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Toxins
Special Issues
Uremic Toxins and Organ Damage
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Uremic Toxins and Organ Damage

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

Deadline for manuscript submissions: closed (31 May 2023) | Viewed by 11930

Special Issue Editors

Prof. Dr. Bang-Gee Hsu

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Guest Editor
1. Division of Nephrology, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 97004, Taiwan
2. School of Medicine, Tzu Chi University, Hualien 97004, Taiwan
Interests: uremic toxins; arterial stiffness; endothelial function; vascular calcification; uremic sarcopenia; acute kidney injury
Special Issues, Collections and Topics in MDPI journals
Dr. Simone Vettoretti

E-Mail Website1 Website2
Guest Editor
Division of Nephrology Dialysis and Renal Transplantation Fondazione IRCCS Ca’ Granda Ospedale Maggiore Policlinico Milano, Milan, Italy
Interests: uremic toxins; cardiovascular disease; chronic renal disease progression; malnutrition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Uremic toxins can be defined as residues of organic compounds which cannot be excreted by the kidneys, and therefore accumulate in the systemic circulation and tissues, which hastens the progression of chronic kidney disease (CKD) and concomitant comorbidities. Uremic toxins are not fully known, but it is well established that they progressively increase in CKD, promoting several functional changes. In accordance with the European Uremic Toxins Working Group (EUTox) database, uremic toxins have been divided into three groups: small substances dissolved in water; medium-sized molecules: peptides and low-molecular-weight proteins; and protein-bound toxins. Although numerous uremic toxins have been identified to date and many of them are believed to play a role in the progression of organ damage, the pathophysiological mechanisms of uremic toxins must be investigated further in order to obtain a better understanding of their roles in organ damage or disease progression. The aim of this Special Issue is to offer a platform for both clinicians and basic researchers to present and discuss novel issues in the pathogenesis and treatment of uremic toxins associated with organ damage. We hope that all published papers will significantly contribute to a better understanding of uremic toxins associated with organ damage, and will be of benefit for suffering patients in the future.

Prof. Dr. Bang-Gee Hsu
Dr. Simone Vettoretti
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 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
  • Cardiovascular disease
  • Chronic kidney disease
  • Cerebrovascular disease
  • Gut microbiota
  • Malnutrition
  • Sarcopenia
  • CKD and mineral-bone disease

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Published Papers (5 papers)

