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Автор: Grafiati
Опубліковано: 10 грудня 2022
Оновлено: 30 січня 2023

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1

Bowry, Sudhir K., Peter Kotanko, Rainer Himmele, Xia Tao, and Michael Anger. "The membrane perspective of uraemic toxins: which ones should, or can, be removed?" Clinical Kidney Journal 14, Supplement_4 (December 2021): i17—i31. http://dx.doi.org/10.1093/ckj/sfab202.

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ABSTRACT Informed decision-making is paramount to the improvement of dialysis therapies and patient outcomes. A cornerstone of delivery of optimal dialysis therapy is to delineate which substances (uraemic retention solutes or ‘uraemic toxins’) contribute to the condition of uraemia in terms of deleterious biochemical effects they may exert. Thereafter, decisions can be made as to which of the accumulated compounds need to be targeted for removal and by which strategies. For haemodialysis (HD), the non-selectivity of membranes is sometimes considered a limitation. Yet, considering that dozens of substances with potential toxicity need to be eliminated, and targeting removal of individual toxins explicitly is not recommended, current dialysis membranes enable elimination of several molecules of a broad size range within a single therapy session. However, because HD solute removal is based on size-exclusion principles, i.e. the size of the substances to be removed relative to the mean size of the ‘pores’ of the membrane, only a limited degree of selectivity of removal is possible. Removal of unwanted substances during HD needs to be weighed against the unavoidable loss of substances that are recognized to be necessary for bodily functions and physiology. In striving to improve the efficiency of HD by increasing the porosity of membranes, there is a greater potential for the loss of substances that are of benefit. Based on this elementary trade-off and availability of recent guidance on the relative toxicity of substances retained in uraemia, we propose a new evidence-linked uraemic toxin elimination (ELUTE) approach whereby only those clusters of substances for which there is a sufficient body of evidence linking them to deleterious biological effects need to be targeted for removal. Our approach involves correlating the physical properties of retention solutes (deemed to express toxicity) with key determinants of membranes and separation processes. Our analysis revealed that in attempting to remove the relatively small number of ‘larger’ substances graded as having only moderate toxicity, uncontrolled (and efficient) removal of several useful compounds would take place simultaneously and may compromise the well-being or outcomes of patients. The bulk of the uraemic toxin load comprises uraemic toxins below <30 000 Da and are adequately removed by standard membranes. Further, removal of a few difficult-to-remove-by-dialysis (protein-bound) compounds that express toxicity cannot be achieved by manipulation of pore size alone. The trade-off between the benefits of effective removal of the bulk of the uraemic toxin load and risks (increased loss of useful substances) associated with targeting the removal of a few larger substances in ‘high-efficiency’ HD treatment strategies needs to be recognized and better understood. The removability during HD of substances, be they toxic, inert or beneficial, needs be revised to establish the pros and cons of current dialytic elimination strategies.
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2

Wang, Xifan, Songtao Yang, Shenghui Li, Liang Zhao, Yanling Hao, Junjie Qin, Lian Zhang, et al. "Aberrant gut microbiota alters host metabolome and impacts renal failure in humans and rodents." Gut 69, no. 12 (April 2, 2020): 2131–42. http://dx.doi.org/10.1136/gutjnl-2019-319766.

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ObjectivePatients with renal failure suffer from symptoms caused by uraemic toxins, possibly of gut microbial origin, as deduced from studies in animals. The aim of the study is to characterise relationships between the intestinal microbiome composition, uraemic toxins and renal failure symptoms in human end-stage renal disease (ESRD).DesignCharacterisation of gut microbiome, serum and faecal metabolome and human phenotypes in a cohort of 223 patients with ESRD and 69 healthy controls. Multidimensional data integration to reveal links between these datasets and the use of chronic kidney disease (CKD) rodent models to test the effects of intestinal microbiome on toxin accumulation and disease severity.ResultsA group of microbial species enriched in ESRD correlates tightly to patient clinical variables and encode functions involved in toxin and secondary bile acids synthesis; the relative abundance of the microbial functions correlates with the serum or faecal concentrations of these metabolites. Microbiota from patients transplanted to renal injured germ-free mice or antibiotic-treated rats induce higher production of serum uraemic toxins and aggravated renal fibrosis and oxidative stress more than microbiota from controls. Two of the species, Eggerthella lenta and Fusobacterium nucleatum, increase uraemic toxins production and promote renal disease development in a CKD rat model. A probiotic Bifidobacterium animalis decreases abundance of these species, reduces levels of toxins and the severity of the disease in rats.ConclusionAberrant gut microbiota in patients with ESRD sculpts a detrimental metabolome aggravating clinical outcomes, suggesting that the gut microbiota will be a promising target for diminishing uraemic toxicity in those patients.Trial registration numberThis study was registered at ClinicalTrials.gov (NCT03010696).
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3

Liabeuf, Sophie, Cédric Villain, and Ziad A. Massy. "Protein-bound toxins: has the Cinderella of uraemic toxins turned into a princess?" Clinical Science 130, no. 23 (October 31, 2016): 2209–16. http://dx.doi.org/10.1042/cs20160393.

