scholarly journals Indoxyl sulfate (IS)-mediated immune dysfunction provokes endothelial damage in patients with end-stage renal disease (ESRD)

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Hee Young Kim ◽  
Tae-Hyun Yoo ◽  
Yuri Hwang ◽  
Ga Hye Lee ◽  
Bonah Kim ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Immune Dysfunction ◽  
Endothelial Damage ◽  
Indoxyl Sulfate ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Indoxyl Sulfate-Mediated Metabolic Alteration of Transcriptome Signatures in Monocytes of Patients with End-Stage Renal Disease (ESRD)

Toxins ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 621
Author(s):  
Hee Young Kim ◽  
Su Jeong Lee ◽  
Yuri Hwang ◽  
Ga Hye Lee ◽  
Chae Eun Yoon ◽  
...  
Keyword(s):  
Renal Disease ◽  
Immune Cells ◽  
End Stage Renal Disease ◽  
Metabolic Pathways ◽  
Esrd Patient ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

End-stage renal disease (ESRD) is the final stage of chronic kidney disease, which is increasingly prevalent worldwide and is associated with the progression of cardiovascular disease (CVD). Indoxyl sulfate (IS), a major uremic toxin, plays a key role in the pathology of CVD via adverse effects in endothelial and immune cells. Thus, there is a need for a transcriptomic overview of IS responsive genes in immune cells of ESRD patients. Here, we investigated IS-mediated alterations in gene expression in monocytes from ESRD patients. Transcriptomic analysis of ESRD patient-derived monocytes and IS-stimulated monocytes from healthy controls was performed, followed by analysis of differentially expressed genes (DEGs) and gene ontology (GO). We found that 148 upregulated and 139 downregulated genes were shared between ESRD patient-derived and IS-stimulated monocytes. Interaction network analysis using STRING and ClueGo suggests that mainly metabolic pathways, such as the pentose phosphate pathway, are modified by IS in ESRD patient-derived monocytes. These findings were confirmed in IS-stimulated monocytes by the increased mRNA expression of genes including G6PD, PGD, and TALDO1. Our data suggest that IS causes alteration of metabolic pathways in monocytes of ESRD patients and, thus, these altered genes may be therapeutic targets.

Upregulation of Inflammatory Mediators In End-Stage Renal Disease as Measured Via Biochip Array Technology

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 5186-5186
Author(s):  
Vinod Bansal ◽  
Rachael Davis ◽  
Evangelos Litinas ◽  
Debra Hoppensteadt ◽  
Indermohan Thethi ◽  
...  
Keyword(s):  
Renal Disease ◽  
Inflammatory Mediators ◽  
End Stage Renal Disease ◽  
Conflicts Of Interest ◽  
Fold Increase ◽  
Endothelial Damage ◽  
Cellular Damage ◽  
Array Technology ◽  
Stage Renal Disease ◽  
End Stage

Abstract Abstract 5186 End-Stage Renal Disease (ESRD) is a complex syndrome in which systemic vascular pathophysiologic changes contribute to adverse cardiovascular and cerebrovascular manifestations. Cardiovascular disease alone is present in over 60% of patients with ESRD and contributes heavily to mortality among this population. Given that inflammatory and hemostatic aberrations contribute to the overall pathogenesis of the syndrome, the purpose of this study is to profile several inflammatory mediators in order to better understand their role in the underlying mechanism of vascular changes in ESRD. Plasma samples from 49 patients with ESRD were collected prior to maintenance hemodialysis sessions. A group of 56 normal individuals, both male and female, was included as control. Cerebral Array II chips were used in the Randox® system to simultaneously measure Neuron Specific Enolase (NSE), Neutrophil Gelatinase-associated Lipocalin (NGAL), Soluble Tumor Necrosis Factor Receptor I (TNFRI), D-Dimer (DD), Thrombomodulin (TM), and C-reactive protein (CRP). The Randox® Evidence Investigator™ is a new biochip array technology that utilizes multiple discrete test regions of immobilized antibody to simultaneously quantify multiple markers from a single patient plasma sample based on the light signal generated from each test region. The data was statistically analyzed using the Mann-Whitney U test (two-tailed with Gaussian approximation). As compared to the normal individual, all of the markers studied showed an upregulation in patients with ESRD. Most notably, TNFRI showed a 19.8 fold increase in patients with ESRD (mean 7.8 ± 2.8 ng/ml, range 0.8 to 13.7) compared to the control (mean 0.4 ± 0.2, range 0.1 to 1.0). TM was increased 5.2 fold (mean 6.5 ± 2.6, range 0.7 to 14.1) compared to control (mean 1.2 ± 0.4, range 0.6 to 2.3). Also, NGAL showed a 4.6 fold increase (mean 1390 ± 257, range 406 to 1729), compared to control (mean 299 ± 99, range 115 to 603), and CRP a 4.2 fold increase (mean 5.7 ± 4.2 ug/ml, range 0.6 to 13.2) compared to control (mean 1.4 ± 1.7, range 0.2 to 11.4). DD and NSE were also increased 3.0 and 1.8 fold respectively. These studies show that some newer markers such as TNFRI, NGAL and NSE are upregulated in ESRD. The marked increase in TM is highly suggestive of endothelial damage. Similarly, the increase in TNFRI supports a state of increased cellular damage. The elevations in NGAL and CRP imply a state of increased inflammation and indicate a polypathologic process, which may predispose ESRD patients to both cardiovascular and cerebrovascular thromboembolic events. Finally, this study further validates the role of endothelial damage and endogenous thrombotic processes in ESRD as evidenced by the increased levels of TM and DD. However, the clinical significance of these markers still needs to be further explored. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Microbiome perturbation by oral vancomycin reduces plasma concentration of two gut-derived uremic solutes, indoxyl sulfate and p-cresyl sulfate, in end-stage renal disease

