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Journal articles on the topic 'Indoxyl sulphate'

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Published: 9 March 2023

Last updated: 10 March 2023

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1

Chou, Chia-An, Hwee-Yeong Ng, Wei-Hung Kuo, Ting-Yu Terry Chiou, Sung-Nan Pei, Lung-Chih Li, Yueh-Ting Lee, and Chien-Te Lee. "Rosiglitazone attenuates indoxyl sulphate-induced endothelial dysfunction." Clinical and Experimental Pharmacology and Physiology 42, no. 3 (February 11, 2015): 287–92. http://dx.doi.org/10.1111/1440-1681.12351.

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2

Mozar, A., L. Louvet, C. Godin, R. Mentaverri, M. Brazier, S. Kamel, and Z. A. Massy. "Indoxyl sulphate inhibits osteoclast differentiation and function." Nephrology Dialysis Transplantation 27, no. 6 (December 1, 2011): 2176–81. http://dx.doi.org/10.1093/ndt/gfr647.

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3

Valko-Rokytovská, Marcela, Beáta Hubková, Anna Birková, Jana Mašlanková, Marek Stupák, Marianna Zábavníková, Beáta Čižmárová, and Mária Mareková. "Specific Urinary Metabolites in Malignant Melanoma." Medicina 55, no. 5 (May 16, 2019): 145. http://dx.doi.org/10.3390/medicina55050145.

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Background and objectives: Melanin, which has a confirmed role in melanoma cell behaviour, is formed in the process of melanogenesis and is synthesized from tryptophan, L-tyrosine and their metabolites. All these metabolites are easily detectable by chromatography in urine. Materials and Methods: Urine samples of 133 individuals (82 malignant melanoma patients and 51 healthy controls) were analysed by reversed-phase high-performance liquid chromatography (RP-HPLC). The diagnosis of malignant melanoma was confirmed histologically. Results: Chromatograms of melanoma patients showed increased levels of 5,6-dihydroxyindole-2-carboxylic acid, vanilmandelic acid, homovanilic acid, tryptophan, 5-hydroxyindole-3-acetic acid, and indoxyl sulphate compared to healthy controls. Concentration of indoxyl sulphate, homovanilic acid and tryptophan were significantly increased even in the low clinical stage 0 of the disease (indoxyl sulphate, homovanilic acid and tryptophan in patients with clinical stage 0 vs. controls expressed as medium/ interquartile range in µmol/mmol creatinine: 28.37/15.30 vs. 5.00/6.91; 47.97/33.08 vs. 7.33/21.25; and 16.38/15.98 vs. 3.46/6.22, respectively). Conclusions: HPLC detection of metabolites of L-tyrosine and tryptophan in the urine of melanoma patients may play a significant role in diagnostics as well as a therapeutic strategy of melanoma cancer.

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4

Wu, I. W., K. H. Hsu, C. C. Lee, C. Y. Sun, H. J. Hsu, C. J. Tsai, C. Y. Tzen, Y. C. Wang, C. Y. Lin, and M. S. Wu. "p-Cresyl sulphate and indoxyl sulphate predict progression of chronic kidney disease." Nephrology Dialysis Transplantation 26, no. 3 (September 29, 2010): 938–47. http://dx.doi.org/10.1093/ndt/gfq580.

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5

Yang, Ke, Cheng Wang, Ling Nie, Xiaohui Zhao, Jun Gu, Xu Guan, Song Wang, et al. "Klotho Protects Against Indoxyl Sulphate-Induced Myocardial Hypertrophy." Journal of the American Society of Nephrology 26, no. 10 (March 24, 2015): 2434–46. http://dx.doi.org/10.1681/asn.2014060543.

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6

Yousef Selim, Nermien, Hazem Farag Mannaa, Ola Atef Sharaki, Tayseer Zaytoun, Noha Elkholy, and Waleed Arafat. "Highlighting Levels of Indoxyl Sulphate among Critically Ill Patients with Acute Nephrotoxicity; Correlations Between Indoxyl Sulphate Levels and Patients’ Characteristics." Reports of Biochemistry and Molecular Biology 10, no. 2 (August 1, 2021): 266–79. http://dx.doi.org/10.52547/rbmb.10.2.266.

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7

Ellis, Robert J., David M. Small, David A. Vesey, David W. Johnson, Ross Francis, Luis Vitetta, Glenda C. Gobe, and Christudas Morais. "Indoxyl sulphate and kidney disease: Causes, consequences and interventions." Nephrology 21, no. 3 (January 28, 2016): 170–77. http://dx.doi.org/10.1111/nep.12580.

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8

Kamiński, Tomasz, Małgorzata Michałowska, and Dariusz Pawlak. "Aryl hydrocarbon receptor (AhR) and its endogenous agonist – indoxyl sulfate in chronic kidney disease." Postępy Higieny i Medycyny Doświadczalnej 71, no. 1 (July 30, 2017): 0. http://dx.doi.org/10.5604/01.3001.0010.3843.

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The indoxyl sulfate (IS, indoxyl sulphate) is the end product of dietary tryptophan degradation by indole pathway and significantly higher serum and tissue concentrations of this compound is observed in patients with impaired renal function. Despite the high albumin binding affinity, the remaining free fraction of IS has a number of biological effects related to the generation of oxidative stress andactivation of signaling pathways related to NF-кB, p53 protein, STAT3, TGF-β and Smad2/3. IS induces the inflammatory process, exerts nephrotoxic activity and is also a factor impairing the cardiovascular system.Its high concentrations are associated with the occurrence of cardiovascular incidents, whose frequency is significantly higher in patients with chronic kidney disease. Evaluation of the mechanisms that underlie the high reactivity of indoxyl sulfate and its biological effects showed that this compound is an agonist of the aryl hydrocarbon receptor (AhR). This receptor plays an important role in maintaining homeostasis Moreover, AhR exerts high transcriptional activity, so ligands of obciążethis receptor may exert different biological effects. The following paper describes the role of indoxyl sulfate as AhR ligand in the context of the excessive accumulation, which appears as one of the symptoms associated with chronic kidney disease.