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Анотація:
Chronic kidney disease (CKD) has emerged as a global public health problem. Although the incidence and prevalence of CKD vary from one country to another, the estimated worldwide prevalence is 8–16%. The complications associated with CKD include progression to end-stage renal disease (ESRD), mineral and bone disorders, anaemia, cognitive decline and elevated all-cause and cardiovascular (CV) mortality. As a result of progressive nephron loss, patients with late-stage CKD are permanently exposed to uraemic toxins. These toxins have been classified into three groups as a function of the molecular mass: small water-soluble molecules, middle molecules and protein-bound uraemic toxins. The compounds can also be classified according to their origin (i.e. microbial or not) or their protein-binding ability. The present review will focus on the best-characterized protein-bound uraemic toxins, namely indoxylsulfate (IS), indole acetic acid (IAA) and p-cresylsulfate (PCS, a cresol metabolite). Recent research suggests that these toxins accelerate the progression of CV disease, kidney disease, bone disorders and neurological complications. Lastly, we review therapeutic approaches that can be used to decrease toxin levels.
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4

Massy, Ziad A., and Sophie Liabeuf. "From old uraemic toxins to new uraemic toxins: place of ‘omics’." Nephrology Dialysis Transplantation 33, suppl_3 (October 1, 2018): iii2—iii5. http://dx.doi.org/10.1093/ndt/gfy212.

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5

Vanholder, R. "Uraemic toxins and cardiovascular disease." Nephrology Dialysis Transplantation 18, no. 3 (March 1, 2003): 463–66. http://dx.doi.org/10.1093/ndt/18.3.463.

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6

Capeillère-Blandin, Chantal, Valérie Gausson, Anh Thu Nguyen, Béatrice Descamps-Latscha, Tilman Drüeke, and Véronique Witko-Sarsat. "Respective role of uraemic toxins and myeloperoxidase in the uraemic state." Nephrology Dialysis Transplantation 21, no. 6 (February 13, 2006): 1555–63. http://dx.doi.org/10.1093/ndt/gfl007.

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7

Masereeuw, Rosalinde, and Marianne C. Verhaar. "Innovations in approaches to remove uraemic toxins." Nature Reviews Nephrology 16, no. 10 (May 7, 2020): 552–53. http://dx.doi.org/10.1038/s41581-020-0299-0.

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8

YE, C., Q. GONG, F. LU, and J. LIANG. "Adsorption of uraemic toxins on carbon nanotubes." Separation and Purification Technology 58, no. 1 (December 1, 2007): 2–6. http://dx.doi.org/10.1016/j.seppur.2007.07.003.

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9

Bowry, Sudhir K., Fatih Kircelli, Mooppil Nandakumar, and Tushar J. Vachharajani. "Clinical relevance of abstruse transport phenomena in haemodialysis." Clinical Kidney Journal 14, Supplement_4 (December 2021): i85—i97. http://dx.doi.org/10.1093/ckj/sfab183.

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Анотація:
ABSTRACT Haemodialysis (HD) utilizes the bidirectional properties of semipermeable membranes to remove uraemic toxins from blood while simultaneously replenishing electrolytes and buffers to correct metabolic acidosis. However, the nonspecific size-dependent transport across membranes also means that certain useful plasma constituents may be removed from the patient (together with uraemic toxins), or toxic compounds, e.g. endotoxin fragments, may accompany electrolytes and buffers of the dialysis fluids into blood and elicit severe biological reactions. We describe the mechanisms and implications of these undesirable transport processes that are inherent to all HD therapies and propose approaches to mitigate the effects of such transport. We focus particularly on two undesirable events that are considered to adversely affect HD therapy and possibly impact patient outcomes. Firstly, we describe how loss of albumin (and other essential substances) can occur while striving to eliminate larger uraemic toxins during HD and why hypoalbuminemia is a clinical condition to contend with. Secondly, we describe the origins and mode of transport of biologically active substances (from dialysis fluids with bacterial contamination) into the blood compartment and biological reactions they elicit. Endotoxin fragments activate various proinflammatory pathways to increase the underlying inflammation associated with chronic kidney disease. Both phenomena involve the physical as well as chemical properties of membranes that must be selected judiciously to balance the benefits with potential risks patients may encounter, in both the short and long term.
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10

Xiong, Siyu, Yaxuan Lyu, Andrew Davenport, and Kwang Leong Choy. "Sponge-like Chitosan Based Porous Monolith for Uraemic Toxins Sorption." Nanomaterials 11, no. 9 (August 30, 2021): 2247. http://dx.doi.org/10.3390/nano11092247.

