vascular access, experiences of haemodialysis and a research priority setting exercise. From these studies, three themes were meta-aggregated: (1) Cannulation for haemodialysis is an unpleasant, abnormal and unique procedure associated with pain, abnormal appearance, vulnerability and dependency. (2) The necessity of cannulation for haemodialysis emphasises the unpleasantness of the procedure. Success had multiple meanings for patients and patients worry about whether the needle insertion will be successful. (3) Patients survive unpleasant, necessary and repetitive cannulation by learning to tolerate cannulation and exerting control over the procedure. Feeling safe can help them tolerate cannulation better and the cannulator can invoke feeling safe. However, some patients still avoid cannulation, due to its unpleasantness. Conclusions: Cannulation is a pervasive procedure that impacts on patients’ experiences of haemodialysis. This review illuminates further patients’ experiences of cannulation for haemodialysis, indicating how improvements can be made to cannulation. Registration: PROSPERO (CRD42019134583).

2022 ◽  
Ying Yang ◽  
Chang Zeng ◽  
Kun Yang ◽  
Zhou Zhang ◽  
Qinyun Cai ◽  

Long-term complications of type 2 diabetes (T2D) are the major causes for T2D-related disability and mortality. Notably, diabetic nephropathy (DN) has become the most frequent cause of end-stage renal disease (ESRD) in most countries. Understanding epigenetic contributors to DN can provide novel insights into this complex disorder and lay the foundation for more effective monitoring tools and preventive interventions, critical for achieving the ultimate goal of improving patient care and reducing healthcare burden. We have used a selective chemical labeling technique (5hmC-Seal) to profile genome-wide distributions of 5-hydroxymethylcytosines (5hmC), a gene activation mark, in patient-derived circulating cell-free DNA (cfDNA). Differentially modified 5hmC genes were identified across T2D patients with DN (n = 12), T2D patients with non-DN vascular complications (non-DN) (n = 29), and T2D patients with no complications (controls) (n = 14). Specifically, differential 5hmC markers between DN and controls revealed relevant pathways such as NOD-like receptor signaling pathway and tyrosine metabolism. A ten-gene panel was shown to provide differential 5hmC patterns between controls and DN, as well as between controls and non-DN patients using a machine learning approach. The 5hmC profiles in cfDNA reflected novel DN-associated epigenetic modifications relevant to the disease pathogenesis of DN. Importantly, these findings in cfDNA, a convenient liquid biopsy, have the potential to be exploited as a clinically useful tool for predicting DN in high risk T2D patients. Keywords: diabetes, nephropathy, epigenetics, 5-hydroxymethylcytosine, cfDNA

2022 ◽  
Vol 8 (4) ◽  
pp. 285-288
S L V Sankeerthi C H ◽  
Sai Ravi Kiran Biri ◽  
Sandhya Rani T ◽  
Rajkumar Gundu ◽  
Aravind Vadlakonda

Diabetes is one of the leading causes for end stage renal disease and nephropathy. Increases of blood urea and serum creatinine are due to abnormal renal function and also reduction in glomerular filtration rate. So, Urea and Creatinine are the ideal biomarkers to correlate the progression of diabetic nephropathy. Aim of the study is to evaluate the blood urea & serum creatinine with HbA1C in Diabetes mellitus patients.: A total of 50 cases and 30 controls were selected in our study. Blood samples were collected for blood urea, serum creatinine, HbA1C, Fasting plasma glucose and Post prandial blood sugar with age limit of 35-65 years. Mean ±SD was calculated for all these parameters. Blood urea and Serum creatinine are statistically significant in Diabetic patients when compared to the controls.Our study shows that blood urea and serum creatinine can be used as biomarkers in the early detection of diabetic nephropathy. These parameters help in reducing the severity of renal failure.

2022 ◽  
Vol 8 ◽  
Xueqin Wu ◽  
Yong Zhong ◽  
Ting Meng ◽  
Joshua Daniel Ooi ◽  
Peter J. Eggenhuizen ◽  

BackgroundA significant proportion of anti-neutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis eventually progresses to end-stage renal disease (ESRD) thus requiring long-term dialysis. There is no consensus about which dialysis modality is more recommended for those patients with associated vasculitis (AAV-ESRD). The primary objective of this study was to compare patient survival in patients with AAV-ESRD treated with hemodialysis (HD) or peritoneal dialysis (PD).MethodsThis double-center retrospective cohort study included dialysis-dependent patients who were treated with HD or PD. Clinical data were collected under standard format. The Birmingham vasculitis activity score (BVAS) was used to evaluate disease activity at diagnosis and organ damage was assessed using the vasculitis damage index (VDI) at dialysis initiation.ResultsIn total, 85 patients were included: 64 with hemodialysis and 21 with peritoneal dialysis. The patients with AAV-PD were much younger than the AAV-HD patients (48 vs. 62, P < 0.01) and more were female (76.2 vs. 51.6%, P = 0.05). The laboratory data were almost similar. The comorbidities, VDI score, and immuno-suppressive therapy at dialysis initiation were almost no statistical difference. Patient survival rates between HD and PD at 1 year were 65.3 vs. 90% (P = 0.062), 3 year were 59.6 vs. 90% (P < 0.001), and 5 years were 59.6 vs. 67.5% (P = 0.569). The overall survival was no significant difference between the two groups (P = 0.086) and the dialysis modality (HD or PD) was not shown to be an independent predictor for all-cause death (hazard ratio (HR) 0.73; 95% confidence interval (CI) 0.31–1.7; P = 0.473). Cardio-cerebrovascular events were the main cause of death among AAV-HD patients while infection in patients with AAV-PD.ConclusionThese results provide real-world data that the use of either hemodialysis or peritoneal dialysis modality does not affect patient survival for patients with AAV-ESRD who need long-term dialysis.

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261789
Xiaoying Liu ◽  
Sarah A. Taylor ◽  
Kyle D. Gromer ◽  
Danny Zhang ◽  
Susan C. Hubchak ◽  

Nonalcoholic fatty liver disease (NAFLD) is one of the most common causes of liver diseases in the United States and can progress to cirrhosis, end-stage liver disease and need for liver transplantation. There are limited therapies for NAFLD, in part, due to incomplete understanding of the disease pathogenesis, which involves different cell populations in the liver. Endoplasmic reticulum stress and its adaptative unfolded protein response (UPR) signaling pathway have been implicated in the progression from simple hepatic steatosis to nonalcoholic steatohepatitis (NASH). We have previously shown that mice lacking the UPR protein X-box binding protein 1 (XBP1) in the liver demonstrated enhanced liver injury and fibrosis in a high fat sugar (HFS) dietary model of NAFLD. In this study, to better understand the role of liver XBP1 in the pathobiology of NAFLD, we fed hepatocyte XBP1 deficient mice a HFS diet or chow and investigated UPR and other cell signaling pathways in hepatocytes, hepatic stellate cells and immune cells. We demonstrate that loss of XBP1 in hepatocytes increased inflammatory pathway expression and altered expression of the UPR signaling in hepatocytes and was associated with enhanced hepatic stellate cell activation after HFS feeding. We believe that a better understanding of liver cell-specific signaling in the pathogenesis of NASH may allow us to identify new therapeutic targets.

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