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9

Adesso, Simona, Ada Popolo, Giuseppe Bianco, Rosalinda Sorrentino, Aldo Pinto, Giuseppina Autore, and Stefania Marzocco. "The Uremic Toxin Indoxyl Sulphate Enhances Macrophage Response to LPS." PLoS ONE 8, no. 9 (September 30, 2013): e76778. http://dx.doi.org/10.1371/journal.pone.0076778.

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10

Deguchi, Tsuneo, Mikio Nakamura, Yasuhiro Tsutsumi, Ayaka Suenaga, and Masaki Otagiri. "Pharmacokinetics and tissue distribution of uraemic indoxyl sulphate in rats." Biopharmaceutics & Drug Disposition 24, no. 8 (2003): 345–55. http://dx.doi.org/10.1002/bdd.370.

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11

De Mauri, Andreana, Deborah Carrera, Matteo Vidali, Marco Bagnati, Roberta Rolla, Sergio Riso, Doriana Chiarinotti, and Massimo Torreggiani. "Does Mediterranean Adequacy Index Correlate with Cardiovascular Events in Patients with Advanced Chronic Kidney Disease? An Exploratory Study." Nutrients 14, no. 9 (April 19, 2022): 1687. http://dx.doi.org/10.3390/nu14091687.

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The Mediterranean Diet (MD) is a healthy dietary pattern, demonstrated to reduce the risk of cancer, diabetes, cardiovascular and neurodegenerative diseases, and early death. The Mediterranean Adequacy Index (MAI) is used to measure adherence to the MD in perspective studies in the general population and correlates with cardiovascular events. The aim of this study was to calculate the MAI among patients with advanced chronic kidney disease (CKD) and correlate it with traditional uremic, microbiota-derived, and proatherogenic toxins as well as nutritional status, quality of life, and cardiovascular events. A total of 60 adult patients with advanced CKD were enrolled and their MAI was calculated. According to the median value, patients were divided into lower (l-MAI, <1.80) and higher (h-MAI, ≥1.80) MAI groups. Biochemical parameters, microbiota-derived and proatherogenic toxins (p-Cresyl sulphate, Indoxyl-sulphate, and Lipoprotein-associated phospholipase A2), nutritional status, quality of life, and cardiovascular events that occurred in the previous three years were recorded. The mean value of the MAI was 2.78 ± 2.86. The MAI was significantly higher in foreigners (median (IQR) 6.38 (8.98) vs. 1.74 (1.67), p < 0.001) and diabetic patients. The l-MAI and h-MAI groups had similar routinary blood, p-Cresyl-sulphate, Indoxyl-sulphate, and Lp-PLA2 as well as nutritional status and quality of life parameters. The MAI was not associated with previous cardiovascular events and did not correlate with cardiovascular events in CKD patients. New and nephro-tailored indexes are warranted to evaluate nutritional therapy in CKD patients.

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12

Abdullah H Drewil, Mohammed A Al-Bayati, and Arif S Malik. "Evaluation of Indoxyl Sulfate in Chronic Kidney Disease associated with Left Ventricular Hypertrophy." International Journal of Research in Pharmaceutical Sciences 11, SPL4 (December 21, 2020): 3073–79. http://dx.doi.org/10.26452/ijrps.v11ispl4.4608.

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Chronic kidney disease CKD is widely prevalent globally and Left ventricular hypertrophy (LVH) is very common among CKD patients and contributes to CV mortality which can be monitored by measuring the levels of indoxyl sulfate (IS). Study the correlation of indoxyl sulphate and the degree of left Ventricular hypertrophy in CKD patients. A case control study was done on 90 patients with Chronic kidney disease CKD, 45 of them with who were recruited the Imamian Al-Khadhemian Medical City and Baghedad Hospital, Baghdad, Iraq between January, and September 2020. The levels of indoxyl sulfate and other parameters were measured in the serum of Left ventricular hypertrophy (LVH) and compared with those with a no evidence of LVH) who considered as BMI and sex matched control group. Indoxyl sulfate (IS) levels in patients with chronic kidney disease and an evidence of lift ventricular hypertrophy (LVH-CKD) group were significantly (p=0.001) higher than those of patients with chronic kidney disease without an evidence of lift ventricular hypertrophy (NLVH-CKD) and IS levels were associated significantly with the severity of LVH. The possibility to use IS as a marker for early diagnosis of LVH in patients suffered from CKD and it can be used to determine the severity of LVH in those patients.

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13

Veldeman, Laurens, Jill Vanmassenhove, Wim Van Biesen, Ziad A. Massy, Sophie Liabeuf, Griet Glorieux, and Raymond Vanholder. "Evolution of protein-bound uremic toxins indoxyl sulphate and p-cresyl sulphate in acute kidney injury." International Urology and Nephrology 51, no. 2 (January 2, 2019): 293–302. http://dx.doi.org/10.1007/s11255-018-2056-x.

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14

Achtergael, W., D. Michielsen, F. K. Gorus, and E. Gerlo. "INDOXYL SULPHATE AND THE PURPLE URINE BAG SYNDROME: A CASE REPORT." Acta Clinica Belgica 61, no. 1 (February 2006): 38–41. http://dx.doi.org/10.1179/acb.2006.008.

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15

Yang, Chih-Yu, and Der-Cherng Tarng. "Diet, gut microbiome and indoxyl sulphate in chronic kidney disease patients." Nephrology 23 (October 2018): 16–20. http://dx.doi.org/10.1111/nep.13452.

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16

Shimazu, Shuzo, Akihiro Hirashiki, Takashi Yamada, Rie Okamoto, Norihiro Shinoda, Yasuko Bandou, Toshimitsu Niwa, and Toyoaki Murohara. "Indoxyl Sulphate is Associated with Cardiac Dysfunction in Patients with Dilated Cardiomyopathy." Journal of Cardiac Failure 17, no. 9 (September 2011): S148. http://dx.doi.org/10.1016/j.cardfail.2011.06.477.