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Анотація:
More than three million patients are treated for kidney failure world-wide. Haemodialysis, the most commonly used treatment, requires large amounts of water and generates mountains of non-recyclable plastic waste. To improve the environmental footprint, dialysis treatments need to develop absorbents to regenerate the waste dialysate. Whereas conventional dialysis clears water-soluble toxins, it is not so effective in clearing protein-bound uraemic toxins (PBUTs), such as indoxyl sulfate (IS). Thus, developing absorption devices to remove both water-soluble toxins and PBUTs would be advantageous. Vapour induced phase separation (VIPS) has been used in this work to produce polycaprolactone/chitosan (PCL/CS) composite symmetric porous monoliths with extra porous carbon additives to increase creatinine and albumin-bound IS absorption. Moreover, these easy-to-fabricate porous monoliths can be formed into the required geometry. The PCL/CS porous monoliths absorbed 436 μg/g of albumin-bound IS and 2865 μg/g of creatinine in a single-pass perfusion model within 1 h. This porous PCL/CS monolith could potentially be used to absorb uraemic toxins, including PBUTs, and thus allow the regeneration of waste dialysate and the development of a new generation of environmentally sustainable dialysis treatments, including wearable devices.
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11

Niwa, Toshimitsu. "Removal of Protein-Bound Uraemic Toxins by Haemodialysis." Blood Purification 35, s2 (2013): 20–25. http://dx.doi.org/10.1159/000350843.

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12

Cohen, G., G. Glorieux, P. Thornalley, E. Schepers, N. Meert, J. Jankowski, V. Jankowski, et al. "Review on uraemic toxins III: recommendations for handling uraemic retention solutes in vitro towards a standardized approach for research on uraemia." Nephrology Dialysis Transplantation 22, no. 12 (August 25, 2007): 3381–90. http://dx.doi.org/10.1093/ndt/gfm210.

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13

Deltombe, Olivier, Annemieke Dhondt, Wim Van Biesen, Griet Glorieux, and Sunny Eloot. "Effect of sample temperature, pH, and matrix on the percentage protein binding of protein-bound uraemic toxins." Analytical Methods 9, no. 12 (2017): 1935–40. http://dx.doi.org/10.1039/c7ay00054e.

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While studying and trying to optimise dialysis clearances of protein-bound uraemic toxins (PBUTs), the percentage protein binding (% PB) may be an important parameter and can be calculated from measured free and total concentrations.
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14

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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15

Nuhu, Faisal, and Sunil Bhandari. "Oxidative Stress and Cardiovascular Complications in Chronic Kidney Disease, the Impact of Anaemia." Pharmaceuticals 11, no. 4 (October 11, 2018): 103. http://dx.doi.org/10.3390/ph11040103.

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Patients with chronic kidney disease (CKD) have significant cardiovascular morbidity and mortality as a result of risk factors such as left ventricular hypertrophy (LVH), oxidative stress, and inflammation. The presence of anaemia in CKD further increases the risk of LVH and oxidative stress, thereby magnifying the deleterious consequence in uraemic cardiomyopathy (UCM), and aggravating progression to failure and increasing the risk of sudden cardiac death. This short review highlights the specific cardio-renal oxidative stress in CKD and provides an understanding of the pathophysiology and impact of uraemic toxins, inflammation, and anaemia on oxidative stress.
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16

Huerta-Uribe, Alejandro, and Andrew J. Roe. "Disarming the enemy: targeting bacterial toxins with small molecules." Emerging Topics in Life Sciences 1, no. 1 (April 21, 2017): 31–39. http://dx.doi.org/10.1042/etls20160013.

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The rapid emergence of antibiotic-resistant bacterial strains has prompted efforts to find new and more efficacious treatment strategies. Targeting virulence factors produced by pathogenic bacteria has gained particular attention in the last few years. One of the inherent advantages of this approach is that it provides less selective pressure for the development of resistance mechanisms. In addition, antivirulence drugs could potentially be the answer for diseases in which the use of conventional antibiotics is counterproductive. That is the case for bacterial toxin-mediated diseases, in which the severity of the symptoms is a consequence of the exotoxins produced by the pathogen. Examples of these are haemolytic-uraemic syndrome produced by Shiga toxins, the profuse and dangerous dehydration caused by Cholera toxin or the life-threatening colitis occasioned by clostridial toxins. This review focuses on the recent advances on the development of small molecules with antitoxin activity against Enterohaemorrhagic Escherichia coli, Vibrio cholerae and Clostridium difficile given their epidemiological importance. The present work includes studies of small molecules with antitoxin properties that act directly on the toxin (direct inhibitors) or that act by preventing expression of the toxin (indirect inhibitors).
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17

Hénaut, Candellier, Boudot, Grissi, Mentaverri, Choukroun, Brazier, Kamel, and Massy. "New Insights into the Roles of Monocytes/Macrophages in Cardiovascular Calcification Associated with Chronic Kidney Disease." Toxins 11, no. 9 (September 12, 2019): 529. http://dx.doi.org/10.3390/toxins11090529.

