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Methods for the Analysis of Gastrointestinal Function
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
Urinalyses may also be performed to detect an excessive growth of bacteria in the small intestines [51]. Analysis for the presence of indican (indoxyl sulfate) may be conducted. Indoles are produced by bacteria, particularly Escherichia coli and Bacterroides.
Kidney Function and Uremia
Published in Sirshendu De, Anirban Roy, Hemodialysis Membranes, 2017
This belongs to the group known as indoles. Indoxyl sulfate, tryptophan, melatonin, and indole-3-acetic acid are all indoles. Indoxyl sulfate enhances drug toxicity, inhibiting active tubular secretion and deiodination.8,9 It is also suspected to be one of the agents behind glomerular sclerosis,10 affecting the function of cellular organic acid. Due to protein binding, the percentage clearance of indoxyl sulfate is greatly reduced and can be as low as 0%–20%.
Analytical Chemistry of Rubins
Published in Karel P. M. Heirwegh, Stanley B. Brown, Bilirubin, 1982
Karel P. M. Heirwegh, Stanley B. Brown
The selectivity of the diazo reaction when applied to biological samples is of major concern. Although diazo positive compounds other than rubins must be present it seems to be tacitly assumed, in general, that for serum and bile their contribution to azo color formation is negligible. Endogenous substances such as indoxyl sulfate (present in uremic serum) and a variety of drugs are diazo positive,87–90 their response de pending on the nature of the reaction accelerator and reactivity of the diazonium salt.88,90
Does the gut microbiome mediate antipsychotic-induced metabolic side effects in schizophrenia?
Published in Expert Opinion on Drug Safety, 2022
Svetlina S. Vasileva, Jack Tucker, Dan Siskind, Darryl Eyles
The other two aforementioned microbial metabolites, indoxyl sulfate and pCS, are both associated with heart failure and cardiac disease in hemodialysis patients. Indoxyl sulfate is a microbial metabolite of tryptophan, and pCS is a microbial metabolite of tyrosine [79]. Indoxyl sulfate induces vascular endothelial damage through induction of apoptosis, as demonstrated on human umbilical vein endothelial cells [105–107], and also contributes to formation of a pro-thrombotic state through enhanced platelet activation [108]. PCS directly contributes to cardiotoxicity of myocytes in patients with renal failure through induction of NADPH oxidase activity and production of superoxides [109,110]. As a result, pCS has been shown to predict cardiovascular events and all-cause mortality in elderly hemodialysis patients [111,112].
Effects of antibiotics on the pharmacokinetics of indoxyl sulfate, a nephro-cardiovascular toxin
Published in Xenobiotica, 2020
Shu-Shang Luo, Chung-Ping Yu, Yow-Wen Hsieh, Pei-Dawn Lee Chao, Douglas H. Sweet, Yu-Chi Hou, Shiuan-Pey Lin
Chronic kidney disease (CKD) is a global health problem. In CKD patients, numerous uremic toxins accumulate in the body (Vanholder et al., 2018). Among the known uremic toxins, indoxyl sulfate (IS) is a small water soluble molecule but with high protein binding (Vanholder et al., 2018), therefore, IS is poorly removed through hemodialysis and accumulates in CKD patients even undergoing hemodialysis treatment (Meijers et al., 2009; Niwa, 1996; Vanholder et al., 2018). Recent studies have reported that IS level is associated with the progression of CKD and high cardiovascular mortality (Ito & Yoshida, 2014; Lin et al., 2012), indicating IS is a nephro-cardiovascular toxin. Due to its strong acidity, IS presents as anions in the systemic circulation, and its renal excretion is via the mediation of organic anion transporter 1 (OAT1) and OAT3 (Deguchi et al., 2004; Wu et al., 2017).
Indoxyl sulfate and high-density lipoprotein cholesterol in early stages of chronic kidney disease
Published in Renal Failure, 2020
Li Wang, Fangfang Xiang, Jun Ji, Xiaoqiang Ding, Bo Shen, Jing Chen, Yunqin Chen, Ning Xue, Lin Zhang, Xiaotian Jiang, Xuesen Cao
Chronic kidney disease (CKD) is associated with higher mortality of cardiovascular disease (CVD) [1]. Indoxyl sulfate (IS), a protein-bound uremic toxin, is one of the organic anions that results from the metabolism of dietary tryptophan and after intestinal absorption is further converted to IS in the liver [2]. Microbiome and intestinal permeability changes induced by hypervolemia may lead to increased IS, inflammation and endothelial dysfunction [3,4]. IS is excreted via proximal tubular secretion in the kidney and it accumulates in the blood of patients with declined renal function. As one of the most extensively studied uremic toxins, IS may predict CKD progression [5]. Cao et al. [6] from our group reported that high serum IS level was associated with higher risk of first heart failure event in patients under hemodialysis. Previous studies [7,8] performed by Xiang and Chen at al. from our group have revealed the regulatory mechanism of IS on vascular calcification and lymphocyte functional disorders, which are both risk factors of CVD.