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17

Hobson, Sam, Samsul Arefin, Awahan Rahman, Leah Hernandez, Thomas Ebert, Henriette de Loor, Pieter Evenepoel, Peter Stenvinkel, and Karolina Kublickiene. "Indoxyl Sulphate Retention Is Associated with Microvascular Endothelial Dysfunction after Kidney Transplantation." International Journal of Molecular Sciences 24, no. 4 (February 11, 2023): 3640. http://dx.doi.org/10.3390/ijms24043640.

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Kidney transplantation (KTx) is the preferred form of renal replacement therapy in chronic kidney disease (CKD) patients, owing to increased quality of life and reduced mortality when compared to chronic dialysis. Risk of cardiovascular disease is reduced after KTx; however, it is still a leading cause of death in this patient population. Thus, we aimed to investigate whether functional properties of the vasculature differed two years post-KTx (postKTx) compared to baseline (time of KTx). Using the EndoPAT device in 27 CKD patients undergoing living-donor KTx, we found that vessel stiffness significantly improved while endothelial function worsened postKTx vs. baseline. Furthermore, baseline serum indoxyl sulphate (IS), but not p-cresyl sulphate, was independently negatively associated with reactive hyperemia index, a marker of endothelial function, and independently positively associated with P-selectin postKTx. Finally, to better understand the functional effects of IS in vessels, we incubated human resistance arteries with IS overnight and performed wire myography experiments ex vivo. IS-incubated arteries showed reduced bradykinin-mediated endothelium-dependent relaxation compared to controls via reduced nitric oxide (NO) contribution. Endothelium-independent relaxation in response to NO donor sodium nitroprusside was similar between IS and control groups. Together, our data suggest that IS promotes worsened endothelial dysfunction postKTx, which may contribute to the sustained CVD risk.

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18

Bergerova, Michaela, Milan Libansky, and Hana Dejmkova. "Determination of Indoxyl Sulphate on Carbon Film Composite Electrode and Carbon Paste Electrode." Current Analytical Chemistry 14, no. 5 (September 3, 2018): 530–35. http://dx.doi.org/10.2174/1573411013666170718095203.

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19

Di Micco, Lucia, Luca Di Lullo, Antonio Bellasi, and Biagio R. Di Iorio. "Very Low Protein Diet for Patients with Chronic Kidney Disease: Recent Insights." Journal of Clinical Medicine 8, no. 5 (May 20, 2019): 718. http://dx.doi.org/10.3390/jcm8050718.

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Use of nutritional therapy (NT) in chronic kidney disease (CKD) patients is still debated among nephrologists, but it represents a fundamental point in the conservative treatment of CKD. It has been used for years and it has new goals today, such as (1) the reduction of edema, diuretics, and blood pressure values with a low sodium-content diet; (2) the dose reduction of phosphate levels and phosphate binders; (3) the administration of bicarbonate with vegetables in order to correct metabolic acidosis and delay CKD progression; (4) the reduction of the number and the doses of drugs and chemical substances; and (5) the lowering of urea levels, the cure of intestinal microbioma, and the reduction of cyanates levels (such as indoxyl-sulphate and p-cresol sulphate), which are the most recent known advantages achievable with NT. In conclusion, NT and especially very low protein diet (VLPD) have several beneficial effects in CKD patients and slows the progression of CKD.

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20

Niwa, T., Y. Emoto, K. Maeda, Y. Uehara, Y. Nobuo, and M. Shibata. "Oral Sorbent Suppresses Accumulation of Albumin-Bound Indoxyl Sulphate in Serum of Haemodialysis Patients." Nephrology Dialysis Transplantation 6, no. 2 (January 1, 1991): 105–9. http://dx.doi.org/10.1093/ndt/6.2.105.

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21

Adijiang, A., S. Goto, S. Uramoto, F. Nishijima, and T. Niwa. "Indoxyl sulphate promotes aortic calcification with expression of osteoblast-specific proteins in hypertensive rats." Nephrology Dialysis Transplantation 23, no. 6 (March 7, 2008): 1892–901. http://dx.doi.org/10.1093/ndt/gfm861.

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22

Renwick, A. G., A. Thakrar, C. A. Lawrie, and C. F. George. "Microbial Amino Acid Metabolites and Bladder Cancer: No Evidence of Promoting Activity in Man." Human Toxicology 7, no. 3 (May 1988): 267–72. http://dx.doi.org/10.1177/096032718800700307.

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1 Indole, p-cresol and phenol are microbial amino acid metabolites which show co-carcinogenic or promoting activity in animal studies. Their involvement in the development of human bladder cancer has been determined by measuring the urinary excretion of indican (indoxyl sulphate) and conjugated phenols. 2 Thirty-two patients (22 males, 10 females) with histologically confirmed carcinoma of the urinary bladder and a similar number of age and sex matched controls took part in the study. The excretion of indican, p-cresol and phenol showed wide interindividual variability, but did not differ significantly between the two groups. 3 The findings indicate that these endogenous metabolites do not contribute significantly to the development of human bladder cancer.

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Bouabdallah, Jeanne, Kazem Zibara, Hawraa Issa, Gaëlle Lenglet, Ghada Kchour, Thierry Caus, Isabelle Six, Gabriel Choukroun, Saïd Kamel, and Youssef Bennis. "Endothelial cells exposed to phosphate and indoxyl sulphate promote vascular calcification through interleukin-8 secretion." Nephrology Dialysis Transplantation 34, no. 7 (November 27, 2018): 1125–34. http://dx.doi.org/10.1093/ndt/gfy325.