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Cardiovascular disease (CVD) is an important cause of death in patients with chronic kidney disease (CKD), and cardiovascular calcification (CVC) is one of the strongest predictors of CVD in this population. Cardiovascular calcification results from complex cellular interactions involving the endothelium, vascular/valvular cells (i.e., vascular smooth muscle cells, valvular interstitial cells and resident fibroblasts), and monocyte-derived macrophages. Indeed, the production of pro-inflammatory cytokines and oxidative stress by monocyte-derived macrophages is responsible for the osteogenic transformation and mineralization of vascular/valvular cells. However, monocytes/macrophages show the ability to modify their phenotype, and consequently their functions, when facing environmental modifications. This plasticity complicates efforts to understand the pathogenesis of CVC—particularly in a CKD setting, where both uraemic toxins and CKD treatment may affect monocyte/macrophage functions and thereby influence CVC. Here, we review (i) the mechanisms by which each monocyte/macrophage subset either promotes or prevents CVC, and (ii) how both uraemic toxins and CKD therapies might affect these monocyte/macrophage functions.
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18

Gallice, Philippe M., Aimé D. Crevat, and Yvon F. Berland. "Scaling up in isolation of medium-size uraemic toxins." Journal of Chromatography A 539, no. 2 (January 1991): 449–53. http://dx.doi.org/10.1016/s0021-9673(01)83954-6.

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19

Nikolov, I., N. Joki, T. Drueke, and Z. Massy. "Beyond phosphate--role of uraemic toxins in cardiovascular calcification." Nephrology Dialysis Transplantation 21, no. 12 (September 23, 2006): 3354–57. http://dx.doi.org/10.1093/ndt/gfl446.

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20

Plé, Hélène, Manon Maltais, Aurélie Corduan, Guy Rousseau, François Madore, and Patrick Provost. "Alteration of the platelet transcriptome in chronic kidney disease." Thrombosis and Haemostasis 108, no. 10 (2012): 605–15. http://dx.doi.org/10.1160/th12-03-0153.

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SummaryBleeding and thrombotic disorders are major complications affecting patients with chronic kidney disease (CKD). Exposure of circulating platelets to uraemic toxins and contact with artificial surfaces during dialysis induce platelet abnormalities and alter the platelet proteome. We hypothesised that these changes may be subsequent to changes in the composition and/or regulation of the platelet transcriptome. In this study, we investigated the circulating platelets of 10 CKD patients (i.e. five chronic haemodialysis patients and five stage 4 CKD uraemic patients) and five age- and sex-matched healthy subjects. We observed an alteration of the platelet messenger RNA (mRNA) and microRNA transcriptome in CKD patients. Impaired in uraemic platelets, the levels of some mRNAs and of most microRNAs appeared to be corrected by dialysis, which is consistent with a beneficial effect of dialysis and a mRNA regulatory role of platelet microRNAs. Reduced in platelets of uraemic patients, phosphatidylcholine transfer protein (PCTP) and WD repeat-containing protein 1 (WDR1) were found to be regulated by microRNAs, the latter of which involving hsa-miR-19b, a microRNA increased in platelets of uraemic patients and involved in platelet reactivity. These results suggest that an alteration of microRNA-based mRNA regulatory mechanisms may underlie the platelet response to uremia and entail the development of platelet-related complications in CKD.
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21

Jandosov, J. M., L. I. Mikhalovska, C. A. Howell, D. I. Chenchik, B. K. Kosher, S. B. Lyubchik, J. Silvestre-Albero, et al. "Synthesis, Morphostructure, Surface Chemistry and Preclinical Studies of Nanoporous Rice Husk-Derived Biochars for Gastrointestinal Detoxification." Eurasian Chemico-Technological Journal 19, no. 4 (December 29, 2017): 303. http://dx.doi.org/10.18321/ectj678.

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This article summarizes the methodology of synthesis, surface functionalization and structural properties of rice husk-derived nanostructured carbon enterosorbents (biochars) in connection with the preliminary in vitro study results of uraemic toxin adsorption in model experiments, as well as preclinical trials in vivo. The obtained nanostructured carbon sorbents were studied using a number of modern physicochemical methods of investigation: low-temperature nitrogen adsorption, isotherms recording and calculation of the specific surface area, pore volumes were carried out using the Autosorb-1 "Quantachrome" device. Scanning electron microscopy and EDS-analysis. Mercury intrusion porosimetry analysis of the ACs were accomplished using "Quantachrome Poremaster" data analysis software. In vitro adsorption results assessed by use of HPLC and UV-spectroscopy for the nanostructured carbon sorbents with respect to the investigated low-molecule toxins suggest that the rice husks-derived carbon enterosorbents modified with the functional groups are able to reduce clinically significant levels of uraemic toxins and are comparable to the commercial enterosorbents. Based on the results of the comparative analysis for biocompatibility of canine kidney epithelial cells it was determined that the samples of the modified sorbents CRH-P-450 and CRH-475-KOH-850-N do not exhibit cytotoxicity in comparison with the commercial carbon enterosorbent «Adsorbix Extra». According to the results of the in vivo studies, it was determined that there was a positive effect of the enterosorbent CRH-P-450 on uremia and intoxication.
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22

Van Assche, Irthe, Eva Schepers, Wim Van Biesen, Griet Glorieux, and Anneleen Pletinck. "SP269EXPLORING THE MECHANISMS LINKING URAEMIC TOXINS TO ENDOTHELIAL GLYCOCALYX DEGRADATION." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii197. http://dx.doi.org/10.1093/ndt/gfx145.sp269.