2017 ◽  
Vol 32 (11) ◽  
pp. 1809-1817 ◽  
Author(s):  
Lama Nazzal ◽  
Julia Roberts ◽  
Prabhjot Singh ◽  
Sachin Jhawar ◽  
Albert Matalon ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Indoxyl Sulfate ◽  
Oral Vancomycin ◽  
Uremic Solutes ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Functional Genomic Analysis Identifies Indoxyl Sulfate as a Major, Poorly Dialyzable Uremic Toxin in End-Stage Renal Disease

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0118703 ◽  
Author(s):  
Sachin Jhawar ◽  
Prabhjot Singh ◽  
Daniel Torres ◽  
Francisco Ramirez-Valle ◽  
Hania Kassem ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Genomic Analysis ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Functional Genomic ◽  
Functional Genomic Analysis ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Effects of Nutritional Supplementation on Fatigue, and Autonomic and Immune Dysfunction in Patients with End-Stage Renal Disease: A Randomized, Double-Blind, Placebo-Controlled, Multicenter Trial

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0119578 ◽  
Author(s):  
Sanae Fukuda ◽  
Hidenori Koyama ◽  
Kazuhiro Kondo ◽  
Hisako Fujii ◽  
Yoshinobu Hirayama ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Immune Dysfunction ◽  
Multicenter Trial ◽  
Nutritional Supplementation ◽  
Double Blind ◽  
Double Blind Placebo ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Generation, clearance, toxicity, and monitoring possibilities of unaccounted uremic toxins for improved dialysis prescriptions

2018 ◽  
Vol 315 (4) ◽  
pp. F890-F902 ◽  
Author(s):  
James G. Atherton ◽  
David S. Hains ◽  
John Bissler ◽  
Bradford D. Pendley ◽  
Ernő Lindner
Keyword(s):  
Renal Function ◽  
Renal Disease ◽  
Normal Renal Function ◽  
End Stage Renal Disease ◽  
Blood Purification ◽  
Uremic Toxins ◽  
Indoxyl Sulfate ◽  
Stage Renal Disease ◽  
End Stage ◽  
Cellular Secretion

Current dialysis-dosing calculations provide an incomplete assessment of blood purification. They exclude clearances of protein-bound uremic toxins (PB-UTs), such as polyamines, p-cresol sulfate, and indoxyl sulfate, relying solely on the clearance of urea as a surrogate for all molecules accumulating in patients with end-stage renal disease (ESRD). PB-UTs clear differently in dialysis but also during normal renal function. The kidney clears PB toxins via the process of secretion, whereas it clears urea through filtration. Herein, we review the clearance, accumulation, and toxicity of various UTs. We also suggest possible methods for their monitoring toward the ultimate goal of a more comprehensive dialysis prescription. A more inclusive dialysis prescription would retain the kidney-filtration surrogate, urea, and consider at least one PB toxin as a surrogate for UTs cleared through cellular secretion. A more comprehensive assessment of UTs that includes both secretion and filtration is expected to result in a better understanding of ESRD toxicity and consequently, to reduce ESRD mortality.

scholarly journals Serum albumin and indoxyl sulfate were predictive of cognitive impairment via amyloid beta and tauopathy, respectively, in end‐stage renal disease patients

2021 ◽  
Vol 17 (S5) ◽  
Author(s):  
Yi‐Chou Hou ◽  
Kuo‐Cheng Lu ◽  
Chuen‐Lin Huang ◽  
Yuh‐Feng Lin ◽  
Ruei‐Ming Chen
Keyword(s):  
Cognitive Impairment ◽  
Renal Disease ◽  
Serum Albumin ◽  
Amyloid Beta ◽  
End Stage Renal Disease ◽  
Indoxyl Sulfate ◽  
Stage Renal Disease ◽  
End Stage

The Accumulation of Gut Microbiome–derived Indoxyl Sulfate and P-Cresyl Sulfate in Patients With End-stage Renal Disease

2021 ◽  
Author(s):  
Xuechun Lin ◽  
Wangqun Liang ◽  
Li Li ◽  
Qianqian Xiong ◽  
Shuiqing He ◽  
...  
Keyword(s):  
Renal Disease ◽  
Gut Microbiome ◽  
End Stage Renal Disease ◽  
Indoxyl Sulfate ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Aspects of Immune Dysfunction in End-stage Renal Disease

2008 ◽  
Vol 3 (5) ◽  
pp. 1526-1533 ◽  
Author(s):  
Sawako Kato ◽  
Michal Chmielewski ◽  
Hirokazu Honda ◽  
Roberto Pecoits-Filho ◽  
Seiichi Matsuo ◽  
...  
Keyword(s):  
Renal Disease ◽  
End Stage Renal Disease ◽  
Immune Dysfunction ◽  
Stage Renal Disease ◽  
End Stage
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