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AbstractBackgroundVascular calcification (VC) is amplified during chronic kidney disease, partly due to uraemic toxins such as inorganic phosphate (Pi) and indoxyl sulphate (IS) that trigger osteogenic differentiation of vascular smooth muscle cells (VSMCs). These toxins also alter endothelial cell (EC) functions but whether this contributes to VC is unknown. Here, we hypothesized that ECs exposed to Pi and IS promote VSMC calcification.MethodsHuman umbilical vein ECs were treated with Pi, IS or both, and then the conditioned media [endothelial cell conditioned medium (EC-CM)] was collected. Human aortic SMCs (HASMCs) were exposed to the same toxins, with or without EC-CM, and then calcification and osteogenic differentiation were evaluated. Procalcifying factors secreted from ECs in response to Pi and IS were screened. Rat aortic rings were isolated to assess Pi+IS-induced calcification at the tissue level.ResultsPi and Pi+IS induced HASMCs calcification, which was significantly exacerbated by EC-CM. Pi+IS induced the expression and secretion of interleukin-8 (IL-8) from ECs. While IL-8 treatment of HASMCs stimulated the Pi+IS-induced calcification in a concentration-dependent manner, IL-8 neutralizing antibody, IL-8 receptors antagonist or silencing IL-8 gene expression in ECs before collecting EC-CM significantly prevented the EC-CM procalcifying effect. IL-8 did not promote the Pi+IS-induced osteogenic differentiation of HASMCs but prevented the induction of osteopontin (OPN), a potent calcification inhibitor. In rat aortic rings, IS also promoted Pi-induced calcification and stimulated the expression of IL-8 homologues. Interestingly, in the Pi+IS condition, IL-8 receptor antagonist lifted the inhibition of OPN expression and partially prevented aortic calcification.ConclusionThese results highlight a novel role of IL-8, whose contribution to VC in the uraemic state results at least from interaction between ECs and VSMCs.

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Wyczalkowska-Tomasik, Aleksandra, Bozena Czarkowska-Paczek, Joanna Giebultowicz, Piotr Wroczynski, and Leszek Paczek. "Age-dependent increase in serum levels of indoxyl sulphate and p-cresol sulphate is not related to their precursors: Tryptophan and tyrosine." Geriatrics & Gerontology International 17, no. 6 (May 31, 2016): 1022–26. http://dx.doi.org/10.1111/ggi.12811.

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25

Giebułtowicz, Joanna, Natalia Korytowska, Bartłomiej Sankowski, and Piotr Wroczyński. "Development and validation of a LC-MS/MS method for quantitative analysis of uraemic toxins p-cresol sulphate and indoxyl sulphate in saliva." Talanta 150 (April 2016): 593–98. http://dx.doi.org/10.1016/j.talanta.2015.12.075.

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26

Rossi, Megan, Kerenaftali Klein, David W. Johnson, and Katrina L. Campbell. "Pre-, Pro-, and Synbiotics: Do They Have a Role in Reducing Uremic Toxins? A Systematic Review and Meta-Analysis." International Journal of Nephrology 2012 (2012): 1–20. http://dx.doi.org/10.1155/2012/673631.

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Objective. This paper assessed the effectiveness of pre-, pro-, and synbiotics on reducing two protein-bound uremic toxins, p-cresyl sulphate (PCS) and indoxyl sulphate (IS).Methods. English language studies reporting serum, urinary, or fecal PCS and/or IS (or their precursors) following pre-, pro-, or synbiotic interventions (>1 day) in human adults were included. Population estimates of differences in the outcomes between the pre- and the postintervention were estimated for subgroups of studies using four meta-analyses. Quality was determined using the GRADE approach.Results. 19 studies met the inclusion criteria, 14 in healthy adults and five in haemodialysis patients. Eight studies investigated prebiotics, six probiotics, one synbiotics, one both pre- and probiotics, and three studies trialled all three interventions. The quality of the studies ranged frommoderatetovery low. 12 studies were included in the meta-analyses with all four meta-analyses reporting statistically significant reductions in IS and PCS with pre- and probiotic therapy.Conclusion. There is a limited but supportive evidence for the effectiveness of pre- and probiotics on reducing PCS and IS in the chronic kidney disease population. Further studies are needed to provide more definitive findings before routine clinical use can be recommended.

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Castillo-Rodriguez, Esmeralda, Raul Fernandez-Prado, Raquel Esteras, Maria Perez-Gomez, Carolina Gracia-Iguacel, Beatriz Fernandez-Fernandez, Mehmet Kanbay, et al. "Impact of Altered Intestinal Microbiota on Chronic Kidney Disease Progression." Toxins 10, no. 7 (July 19, 2018): 300. http://dx.doi.org/10.3390/toxins10070300.

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In chronic kidney disease (CKD), accumulation of uremic toxins is associated with an increased risk of CKD progression. Some uremic toxins result from nutrient processing by gut microbiota, yielding precursors of uremic toxins or uremic toxins themselves, such as trimethylamine N-Oxide (TMAO), p-cresyl sulphate, indoxyl sulphate and indole-3 acetic acid. Increased intake of some nutrients may modify the gut microbiota, increasing the number of bacteria that process them to yield uremic toxins. Circulating levels of nutrient-derived uremic toxins are associated to increased risk of CKD progression. This offers the opportunity for therapeutic intervention by either modifying the diet, modifying the microbiota, decreasing uremic toxin production by microbiota, increasing toxin excretion or targeting specific uremic toxins. We now review the link between nutrients, microbiota and uremic toxin with CKD progression. Specific focus will be placed on the generation specific uremic toxins with nephrotoxic potential, the decreased availability of bacteria-derived metabolites with nephroprotective potential, such as vitamin K and butyrate and the cellular and molecular mechanisms linking these toxins and protective factors to kidney diseases. This information provides a conceptual framework that allows the development of novel therapeutic approaches.

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Dalal, N., T. K. Dhiman, G. B. V. S. Lakshmi, A. K. Singh, R. Singh, P. R. Solanki, and A. Kumar. "MIP-based sensor for the detection of gut microbiota-derived indoxyl sulphate using PANI-graphene-NiS2." Materials Today Chemistry 26 (December 2022): 101157. http://dx.doi.org/10.1016/j.mtchem.2022.101157.

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Odamaki, M., A. Kato, H. Kumagai, and A. Hishida. "Counter-regulatory effects of procalcitonin and indoxyl sulphate on net albumin secretion by cultured rat hepatocytes." Nephrology Dialysis Transplantation 19, no. 4 (March 18, 2004): 797–804. http://dx.doi.org/10.1093/ndt/gfh023.