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23

Sakata, K., K. Kashiwagi, S. Sharmin, S. Ueda, and K. Igarashi. "Acrolein produced from polyamines as one of the uraemic toxins." Biochemical Society Transactions 31, no. 2 (April 1, 2003): 371–74. http://dx.doi.org/10.1042/bst0310371.

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It is well known that the addition of spermine or spermidine to culture medium containing ruminant serum inhibits cellular proliferation. This effect is caused by the products of oxidation of polyamines that are generated by serum amine oxidase. Among the products, we found that acrolein is a major toxic compound produced from spermine and spermidine by amine oxidase. We then analysed the level of polyamines (putrescine, spermidine and spermine) and amine oxidase activity in plasma of patients with chronic renal failure. It was found that the levels of putrescine and the amine oxidase activity were increased, whereas spermidine and spermine were decreased in plasma of patients with chronic renal failure. The levels of free and protein-conjugated acrolein were also increased in plasma of patients with chronic renal failure. An increase in putrescine, amine oxidase and acrolein in plasma was observed in all cases such as diabetic nephropathy, chronic glomerulonephritis and nephrosclerosis. These results suggest that acrolein is produced during the early stage of nephritis through kidney damage and also during uraemia through accumulation of polyamines in blood due to the decrease in their excretion into urine.
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24

Popławska, Magdalena, and Hanna Krawczyk. "Uraemic Toxins Generated in the Presence of FullereneC60, Carbon-Encapsulated Magnetic Nanoparticles, and Multiwalled Carbon Nanotubes." BioMed Research International 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/168512.

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Uraemic toxins—creatol and N-methylguanidine—are generated in conversion of creatinine in water in the presence of various forms of carbon such as fullerene C60, carbon-encapsulated magnetic nanoparticles, and multiwalled carbon nanotubes and oxygen. The conversion degree for creatinine was different for fullerene C60, CEMNPs, and MWCNTs and was 9% (3.6% creatol, 5.4% N-methylguanidine), 35% (12% creatol, 23% N-methylguanidine), and 75% (16% creatol, 59% N-methylguanidine), respectively.
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25

Locatelli, F., and R. Minutolo. "Intestinal adsorption of uraemic toxins: a new strategy for anaemia management?" Nephrology Dialysis Transplantation 29, no. 9 (May 2, 2014): 1620–24. http://dx.doi.org/10.1093/ndt/gfu102.

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26

Rroji, Merita, Sunny Eloot, Annemie Dhondt, Wim Van Biesen, Griet Glorieux, Nathalie Neirynck, Nele Vandennoortgate, Sophie Liabeuf, Ziad Massy, and Raymond Vanholder. "Association of advanced age with concentrations of uraemic toxins in CKD." Journal of Nephrology 29, no. 1 (April 10, 2015): 81–91. http://dx.doi.org/10.1007/s40620-015-0195-z.

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27

Lin, C. J., C. J. Wu, C. F. Pan, Y. C. Chen, F. J. Sun, and H. H. Chen. "Serum protein-bound uraemic toxins and clinical outcomes in haemodialysis patients." Nephrology Dialysis Transplantation 25, no. 11 (May 13, 2010): 3693–700. http://dx.doi.org/10.1093/ndt/gfq251.

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28

Garikapati, Kartheek, Daniel Goh, Shaun Khanna, and Krishna Echampati. "Uraemic Cardiomyopathy: A Review of Current Literature." Clinical Medicine Insights: Cardiology 15 (January 2021): 117954682199834. http://dx.doi.org/10.1177/1179546821998347.

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Uraemic Cardiomyopathy (UC) is recognised as an intricate and multifactorial disease which portends a significant burden in patients with End-Stage Renal Disease (ESRD). The cardiovascular morbidity and mortality associated with UC is significant and can be associated with the development of arrythmias, cardiac failure and sudden cardiac death (SCD). The pathophysiology of UC involves a complex interplay of traditional implicative factors such as haemodynamic overload and circulating uraemic toxins as well as our evolving understanding of the Chronic Kidney Disease-Mineral Bone Disease pathway. There is an instrumental role for multi-modality imaging in the diagnostic process; including transthoracic echocardiography and cardiac magnetic resonance imaging in identifying the hallmarks of left ventricular hypertrophy and myocardial fibrosis that characterise UC. The appropriate utilisation of the aforementioned diagnostics in the ESRD population may help guide therapeutic approaches, such as pharmacotherapy including beta-blockers and aldosterone-antagonists as well as haemodialysis and renal transplantation. Despite this, there remains limitations in effective therapeutic interventions for UC and ongoing research on a cellular level is vital in establishing further therapies.
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29

Ferraz, Natalia, Daniel O. Carlsson, Jaan Hong, Rolf Larsson, Bengt Fellström, Leif Nyholm, Maria Strømme, and Albert Mihranyan. "Haemocompatibility and ion exchange capability of nanocellulose polypyrrole membranes intended for blood purification." Journal of The Royal Society Interface 9, no. 73 (February 2012): 1943–55. http://dx.doi.org/10.1098/rsif.2012.0019.

