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Toxins
Special Issues
Uremic Toxins and Hemodialysis: Mechanisms, Challenges, and Therapeutic Advances
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Uremic Toxins and Hemodialysis: Mechanisms, Challenges, and Therapeutic Advances

A special issue of Toxins (ISSN 2072-6651).

Deadline for manuscript submissions: 31 October 2026 | Viewed by 5364

Editors

Prof. Dr. Joëlle Nortier

E-Mail Website
Guest Editor
1. Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium
2. Nephrology & Dialysis Department, University Hospital Brugmann, Université Libre de Bruxelles, 4 Place Van Gehuchten, 1020 Brussels, Belgium
Interests: toxic nephropathies; renal fibrosis; end-stage kidney disease; renal replacement therapies; tubular and endothelial dysfunctions
Prof. Dr. Marie-Hélène Antoine

E-Mail Website
Guest Editor
Laboratory of Experimental Nephrology, Faculty of Medicine, Université Libre de Bruxelles, Erasme Campus, 808 Route de Lennik, 1070 Brussels, Belgium
Interests: uremic toxins; oxidative stress; renal cell cultures; tubulo–endothelial cell cross-talk

Special Issue Information

Dear Colleagues,

Hemodialysis (HD) is the world's most widely used renal replacement therapy for the management of end-stage kidney disease. Despite technological advances, plasma depuration performances remain limited and the accumulation of unremoved uremic toxins is still a major unsolved problem. In addition to the acute phase of potentially reversible renal damage, the transition to a chronic phase may be unavoidable. Moreover, because of the comorbidities frequently associated with advanced age (diabetes, hypertension, cardiovascular disease, overweight, dyslipidemia, smoking, etc.), access to transplantation will not be possible for the vast majority of patients worldwide.

Research is therefore still needed to better understand the key pathophysiological mechanisms behind the deleterious impact of uremic toxins on oxidative stress, endothelial dysfunction, and alterations to the microbiota, among other issues. Indeed, the therapeutic strategies depend on such research—whether they be medicinal or dietary, or combined with more sophisticated purification techniques. More than ever, an interdisciplinary approach to basic and clinical research on HD patients is crucial to improve the currently unfavorable overall prognosis linked to the numerous multi-systemic consequences.

This Special Issue aims to bring together as many varied contributions as possible in this field.

Prof. Dr. Joëlle Nortier
Prof. Dr. Marie-Hélène Antoine
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • end-stage kidney disease
  • hemodialysis/hemodiafiltration
  • uremic toxins
  • endothelial dysfunction
  • gut microbiome

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Published Papers (3 papers)

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Research

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15 pages, 4529 KB  
Article
Effect of Dietary Aryl Hydrocarbon Receptor Ligands on Indoxyl Sulfate-Induced Endothelial Activation
by Flora Lefevre, Rania Chermiti, Julien Cebile, Nathalie McKay, Stanislas Bataille, Stéphane Burtey and Laetitia Dou
Toxins 2026, 18(7), 298; https://doi.org/10.3390/toxins18070298 - 10 Jul 2026
Viewed by 389
Abstract
Patients with chronic kidney disease (CKD) are exposed to high levels of uremic toxins and have an increased risk of cardiovascular disease. Among these toxins, indolic compounds such as indoxyl sulfate (IS) are predictors of cardiovascular events and mortality in CKD patients and [...] Read more.
Patients with chronic kidney disease (CKD) are exposed to high levels of uremic toxins and have an increased risk of cardiovascular disease. Among these toxins, indolic compounds such as indoxyl sulfate (IS) are predictors of cardiovascular events and mortality in CKD patients and induce a procoagulant and proinflammatory vascular phenotype through activation of the aryl hydrocarbon receptor (AhR). Targeting AhR activation by indolic toxins may therefore help prevent cardiovascular complications in CKD. To this end, we investigated in vitro whether natural dietary AhR ligands (galangin, quercetin, curcumin and indole-3-carbinol) could antagonize IS-induced AhR activation and the associated inflammatory response in endothelial cells. The activation of the AhR genomic pathway was assessed by measuring the expression of AhR target genes (CYP1A1, CYP1B1, and AHRR) in endothelial cells and by evaluating AhR-dependent transcriptional activity using a CALUX-AHRE luciferase reporter assay in HG40/6 cells. In parallel, endothelial inflammation was evaluated by analyzing the expression of AhR-related inflammatory genes: F3/tissue factor, PTGS2/COX-2, CCL2/MCP-1, and CXCL8/IL-8. Quercetin was the only ligand capable of antagonizing IS-induced AhR transcriptional activity, as well as the upregulation of the endothelial AhR target genes CYP1A1 and CYP1B1. In contrast, galangin, curcumin, and I3C exhibited no inhibitory effects. Moreover, none of the tested dietary AhR ligands suppressed the IS-induced upregulation of endothelial inflammatory genes; instead, they tended to potentiate IS-induced inflammatory responses at high concentrations. In conclusion, among the AhR ligands tested, quercetin was the only one that attenuated IS-induced activation of the AhR genomic pathway in endothelial cells. However, it may also enhance IS-mediated endothelial inflammation, an effect also observed at specific concentrations of galangin, curcumin, and I3C. These findings suggest that the potential beneficial effects of natural dietary AhR ligands should be carefully considered in the context of CKD patients exhibiting high levels of indolic uremic toxins. Full article
(This article belongs to the Special Issue Uremic Toxins and Hemodialysis: Mechanisms, Challenges, and Therapeutic Advances)
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14 pages, 1112 KB  
Article
Furosemide and the Symptom Burden: The Potential Mediating Role of Uremic Toxins in Patients with CKD
by Margaux Costes-Albrespic, Sophie Liabeuf, Islam-Amine Larabi, Solène M. Laville, Bénédicte Stengel, Abdou Y. Omorou, Luc Frimat, Jean-Claude Alvarez, Ziad A. Massy, Natalia Alencar de Pinho and the CKD-REIN Study Group
Toxins 2025, 17(11), 541; https://doi.org/10.3390/toxins17110541 - 1 Nov 2025
Cited by 1 | Viewed by 1841
Abstract
Furosemide appears to contribute to the accumulation of protein-bound uremic toxins (PBUTs) and to induce adverse drug reactions. We investigated the extent to which the association between the furosemide dose and serum PBUT concentrations mediates the relationship between the furosemide dose and the [...] Read more.
Furosemide appears to contribute to the accumulation of protein-bound uremic toxins (PBUTs) and to induce adverse drug reactions. We investigated the extent to which the association between the furosemide dose and serum PBUT concentrations mediates the relationship between the furosemide dose and the symptom burden in patients with chronic kidney disease (CKD). This cross-sectional analysis included patients with CKD stages 2 to 5 from the CKD-REIN cohort and with data on the baseline serum concentrations of the free fractions of indoxyl sulphate (IS), kynurenine (KYN), p-cresyl sulphate (PCS), and indole-3-acetic acid (IAA), as measured by liquid chromatography–tandem mass spectrometry. The symptom burden was also assessed with a modified (8-item) symptom subscale from the Kidney Disease Quality of Life-36 (e.g., muscle soreness, cramps, itchy skin, dry skin, dizziness, appetite, numbness, and nausea). We used beta regressions to model the association between the furosemide dose and the symptom burden and used structural equation models to quantify the mediating effect of PBUT on this association. Among the 2053 included patients (males: 66%, median age: 68; mean estimated glomerular filtration rate: 35 mL/min/1.73 m2), those prescribed high-dose furosemide (>120 mg/day) had higher symptom burden than those not prescribed furosemide (i.e., a 5.67-point lower symptom score, 95%CI 1.41–9.93). The sum of PBUTs explained 3.78% (95%CI 0.10–18.01%) of this association. Similar results were observed for IS, KYN, and IAA, considered separately, but not for PCS, whose estimated mediation effect was nearly null. Although high-dose furosemide was associated with a greater symptom burden in patients with CKD, mediation by PBUT accumulation appeared to be minimal. Full article
(This article belongs to the Special Issue Uremic Toxins and Hemodialysis: Mechanisms, Challenges, and Therapeutic Advances)
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Review