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30

Kompa, A., C. Nguyen, A. Edgley, and D. Kelly. "Arly Hydrocarbon Receptor Inhibition Restores Indoxyl Sulphate-Mediated Endothelial Dysfunction: A Novel Target for Cardiovascular Disease." Heart, Lung and Circulation 27 (2018): S64. http://dx.doi.org/10.1016/j.hlc.2018.06.046.

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Wu, Mengyin, Xianlei Cai, Jingjing Lin, Xinhan Zhang, E. Marian Scott, and Xiuyang Li. "Association between fibre intake and indoxyl sulphate/P-cresyl sulphate in patients with chronic kidney disease: Meta-analysis and systematic review of experimental studies." Clinical Nutrition 38, no. 5 (October 2019): 2016–22. http://dx.doi.org/10.1016/j.clnu.2018.09.015.

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32

Foudi, Nabil, Maeva Palayer, Marie Briet, and Anne-Sophie Garnier. "Arterial Remodelling in Chronic Kidney Disease: Impact of Uraemic Toxins and New Pharmacological Approaches." Journal of Clinical Medicine 10, no. 17 (August 25, 2021): 3803. http://dx.doi.org/10.3390/jcm10173803.

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Chronic kidney disease (CKD) is a major public health concern that affects around 10 percent of the world’s population. The severity of CKD is mainly due to the high prevalence of cardiovascular (CV) complications in this population. The aim of this review is to describe the arterial remodelling associated with CKD, to provide a quick overview of the mechanisms involved and to review the recent pharmacological approaches aimed at improving vascular health in CKD. CKD patients are exposed to metabolic and haemodynamic disorders that may affect the CV system. Large artery functional and geometric abnormalities have been well documented in CKD patients and are associated with an increase in arterial stiffness and a maladaptive remodelling. Uraemic toxins, such as indoxyl sulphate, p-cresyl sulphate, protein carbamylation and advanced glycation products, exert various effects on vascular smooth muscle cell functions. The low-grade inflammation associated with CKD may also affect arterial wall composition and remodelling. It is worth noting that the CV risk for CKD patients remains high despite the pharmacological control of traditional CV risk factors, suggesting the need for innovative therapeutic strategies. An interventional study targeting the NLRP3 inflammasome has provided some interesting preliminary results that need to be confirmed, especially in terms of safety.

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Lau, Wei Ling, Javad Savoj, Michael B. Nakata, and Nosratola D. Vaziri. "Altered microbiome in chronic kidney disease: systemic effects of gut-derived uremic toxins." Clinical Science 132, no. 5 (March 9, 2018): 509–22. http://dx.doi.org/10.1042/cs20171107.

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In chronic kidney disease (CKD), influx of urea and other retained toxins exerts a change in the gut microbiome. There is decreased number of beneficial bacteria that produce short-chain fatty acids, an essential nutrient for the colonic epithelium, concurrent with an increase in bacteria that produce uremic toxins such as indoxyl sulphate, p-cresyl sulphate, and trimethylamine-N-oxide (TMAO). Due to intestinal wall inflammation and degradation of intercellular tight junctions, gut-derived uremic toxins translocate into the bloodstream and exert systemic effects. In this review, we discuss the evidence supporting a role for gut-derived uremic toxins in promoting multiorgan dysfunction via inflammatory, oxidative stress, and apoptosis pathways. End-organ effects include vascular calcification, kidney fibrosis, anemia, impaired immune system, adipocyte dysfunction with insulin resistance, and low turnover bone disease. Higher blood levels of gut-derived uremic toxins are associated with increased cardiovascular events and mortality in the CKD population. Clinical trials that have examined interventions to trap toxic products or reverse gut microbial dysbiosis via oral activated charcoal AST-120, prebiotics and probiotics have not shown impact on cardiovascular or survival outcomes but were limited by sample size and short trials. In summary, the gut microbiome is a major contributor to adverse cardiovascular outcomes and progression of CKD.

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Takeda, Naohito, Toshimitsu Niwa, Kenji Maeda, Masao Shibata, and Akira Tatematsu. "Rapid assay for indoxyl sulphate in uremic serum by internal-surface reversed-phase high-performance liquid chromatography." Journal of Chromatography B: Biomedical Sciences and Applications 431 (January 1988): 418–23. http://dx.doi.org/10.1016/s0378-4347(00)83112-6.

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35

Muteliefu, G., A. Enomoto, P. Jiang, M. Takahashi, and T. Niwa. "Indoxyl sulphate induces oxidative stress and the expression of osteoblast-specific proteins in vascular smooth muscle cells." Nephrology Dialysis Transplantation 24, no. 7 (January 22, 2009): 2051–58. http://dx.doi.org/10.1093/ndt/gfn757.

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36

Hirata, Kenshiro, Tokunori Ikeda, Hiroshi Watanabe, Toru Maruyama, Motoko Tanaka, Victor Chuang, Yuji Uchida, et al. "The Binding of Aripiprazole to Plasma Proteins in Chronic Renal Failure Patients." Toxins 13, no. 11 (November 18, 2021): 811. http://dx.doi.org/10.3390/toxins13110811.

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The binding of drugs to plasma protein is frequently altered in certain types of renal diseases. We recently reported on the effects of oxidation and uremic toxins on the binding of aripiprazole (ARP) to human serum albumin. In our continuing investigations, we examined the binding of ARP to plasma pooled from patients with chronic renal dysfunction. We examined the issue of the molecular basis for which factors affect the changes in drug binding that accompany renal failure. The study was based on the statistical relationships between ARP albumin binding and biochemical parameters such as the concentrations of oxidized albumin and uremic toxins. The binding of ARP to plasma from chronic renal patients was significantly lower than healthy volunteers. A rational relationship between the ARP binding rate and the concentration of toxins, including indoxyl sulphate (IS) and p-cresyl sulphate (PCS), was found, particularly for IS. Moreover, multiple regression analyses that involved taking other parameters such as PCS or oxidized albumin ratio to IS into account supports the above hypothesis. In conclusion, the limited data reported in this present study indicates that monitoring IS in the blood is a very important determinant in the dosage plan for the administration of site II drugs such as ARP, if the efficacy of the drug in renal disease is to be considered.