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Composites of nanocellulose and the conductive polymer polypyrrole (PPy) are presented as candidates for a new generation of haemodialysis membranes. The composites may combine active ion exchange with passive ultrafiltration, and the large surface area (about 80 m 2 g −1 ) could potentially provide compact dialysers. Herein, the haemocompatibility of the novel membranes and the feasibility of effectively removing small uraemic toxins by potential-controlled ion exchange were studied. The thrombogenic properties of the composites were improved by applying a stable heparin coating. In terms of platelet adhesion and thrombin generation, the composites were comparable with haemocompatible polymer polysulphone, and regarding complement activation, the composites were more biocompatible than commercially available membranes. It was possible to extract phosphate and oxalate ions from solutions with physiological pH and the same tonicity as that of the blood. The exchange capacity of the materials was found to be 600 ± 26 and 706 ± 31 μmol g −1 in a 0.1 M solution (pH 7.4) and in an isotonic solution of phosphate, respectively. The corresponding values with oxalate were 523 ± 5 in a 0.1 M solution (pH 7.4) and 610 ± 1 μmol g −1 in an isotonic solution. The heparinized PPy–cellulose composite is consequently a promising haemodialysis material, with respect to both potential-controlled extraction of small uraemic toxins and haemocompatibility.
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30

Ammon, A. "Surveillance of enterohaemorrhagic E. coli (EHEC) infections and haemolytic uraemic syndrome (HUS) in Europe." Eurosurveillance 2, no. 12 (December 1, 1997): 91–96. http://dx.doi.org/10.2807/esm.02.12.00133-en.

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Since they were first described, Escherichia coliO157: H7 and other related enterohaemorrhagic E. coli(EHEC) have become known as a major infectious cause of bloody diarrhoea. These E. coliproduce one or more shiga-toxins (stx) or Vero cytotoxins. Strictl
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31

Liu, Shan, Suree Lekawanvijit, Andrew R. Kompa, Bing H. Wang, Darren J. Kelly, and Henry Krum. "Cardiorenal syndrome: Pathophysiology, preclinical models, management and potential role of uraemic toxins." Clinical and Experimental Pharmacology and Physiology 39, no. 8 (July 25, 2012): 692–700. http://dx.doi.org/10.1111/j.1440-1681.2011.05632.x.

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32

Deltombe, Olivier, Henriette de Loor, Griet Glorieux, Annemieke Dhondt, Wim Van Biesen, Björn Meijers, and Sunny Eloot. "MP310EXPLORING BINDING CHARACTERISTICS AND RELATED COMPETITION OF DIFFERENT PROTEIN-BOUND URAEMIC TOXINS." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii539—iii540. http://dx.doi.org/10.1093/ndt/gfx168.mp310.

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33

Vanholder, R., S. V. Laecke, F. Verbeke, G. Glorieux, and W. V. Biesen. "Uraemic toxins and cardiovascular disease: in vitro research versus clinical outcome studies." Clinical Kidney Journal 1, no. 1 (December 19, 2007): 2–10. http://dx.doi.org/10.1093/ndtplus/sfm024.

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34

Joossens, Marie, Karoline Faust, Tessa Gryp, Anh Thi Loan Nguyen, Jun Wang, Sunny Eloot, Eva Schepers, et al. "Gut microbiota dynamics and uraemic toxins: one size does not fit all." Gut 68, no. 12 (November 21, 2018): 2257.1–2260. http://dx.doi.org/10.1136/gutjnl-2018-317561.

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35

Yokozawa, Takako, Koji Fujioka, Hikokichi Oura, Takashi Tanaka, Gen-Ichiro Nonaka, and Itsuo Nishioka. "Decrease in uraemic toxins, a newly found beneficial effect of Ephedrae Herba." Phytotherapy Research 9, no. 5 (August 1995): 382–84. http://dx.doi.org/10.1002/ptr.2650090516.

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36

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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37

Griener, Thomas P., George L. Mulvey, Paola Marcato, and Glen D. Armstrong. "Differential binding of Shiga toxin 2 to human and murine neutrophils." Journal of Medical Microbiology 56, no. 11 (November 1, 2007): 1423–30. http://dx.doi.org/10.1099/jmm.0.47282-0.