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27 pages, 1328 KB  
Review
Uremic Toxins and the Lung Alveolar Capillary Barrier: A Narrative Review
by Saleh Kaysi, Maxime Taghavi, Alissa El Mourabi, Marie-Hélène Antoine, Eric De Prez and Joëlle Nortier
Toxins 2026, 18(3), 126; https://doi.org/10.3390/toxins18030126 - 2 Mar 2026
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Abstract
Introduction: Uremic toxins have been shown to cause adverse pulmonary effects by inducing endothelial and epithelial dysfunction, disrupting the alveolar-capillary barrier, and increasing inflammation and oxidative stress. This article reviews these effects with a specific focus on chronic kidney disease and the mechanisms [...] Read more.
Introduction: Uremic toxins have been shown to cause adverse pulmonary effects by inducing endothelial and epithelial dysfunction, disrupting the alveolar-capillary barrier, and increasing inflammation and oxidative stress. This article reviews these effects with a specific focus on chronic kidney disease and the mechanisms by which uremic toxins affect lung tissue. Methods: A narrative review was conducted using keywords related to uremic toxins and lung injury to search the PubMed database. An advanced literature review was conducted in PubMed to identify studies explaining the mechanisms underlying lung pathophysiology in chronic kidney disease (CKD), with particular focus on CKD-induced pulmonary epithelial and endothelial dysfunction. Additionally, to highlight the pathological processes of lung congestion in CKD, studies on CKD-induced dysfunction of the alveolar-capillary barrier were retrieved. Studies published up to November 2025 were evaluated. Results: A total of 148 articles were reviewed in full text. Uremic toxins negatively impact lung tissue structure and function through multiple mechanisms, including oxidative stress, inflammation, and direct effects. Uremic toxins appear to share signaling pathways in endothelial cells, including those linked to Mitogen-activated protein kinases (MAPK), the Aryl Hydrocarbon Receptor (AhR), the receptor for advanced glycation end products (RAGE), and pro-inflammatory transcription factors such as nuclear factor κB (NF-κB). Additionally, oxidative stress acts as a pro-inflammatory signal shared by several uremic toxins. The mechanisms behind the harmful interactions between CKD and lung disease are mostly unknown, although more evidence exists for acute kidney injury (AKI). Conclusions: Chronic kidney disease, which leads to the buildup of uremic toxins, negatively affects the lungs. Overall, the accumulation of uremic toxins in CKD impairs endothelial and epithelial cells and the alveolar capillary barrier. Further research is needed to understand the specific mechanisms underlying these effects and to identify therapeutic options to protect the lungs in these patients. Full article
(This article belongs to the Special Issue Uremic Toxins and Hemodialysis: Mechanisms, Challenges, and Therapeutic Advances)
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