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De Mauri, Andreana, Deborah Carrera, Matteo Vidali, Marco Bagnati, Roberta Rolla, Sergio Riso, Massimo Torreggiani, and Doriana Chiarinotti. "Compliance, Adherence and Concordance Differently Predict the Improvement of Uremic and Microbial Toxins in Chronic Kidney Disease on Low Protein Diet." Nutrients 14, no. 3 (January 23, 2022): 487. http://dx.doi.org/10.3390/nu14030487.

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Background. In medicine, “compliance” indicates that the patient complies with the prescriber’s recommendations, “adherence” means that “the patient matches the recommendations” and “concordance” means “therapeutic alliance” between patient and clinician. While a low protein diet (LPD) is a cornerstone treatment of chronic kidney disease (CKD), monitoring the actual performance of LPD is a challenge. Patients. Fifty-seven advanced CKD adult patients were enrolled and LPD prescribed. Compliance was evaluated through the normalized protein catabolic rate (nPCR), adherence by the dietitian by means of a 24-h dietary recall and concordance by the nephrologist during consultations. Traditional parameters as well as total p-Cresyl Sulphate (t-PCS), total Indoxyl Sulphate (t-IS) and Lipoprotein-associated phspholipase A2 (Lp-PLA2) were compared between adherent/not adherent and concordant/not concordant subjects at enrolment and after two months. Results. nPCR, blood urea nitrogen, cholesterol and triglycerides significantly decreased in all patients. t-PCS and t-IS decreased among adherent subjects. Lp-PLA2, t-PCS, free-PCS and t-IS decreased among concordant subjects, while these increased in non-concordant ones. Conclusion. This study demonstrates that LPD may improve the control of traditional uremic toxins and atherogenic toxins in “adherent” and “concordant” patients. A comprehensive and multidisciplinary approach is needed to evaluate the compliance/adherence/concordance to LPD for optimizing nutritional interventions.

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Barisione, Chiara, Silvano Garibaldi, Daniela Verzola, Paola Altieri, Giorgio Ghigliotti, Anna Lisa Furfaro, Mariapaola Nitti, Domenico Palombo, and Pietro Ameri. "Effects of the AhR inhibitor CH-223191 on the indoxyl sulphate-induced cardiac fibroblast activation. Role of Nrf2." Vascular Pharmacology 146 (October 2022): 107030. http://dx.doi.org/10.1016/j.vph.2022.107030.

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Miyazaki, Takashi, Isao Aoyama, Michihito Ise, Hisao Seo, and Toshimitsu Niwa. "An oral sorbent reduces overload of indoxyl sulphate and gene expression of TGF‐β1 in uraemic rat kidneys." Nephrology Dialysis Transplantation 15, no. 11 (November 1, 2000): 1773–81. http://dx.doi.org/10.1093/ndt/15.11.1773.

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Gomolka, Malgorzata, Longin Niemczyk, Jerzy Smoszna, Katarzyna Szamotulska, Leszek Paczek, and Stanislaw Niemczyk. "MP518REMOVAL OF INDOXYL SULPHATE AND P-CRESOL SULPHATE AS WELL AS STIMULATION OF FORMING PROTEOLYTIC ENZYMES DURING LOW-FLUX (HDLF), HIGH-FLUX HEMODIALYSIS (HDHF) AND HEMODIAFILTRATION (HDF)." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii618—iii619. http://dx.doi.org/10.1093/ndt/gfx175.mp518.

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Margiotta, Elisabetta, Lara Caldiroli, Maria Luisa Callegari, Francesco Miragoli, Francesca Zanoni, Silvia Armelloni, Vittoria Rizzo, Piergiorgio Messa, and Simone Vettoretti. "Association of Sarcopenia and Gut Microbiota Composition in Older Patients with Advanced Chronic Kidney Disease, Investigation of the Interactions with Uremic Toxins, Inflammation and Oxidative Stress." Toxins 13, no. 7 (July 8, 2021): 472. http://dx.doi.org/10.3390/toxins13070472.

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Sarcopenia is a prevalent condition in chronic kidney disease (CKD). We determined gut microbiota (gMB) composition in CKD patients with or without sarcopenia. Furthermore, we investigated whether in these patients, there was any association between gMB, uremic toxins, inflammation and oxidative stress. We analyzed gMB composition, uremic toxins (indoxyl sulphate and p-cresyl sulphate), inflammatory cytokines (interleukin 10, tumor necrosis factor α, interleukin 6, interleukin 17, interleukin 12 p70, monocyte chemoattractant protein-1 and fetuin-A) and oxidative stress (malondialdehyde) of 64 elderly CKD patients (10 < eGFR < 45 mL/min/1.73 m2, not on dialysis) categorized as sarcopenic and not-sarcopenic. Sarcopenia was defined according to European Working Group on Sarcopenia in Older People 2 criteria. Sarcopenic patients had a greater abundance of the Micrococcaceae and Verrucomicrobiaceae families and of Megasphaera, Rothia, Veillonella, Akkermansia and Coprobacillus genera. They had a lower abundance of the Gemellaceae and Veillonellaceae families and of Acidaminococcus and Gemella genera. GMB was associated with uremic toxins, inflammatory cytokines and MDA. However, uremic toxins, inflammatory cytokines and MDA were not different in sarcopenic compared with not-sarcopenic individuals, except for interleukin 10, which was higher in not-sarcopenic patients. In older CKD patients, gMB was different in sarcopenic than in not-sarcopenic ones. Several bacterial families and genera were associated with uremic toxins and inflammatory cytokines, although none of these latter substantially different in sarcopenic versus not-sarcopenic patients.

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Barisone, C., E. Lazzarini, C. Ruggeri, S. Garibaldi, P. Fabbi, D. Verzola, S. Ravera, C. Brunelli, G. Ghigliotti, and P. Ameri. "Indoxyl sulphate activates cardiac fibroblasts with enhanced collagen synthesis, upregulated angiotensin-neprilysin system, and paracrine induction of cardiomyocyte hypertrophy." Vascular Pharmacology 103-105 (April 2018): 48. http://dx.doi.org/10.1016/j.vph.2017.12.005.