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Shiga toxins (Stx1 and Stx2) are responsible for initiating haemolytic uraemic syndrome, a serious extraintestinal complication caused by enterohaemorrhagic Escherichia coli O157 : H7 infection in humans. Shiga toxins are classical AB5-type exotoxins, consisting of a globotriaosylceramide (Gb3)-binding B subunit pentamer and an enzymic A subunit. It is demonstrated in this study that Stx2 binds to human neutrophils by a non-classical mechanism that is independent of Gb3. In contrast, the investigation revealed that Stx2 binds to murine neutrophils by the classical Gb3-dependent mechanism. Moreover, whereas the human serum amyloid P (HuSAP) component inhibited Stx2 binding to murine neutrophils, HuSAP increased Stx2 binding to human neutrophils by 84.2 % (P≤0.002, Student's t-test). These observations may explain why HuSAP protects mice from the lethal effects of Stx2, whereas there is no indication that HuSAP plays a similar protective role in humans infected by E. coli O157 : H7.
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38

Motojima, Masaru, Atsuko Hosokawa, Hideyuki Yamato, Takamura Muraki, and Toshimasa Yoshioka. "Uraemic toxins induce proximal tubular injury via organic anion transporter 1-mediated uptake." British Journal of Pharmacology 135, no. 2 (January 2002): 555–63. http://dx.doi.org/10.1038/sj.bjp.0704482.

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39

Sarnatskaya, Veronika V., W. Edward Lindup, Adrej I. Ivanov, Larisa A. Yushko, John Tjia, Vitaly N. Maslenny, Natalia M. Gurina, and Vladimir G. Nikolaev. "Extraction of Uraemic Toxins with Activated Carbon Restores the Functional Properties of Albumin." Nephron Physiology 95, no. 1 (2003): p10—p18. http://dx.doi.org/10.1159/000073024.

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40

Kandouz, Sakina, Ali Shendi Mohamed, Yishan Zheng, Susan Sandeman, and Andrew Davenport. "Reduced protein bound uraemic toxins in vegetarian kidney failure patients treated by haemodiafiltration." Hemodialysis International 20, no. 4 (April 4, 2016): 610–17. http://dx.doi.org/10.1111/hdi.12414.

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41

Macías, Nicolás, Soraya Abad, Inés Aragoncillo, Andrés Hernández, Esther Torres, Alba Santos, Juan Manuel López Gómez, José Luño, and Almudena Vega. "Body composition influences the elimination of protein-bound uraemic toxins in online haemodiafiltration." Nefrología (English Edition) 39, no. 4 (July 2019): 434–36. http://dx.doi.org/10.1016/j.nefroe.2018.09.005.

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42

Sarnatskaya, Veronika V., W. Edward Lindup, Toshimitsu Niwa, Andrey I. Ivanov, Larisa A. Yushko, John Tjia, Vitaly N. Maslenny, Ludmila N. Korneeva, and Vladimir G. Nikolaev. "Effect of protein-bound uraemic toxins on the thermodynamic characteristics of human albumin." Biochemical Pharmacology 63, no. 7 (April 2002): 1287–96. http://dx.doi.org/10.1016/s0006-2952(02)00869-9.

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43

Vanholder, R. "The ultimate salt war? Uraemic toxins are all that count in dialysis patients." Nephrology Dialysis Transplantation 27, no. 1 (January 1, 2012): 62–66. http://dx.doi.org/10.1093/ndt/gfr637.

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44

JöRstad, S., and S. Kvernes. "URAEMIC TOXINS OF HIGH MOLECULAR WEIGHT INHIBITING HUMAN MONONUCLEAR PHAGOCYTES CULTURED IN VITRO." Acta Pathologica Microbiologica Scandinavica Section C Immunology 86C, no. 1-6 (August 15, 2009): 221–26. http://dx.doi.org/10.1111/j.1699-0463.1978.tb02584.x.

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45

Sandeman, Susan R., Carol A. Howell, Gary J. Phillips, Yishan Zheng, Guy Standen, Robert Pletzenauer, Andrew Davenport, et al. "An adsorbent monolith device to augment the removal of uraemic toxins during haemodialysis." Journal of Materials Science: Materials in Medicine 25, no. 6 (February 27, 2014): 1589–97. http://dx.doi.org/10.1007/s10856-014-5173-9.

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46

Vila Cuenca, Marc, Peter L. Hordijk, and Marc G. Vervloet. "Most exposed: the endothelium in chronic kidney disease." Nephrology Dialysis Transplantation 35, no. 9 (April 8, 2019): 1478–87. http://dx.doi.org/10.1093/ndt/gfz055.

