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Toxins
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The Role of Uremic Toxins in Comorbidities of Chronic Kidney...
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The Role of Uremic Toxins in Comorbidities of Chronic Kidney Disease

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Uremic Toxins".

Deadline for manuscript submissions: 20 June 2025 | Viewed by 2122

Special Issue Editor

Prof. Dr. Suguru Yamamoto

E-Mail Website
Guest Editor
Division of Clinical Nephrology and Rheumatology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan
Interests: clinical study about uremic toxins-related disease; basic study about uremic toxins-related functional abnormalities of macrophages
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The number of patients with chronic kidney disease (CKD) has increased worldwide. Although treatments to slow the progression of CKD and address CKD-related systemic disorders have advanced, the mortality risk for CKD patients, particularly those on dialysis, remains high. Additionally, both physical activity and quality of life are impaired in CKD patients, especially those undergoing dialysis treatment. Given the association between longer dialysis duration and the onset of frailty, it is crucial to identify and address unknown and unresolved CKD-related factors and develop new treatment strategies.

While uremic toxins are becoming more recognized in kidney disease research, our understanding of the pathophysiology is still insufficient. Moreover, the routine monitoring of blood toxin levels has not yet been implemented in daily clinical practice.

This Special Issue, titled "The Role of Uremic Toxins in Comorbidities of Chronic Kidney Disease", aims to explore the roles of uremic toxins in CKD-related systemic disorders and their treatment. We welcome submissions on basic research that evaluates any uremic toxins in CKD-related systemic diseases, clinical studies that assess the role of these toxins in clinical outcomes, and therapeutic strategies aimed at countering their toxicity.

Prof. Dr. Suguru Yamamoto
Guest Editor

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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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

  • uremic toxins
  • chronic kidney disease
  • hemodialysis
  • blood purification
  • frailty
  • mortality
  • cardiovascular
  • fracture
  • infection
  • pruritus
  • cognitive disorder

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Published Papers (2 papers)

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Research

16 pages, 1769 KiB  
Article
The Role of Indoxyl Sulfate in Exacerbating Colorectal Cancer During Chronic Kidney Disease Progression: Insights into the Akt/β-Catenin/c-Myc and AhR/c-Myc Pathways in HCT-116 Colorectal Cancer Cells
by Yu Ichisaka, Chihiro Takei, Kazuma Naito, Manami Higa, Shozo Yano, Toshimitsu Niwa and Hidehisa Shimizu
Toxins 2025, 17(1), 17; https://doi.org/10.3390/toxins17010017 - 1 Jan 2025
Viewed by 898
Abstract
Epidemiological studies suggest an increased risk of colorectal cancer (CRC) aggravation in patients with chronic kidney disease (CKD). Our previous study demonstrated that indoxyl sulfate, a uremic toxin whose concentration increases with CKD progression, exacerbates CRC through activation of the AhR and Akt [...] Read more.
Epidemiological studies suggest an increased risk of colorectal cancer (CRC) aggravation in patients with chronic kidney disease (CKD). Our previous study demonstrated that indoxyl sulfate, a uremic toxin whose concentration increases with CKD progression, exacerbates CRC through activation of the AhR and Akt pathways. Consequently, indoxyl sulfate has been proposed to be a significant link between CKD progression and CRC aggravation. The present study aimed to investigate the roles of c-Myc and β-Catenin, which are hypothesized to be downstream factors of indoxyl sulfate-induced AhR and Akt activation, in CRC cell proliferation and EGF sensitivity in HCT-116 CRC cells. Indoxyl sulfate significantly induced CRC cell proliferation at concentrations exceeding 62.5 µM, a process suppressed by the c-Myc inhibitor 10058-F4. Indoxyl sulfate activated the Akt/β-Catenin/c-Myc pathway as evidenced by the Akt inhibitor MK2206, which decreased both β-Catenin and c-Myc protein levels, and the β-Catenin inhibitor XAV-939, which reduced c-Myc protein levels. The AhR antagonist CH223191 also inhibited c-Myc upregulation, indicating involvement of the AhR/c-Myc pathway. MK2206 partially attenuated the indoxyl sulfate-induced AhR transcriptional activity, suggesting that Akt activation influences the AhR/c-Myc pathway. MK2206, CH223191, and 10058-F4 suppressed the increase in EGFR protein levels induced by indoxyl sulfate, indicating that the Akt/β-Catenin/c-Myc and AhR/c-Myc pathways enhance the sensitivity of HCT-116 CRC cells to EGF. These findings indicate that the elevation of indoxyl sulfate levels in the blood, due to CKD progression, could worsen CRC by promoting the proliferation of CRC cells and enhancing EGF signaling. Therefore, indoxyl sulfate could potentially serve as a therapeutic target for CRC aggravation in patients with CKD. Full article
(This article belongs to the Special Issue The Role of Uremic Toxins in Comorbidities of Chronic Kidney Disease)
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18 pages, 4767 KiB  
Article
The Ability of AST-120 to Lower the Serum Indoxyl Sulfate Level Improves Renal Outcomes and the Lipid Profile in Diabetic and Nondiabetic Animal Models of Chronic Kidney Disease: A Meta-Analysis
by Hande O. Altunkaynak, Eda Karaismailoglu and Ziad A. Massy
Toxins 2024, 16(12), 544; https://doi.org/10.3390/toxins16120544 - 16 Dec 2024
Viewed by 978
Abstract
The therapeutic benefit of the oral adsorbent drug AST-120 in chronic kidney disease (CKD) is related to an indoxyl sulfate (IS)-lowering action. Diabetes and dyslipidemia might worsen kidney damage in CKD. However, it is not known whether AST-120 influences lipid abnormalities as well [...] Read more.
The therapeutic benefit of the oral adsorbent drug AST-120 in chronic kidney disease (CKD) is related to an indoxyl sulfate (IS)-lowering action. Diabetes and dyslipidemia might worsen kidney damage in CKD. However, it is not known whether AST-120 influences lipid abnormalities as well as renal function in patients with CKD and diabetes. The objective of the present meta-analysis was to evaluate the efficacy of AST-120 treatment in CKD using data from preclinical studies. Mixed-effect or random-effect models were used to estimate the standardized mean difference (SMD) and the 95% confidence interval (CI). Publication bias was assessed with a funnel plot and Egger’s test. The potential influence of some variables (the dose and duration of AST-120 treatment, the animal species, and the CKD model’s diabetic status) was evaluated in subgroup analyses. Treatment with AST-120 was associated with a significantly lower IS level in animals with CKD (SMD = −1.75; 95% CI = −2.00, −1.49; p < 0.001). Significant improvements in markers of renal function and the lipid profile were also observed. In subgroup analyses of the cholesterol level, the diabetic status, the AST-120 dose, and the animal species were found to be influential factors. AST-120 lowered serum IS and triglyceride levels and improved renal function in animal models of CKD independent of diabetes status. However, AST-120’s ability to lower the total cholesterol level was more prominent in animals with diabetic CKD. Full article
(This article belongs to the Special Issue The Role of Uremic Toxins in Comorbidities of Chronic Kidney Disease)
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