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Yaker, Linda, Saïd Kamel, Jérôme Ausseil, and Agnès Boullier. "Effects of Chronic Kidney Disease and Uremic Toxins on Extracellular Vesicle Biology." Toxins 12, no. 12 (December 21, 2020): 811. http://dx.doi.org/10.3390/toxins12120811.

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Vascular calcification (VC) is a cardiovascular complication associated with a high mortality rate, especially in patients with diabetes, atherosclerosis or chronic kidney disease (CKD). In CKD patients, VC is associated with the accumulation of uremic toxins, such as indoxyl sulphate or inorganic phosphate, which can have a major impact in vascular remodeling. During VC, vascular smooth muscle cells (VSMCs) undergo an osteogenic switch and secrete extracellular vesicles (EVs) that are heterogeneous in terms of their origin and composition. Under physiological conditions, EVs are involved in cell-cell communication and the maintenance of cellular homeostasis. They contain high levels of calcification inhibitors, such as fetuin-A and matrix Gla protein. Under pathological conditions (and particularly in the presence of uremic toxins), the secreted EVs acquire a pro-calcifying profile and thereby act as nucleating foci for the crystallization of hydroxyapatite and the propagation of calcification. Here, we review the most recent findings on the EVs’ pathophysiological role in VC, the impact of uremic toxins on EV biogenesis and functions, the use of EVs as diagnostic biomarkers and the EVs’ therapeutic potential in CKD.

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Filipska, Iwona, Agata Winiarska, Monika Knysak, and Tomasz Stompór. "Contribution of Gut Microbiota-Derived Uremic Toxins to the Cardiovascular System Mineralization." Toxins 13, no. 4 (April 10, 2021): 274. http://dx.doi.org/10.3390/toxins13040274.

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Chronic kidney disease (CKD) affects more than 10% of the world population and leads to excess morbidity and mortality (with cardiovascular disease as a leading cause of death). Vascular calcification (VC) is a phenomenon of disseminated deposition of mineral content within the media layer of arteries preceded by phenotypic changes in vascular smooth muscle cells (VSMC) and/or accumulation of mineral content within the atherosclerotic lesions. Medial VC results in vascular stiffness and significantly contributes to increased cardio-vascular (CV) morbidity, whereas VC of plaques may rather increase their stability. Mineral and bone disorders of CKD (CKD-MBD) contribute to VC, which is further aggravated by accumulation of uremic toxins. Both CKD-MBD and uremic toxin accumulation affect not only patients with advanced CKD (glomerular filtration rate (GFR) less than 15 mL/min./1.72 m2, end-stage kidney disease) but also those on earlier stages of a disease. The key uremic toxins that contribute to VC, i.e., p-cresyl sulphate (PCS), indoxyl sulphate (IS) and trimethylamine-N-oxide (TMAO) originate from bacterial metabolism of gut microbiota. All mentioned toxins promote VC by several mechanisms, including: Transdifferentiation and apoptosis of VSMC, dysfunction of endothelial cells, oxidative stress, interaction with local renin–angiotensin–aldosterone system or miRNA profile modification. Several attractive methods of gut microbiota manipulations have been proposed in order to modify their metabolism and to limit vascular damage (and VC) triggered by uremic toxins. Unfortunately, to date no such method was demonstrated to be effective at the level of “hard” patient-oriented or even clinically relevant surrogate endpoints.

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Liu, Shuxin, Lingyun Jia, Jia Xiao, Jingyu Li, Fangfang Mei, Jianan Zhou, Lulu Han, Lin Li, and Jing Shan. "Increased clearance of indoxyl sulphate in renal failure rats with the addition of water‐soluble poly‐β‐cyclodextrin to the dialysate." Nephrology 27, no. 4 (December 7, 2021): 376–82. http://dx.doi.org/10.1111/nep.14008.

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Lin, Cheng-Jui, Chiao-Yin Sun, Chih-Jen Wu, Chau-Chung Wu, Vincent Wu, and Feng-Huei Lin. "CharXgen-Activated Bamboo Charcoal Encapsulated in Sodium Alginate Microsphere as the Absorbent of Uremic Toxins to Retard Kidney Function Deterioration." International Journal of Molecular Sciences 21, no. 4 (February 13, 2020): 1257. http://dx.doi.org/10.3390/ijms21041257.

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Indoxyl sulphate (IS) and p-cresyl sulphate (PCS) are two protein bound uraemic toxins accumulated in chronic kidney disease (CKD) and associated with adverse outcomes. The purpose of this study isto evaluate the effect of the new activated charcoal, CharXgen, on renal function protection and lowering serum uraemic toxins in CKD animal model. The physical character of CharXgen was analyzed before and after activation procedure by Scanning Electron Microscope (SEM) and X-ray diffractometer (XRD). The effect of CharXgen on biochemistry and lowering uremic toxins was evaluated by in vitro binding assay and CKD animal model. CharXgen have high interior surface area analyzed by SEM and XRD and have been produced from local bamboo after an activation process. CharXgen was able to effectively absorb IS, p-cresol and phosphate in an in vitro gastrointestinal tract simulation study. The animal study showed that CharXgen did not cause intestine blackening. Serum albuminand liver function did not change after feeding with CharXgen. Moreover, renal function was improved in CKD rats fed with CharXgen as compared to the CKD group, and there were no significant differences in the CKD and the CKD + AST-120 groups. Serum IS and PCS were higher in the CKD group and lower in rats treated with CharXgen and AST-120. In rats treated with CharXgen, Fibroblast growth factor 23 was significantly decreased as compared to the CKD group. This change cannot be found in rats fed with AST-120.It indicates that CharXgen is a new safe and non-toxic activated charcoal having potential in attenuating renal function deterioration and lowering protein-bound uraemic toxins. Whether the introduction of this new charcoal could further have renal protection in CKD patients will need to be investigated further.