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Abstract Accumulating evidence indicates that the pathological changes of the endothelium may contribute to the development of cardiovascular complications in chronic kidney disease (CKD). Non-traditional risk factors related to CKD are associated with the incidence of cardiovascular disease, but their role in uraemic endothelial dysfunction has often been disregarded. In this context, soluble α-Klotho and vitamin D are of importance to maintain endothelial integrity, but their concentrations decline in CKD, thereby contributing to the dysfunction of the endothelial lining. These hormonal disturbances are accompanied by an increment of circulating fibroblast growth factor-23 and phosphate, both exacerbating endothelial toxicities. Furthermore, impaired renal function leads to an increment of inflammatory mediators, reactive oxygen species and uraemic toxins that further aggravate the endothelial abnormalities and in turn also inhibit the regeneration of disrupted endothelial lining. Here, we highlight the distinct endothelial alterations mediated by the abovementioned non-traditional risk factors as demonstrated in experimental studies and connect these to pathological changes in CKD patients, which are driven by endothelial disturbances, other than atherosclerosis. In addition, we describe therapeutic strategies that may promote restoration of endothelial abnormalities by modulating imbalanced mineral homoeostasis and attenuate the impact of uraemic retention molecules, inflammatory mediators and reactive oxygen species. A clinical perspective on endothelial dysfunction in CKD may translate into reduced structural and functional abnormalities of the vessel wall in CKD, and ultimately improved cardiovascular disease.
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47

El Amouri, Amina, Evelien Snauwaert, Aurélie Foulon, Charlotte Vande Moortel, Maria Van Dyck, Koen Van Hoeck, Nathalie Godefroid, et al. "Dietary Fibre Intake Is Associated with Serum Levels of Uraemic Toxins in Children with Chronic Kidney Disease." Toxins 13, no. 3 (March 19, 2021): 225. http://dx.doi.org/10.3390/toxins13030225.

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Imbalanced colonic microbial metabolism plays a pivotal role in generating protein-bound uraemic toxins (PBUTs), which accumulate with deteriorating kidney function and contribute to the uraemic burden of children with chronic kidney disease (CKD). Dietary choices impact the gut microbiome and metabolism. The aim of this study was to investigate the relation between dietary fibre and gut-derived PBUTs in paediatric CKD. Sixty-one (44 male) CKD children (9 ± 5 years) were prospectively followed for two years. Dietary fibre intake was evaluated by either 24-h recalls (73%) or 3-day food records (27%) at the same time of blood sampling for assessment of total and free serum levels of different PBUTs using liquid chromatography. We used linear mixed models to assess associations between fibre intake and PBUT levels. We found an inverse association between increase in fibre consumption (g/day) and serum concentrations of free indoxyl sulfate (−3.1% (−5.9%; −0.3%) (p = 0.035)), free p-cresyl sulfate (−2.5% (−4.7%; −0.3%) (p = 0.034)), total indole acetic acid (IAA) (−1.6% (−3.0%; −0.3%) (p = 0.020)), free IAA (−6.6% (−9.3%; −3.7%) (p < 0.001)), total serum p-cresyl glucuronide (pCG) (−3.0% (−5.6%; −0.5%) (p = 0.021)) and free pCG levels (−3.3% (−5.8%; −0.8%) (p = 0.010)). The observed associations between dietary fibre intake and the investigated PBUTs highlight potential benefits of fibre intake for the paediatric CKD population. The present observational findings should inform and guide adaptations of dietary prescriptions in children with CKD.
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48

Ponticelli, Claudio, and Mariarosaria Campise. "COVID-19 Vaccination in Kidney Transplant Candidates and Recipients." Vaccines 10, no. 11 (October 27, 2022): 1808. http://dx.doi.org/10.3390/vaccines10111808.

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Kidney transplant candidates and kidney transplant recipients (KTRs) are at particular risk of severe complications of COVID-19 disease. In Western countries, mortality in affected hospitalized KTRs ranges between 19% and 50%. COVID-19 vaccination remains the most important measure to prevent the severity of infection in candidates and recipients of kidney transplant. However, the uraemic condition may affect the vaccine-induced immunity in patients with advanced chronic kidney disease (CKD) and in KTRs. Retention of uraemic toxins, dysbiosis, dysmetabolism, and dialysis can diminish the normal response to vaccination, leading to dysfunction of inflammatory and immune cells. In KTRs the efficacy of vaccines may be reduced by the immunosuppressive medications, and more than half of kidney transplant recipients are unable to build an immune response even after four administrations of anti-COVID-19 vaccines. The lack of antibody response leaves these patients at high risk for SARS-CoV-2 infection and severe COVID-19 disease. The aim of the present review is to focus on the main reasons for the impaired immunological response among candidates and kidney transplant recipients and to highlight some of the present options available to solve the problem.
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49

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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50

Deltombe, Olivier, Annemie Dhondt, Griet Glorieux, Wim Van Biesen, and Sunny Eloot. "FP245EXPLORING MECHANISMS OF PROTEIN BINDING OF URAEMIC TOXINS IN CKD2-5 AND HAEMODIALYSIS PATIENTS." Nephrology Dialysis Transplantation 30, suppl_3 (May 2015): iii149. http://dx.doi.org/10.1093/ndt/gfv173.27.

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