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Meibaum, Jörn, Silvie Krause, Hartmut Hillmer, Daniele Marcelli, and Christof Strohhöfer. "Identification and characterisation of fluorescent substances in spent dialysis fluid." International Journal of Artificial Organs 43, no. 9 (February 4, 2020): 579–86. http://dx.doi.org/10.1177/0391398820901826.

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Patients who suffer from end-stage renal disease require renal replacement therapy, including haemodialysis. While applying extracorporeal blood treatment, uraemic toxins accumulated in the patients’ blood pass into a physiological solution, the dialysis fluid. Thus, important information about the patient’s health status can be obtained by analysing the spent dialysis fluid. To make use of this information, corresponding analysis concepts must be developed. In this context, this article reports the analysis of fluorescence in spent dialysis fluid. Excitation and emission maxima of fluorescence in spent dialysis fluid were recorded, and the main fluorescent substances were identified and quantified using high-performance liquid chromatography analysis. Fluorescence in spent dialysis fluid has two prominent excitation maxima at λex1 = 228 nm and λex2 = 278 nm. However, both excitation maxima cause emission with maxima at λem = 350 nm. Identification of fluorescent substances using high-performance liquid chromatography showed that the main contributors to the overall fluorescence in spent dialysis fluid are tyrosine, tryptophan, indoxyl sulphate and indole-3-acetic acid. However, these substances are responsible for only one-third of the overall fluorescence of spent dialysis fluid. A large number of substances, each of which contributes only to a small part to the overall fluorescence, emit the remaining fluorescence.

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Pretorius, Carel J., Brett C. McWhinney, Bilyana Sipinkoski, Lambro A. Johnson, Megan Rossi, Katrina L. Campbell, and Jacobus P. J. Ungerer. "Reference ranges and biological variation of free and total serum indoxyl- and p-cresyl sulphate measured with a rapid UPLC fluorescence detection method." Clinica Chimica Acta 419 (April 2013): 122–26. http://dx.doi.org/10.1016/j.cca.2013.02.008.

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Lisowska-Myjak, Barbara, Hanna Zborowska, Radosław Jaźwiec, Maria Karlińska, and Ewa Skarżyńska. "Serum indoxyl sulphate and its relation to albumin and α1-acid glycoprotein as a potential biomarkers of maternal intestinal metabolism during pregnancy and postpartum." PLOS ONE 16, no. 11 (November 5, 2021): e0259501. http://dx.doi.org/10.1371/journal.pone.0259501.

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Background Serum indoxyl sulfate (IS) levels depend on the production of indole in the gut. The biological effects of IS in the vascular bed could be confirmed by changes in the levels of individual serum proteins during normal pregnancy and in the postpartum period as compared with non-pregnant controls. Albumin (Alb) and α1-acid glycoprotein (AGP, orosomucoid) are the most abundant serum carrier proteins with potential interrelationships with serum levels of IS. Methods Serum levels of IS, Alb and AGP were measured in 84 pregnant women in the first, second and third trimester of pregnancy and in the postpartum period, as well as in non-pregnant controls (n = 20), using ultra-performance liquid chromatography (UPLC) coupled to mass spectrometry (IS), colorimetric assay (Alb) and immunoturbidimetric assay (AGP). Results The postpartum serum levels [mg/L] of IS were lower (p = 0.027) than in the second trimester (mean±SD: 0.85±0.39 vs 0.58±0.32). There were no differences in the IS to ALB ratio calculated in the three trimesters of pregnancy, the postpartum period, and in the non-pregnant controls. The IS/AGP ratio increased from the first to the second trimester (p = 0.039), and decreased in the postpartum period (p<0.05), when it was lower than in the second and third trimester. Conclusions The variability of the serum IS/AGP ratio during pregnancy and in the postpartum period may reflect shared involvement in the regulation of their intravascular relationships. The link between serum levels of IS derived from the gut and AGP could serve a potential biomarkers of maternal intestinal metabolism during pregnancy and postpartum.

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De Mauri, Andreana, Deborah Carrera, Marco Bagnati, Roberta Rolla, Matteo Vidali, Doriana Chiarinotti, Marco Pane, Angela Amoruso, and Mario Del Piano. "Probiotics-Supplemented Low-Protein Diet for Microbiota Modulation in Patients with Advanced Chronic Kidney Disease (ProLowCKD): Results from a Placebo-Controlled Randomized Trial." Nutrients 14, no. 8 (April 14, 2022): 1637. http://dx.doi.org/10.3390/nu14081637.

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The probiotics-supplemented low-protein diet in chronic kidney disease (ProLowCKD) was a single-centre, double-blind, placebo-controlled, randomised trial that was conducted to investigate whether the association between a low protein diet (LPD) and a new formulation of probiotics (Bifidobacterium longum and Lactobacillus reuteri) was effective at reducing traditional uremic, microbiota-derived, and proatherogenic toxins in sixty patients affected by advanced CKD. After 2 months of a LPD—a reduction in blood urea nitrogen (52 ± 17 vs. 46 ± 15 mg/dL, p = 0.003), total cholesterol (185 ± 41 vs. 171 ± 34 mg/dL, p = 0.001), and triglycerides (194 ± 148 vs. 161 ± 70 mg/dL, p = 0.03) was observed; 57 subjects were then randomized to receive probiotics or a placebo for the subsequent 3 months. A total of 27 patients in the placebo group showed increased serum values of total cholesterol (169 ± 36 vs. 185 ± 40 mg/dL, p = 0.01), LDL cholesterol (169 ± 36 vs. 185 ± 40 mg/dL, p = 0.02), lipoprotein-associated phospholipase A2 (155.4 ± 39.3 vs. 167.5 ± 51.4 nmol/mL/min, p = 0.006), and indoxyl-sulphate (30.1 ± 17.6 vs. 34.5 ± 20.2 μM, p = 0.026), while the 24 subjects in the probiotics group showed a trend in the reduction of microbiota toxins. A reduction of antihypertensive and diuretic medications was possible in the probiotics group. This study shows that associating probiotics to LPD may have an additional beneficial effect on the control and modulation of microbiota-derived and proatherogenic toxins in CKD patients.

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