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Research

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18 pages, 7807 KiB  
Article
The Uremic Toxin Indoxyl Sulfate Accelerates Senescence in Kidney Proximal Tubule Cells
by Yi Yang, Milos Mihajlovic, Manoe J. Janssen and Rosalinde Masereeuw
Toxins 2023, 15(4), 242; https://doi.org/10.3390/toxins15040242 - 25 Mar 2023
Cited by 7 | Viewed by 2032
Abstract
Kidney fibrosis is the common final pathway of nearly all chronic and progressive nephropathies. One cause may be the accumulation of senescent cells that secrete factors (senescence associated secretory phenotype, SASP) promoting fibrosis and inflammation. It has been suggested that uremic toxins, such [...] Read more.
Kidney fibrosis is the common final pathway of nearly all chronic and progressive nephropathies. One cause may be the accumulation of senescent cells that secrete factors (senescence associated secretory phenotype, SASP) promoting fibrosis and inflammation. It has been suggested that uremic toxins, such as indoxyl sulfate (IS), play a role in this. Here, we investigated whether IS accelerates senescence in conditionally immortalized proximal tubule epithelial cells overexpressing the organic anion transporter 1 (ciPTEC-OAT1), thereby promoting kidney fibrosis. Cell viability results suggested that the tolerance of ciPTEC-OAT1 against IS increased in a time-dependent manner at the same dose of IS. This was accompanied by SA-β-gal staining, confirming the accumulation of senescent cells, as well as an upregulation of p21 and downregulation of laminB1 at different time points, accompanied by an upregulation in the SASP factors IL-1β, IL-6 and IL-8. RNA-sequencing and transcriptome analysis revealed that IS accelerates senescence, and that cell cycle appears to be the most relevant factor during the process. IS accelerates senescence via TNF-α and NF-ĸB signalling early on, and the epithelial-mesenchymal transition process at later time points. In conclusion, our results suggest that IS accelerates cellular senescence in proximal tubule epithelial cells. Full article
(This article belongs to the Special Issue Uremic Toxins and Organ Damage)
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14 pages, 2113 KiB  
Article
Advanced Oxidation Protein Products Contribute to Chronic-Kidney-Disease-Induced Adipose Inflammation through Macrophage Activation
by Nanaka Arimura, Hiroshi Watanabe, Hiromasa Kato, Tadashi Imafuku, Takehiro Nakano, Miyu Sueyoshi, Mayuko Chikamatsu, Kai Tokumaru, Taisei Nagasaki, Hitoshi Maeda, Motoko Tanaka, Kazutaka Matsushita and Toru Maruyama
Toxins 2023, 15(3), 179; https://doi.org/10.3390/toxins15030179 - 26 Feb 2023
Cited by 4 | Viewed by 1989
Abstract
Fat atrophy and adipose tissue inflammation can cause the pathogenesis of metabolic symptoms in chronic kidney disease (CKD). During CKD, the serum levels of advanced oxidation protein products (AOPPs) are elevated. However, the relationship between fat atrophy/adipose tissue inflammation and AOPPs has remained [...] Read more.
Fat atrophy and adipose tissue inflammation can cause the pathogenesis of metabolic symptoms in chronic kidney disease (CKD). During CKD, the serum levels of advanced oxidation protein products (AOPPs) are elevated. However, the relationship between fat atrophy/adipose tissue inflammation and AOPPs has remained unknown. The purpose of this study was to investigate the involvement of AOPPs, which are known as uremic toxins, in adipose tissue inflammation and to establish the underlying molecular mechanism. In vitro studies involved co-culturing mouse-derived adipocytes (differentiated 3T3-L1) and macrophages (RAW264.7). In vivo studies were performed using adenine-induced CKD mice and AOPP-overloaded mice. Fat atrophy, macrophage infiltration and increased AOPP activity in adipose tissue were identified in adenine-induced CKD mice. AOPPs induced MCP-1 expression in differentiated 3T3-L1 adipocytes via ROS production. However, AOPP-induced ROS production was suppressed by the presence of NADPH oxidase inhibitors and the scavengers of mitochondria-derived ROS. A co-culturing system showed AOPPs induced macrophage migration to adipocytes. AOPPs also up-regulated TNF-α expression by polarizing macrophages to an M1-type polarity, and then induced macrophage-mediated adipose inflammation. In vitro data was supported by experiments using AOPP-overloaded mice. AOPPs contribute to macrophage-mediated adipose inflammation and constitute a potential new therapeutic target for adipose inflammation associated with CKD. Full article
(This article belongs to the Special Issue Uremic Toxins and Organ Damage)
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10 pages, 603 KiB  
Article
Indoxyl Sulfate Might Play a Role in Sarcopenia, While Myostatin Is an Indicator of Muscle Mass in Patients with Chronic Kidney Disease: Analysis from the RECOVERY Study
by Su Mi Lee, Mi Yeun Han, Su Hyun Kim, Ran Hui Cha, Seock Hui Kang, Jun Chul Kim and Won Suk An
Toxins 2022, 14(10), 660; https://doi.org/10.3390/toxins14100660 - 23 Sep 2022
Cited by 4 | Viewed by 1844
Abstract
Serum myostatin and indoxyl sulfate (IS) levels increase with kidney function decline and may function as uremic toxins in chronic kidney disease (CKD)-related sarcopenia. Herein, we analyzed the association between serum myostatin and IS levels and sarcopenia in patients with CKD, by performing [...] Read more.
Serum myostatin and indoxyl sulfate (IS) levels increase with kidney function decline and may function as uremic toxins in chronic kidney disease (CKD)-related sarcopenia. Herein, we analyzed the association between serum myostatin and IS levels and sarcopenia in patients with CKD, by performing a post hoc analysis of baseline data extracted from the RECOVERY study (clinicaltrials.gov: NCT03788252) of 150 patients with CKD. We stratified patients into two groups according to the median value of myostatin (cutoff 4.5 ng/mL) and IS levels (cutoff 0.365 mg/dL). The proportion of patients with sarcopenia was higher in those with high IS levels but lower in those with high myostatin levels. The skeletal muscle mass index (SMI) and handgrip strength (HGS) were significantly lower in patients with high IS levels but significantly higher in patients with high myostatin levels. IS levels showed a negative correlation with glomerular filtration rate (GFR), SMI, and HGS. However, myostatin levels were positively correlated with SMI and HGS, but not with GFR. Sarcopenia was independently associated with age and IS level after adjustment. Increased levels of serum total IS might play a role in sarcopenia, while increased levels of serum myostatin are associated with muscle mass in patients with CKD. Full article
(This article belongs to the Special Issue Uremic Toxins and Organ Damage)
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10 pages, 448 KiB  
Article
Serum P-Cresyl Sulfate Level Is an Independent Marker of Peripheral Arterial Stiffness as Assessed Using Brachial-Ankle Pulse Wave Velocity in Patients with Non-Dialysis Chronic Kidney Disease Stage 3 to 5
by Yu-Chi Chang, Yu-Li Lin, Yu-Hsien Lai, Chih-Hsien Wang and Bang-Gee Hsu
Toxins 2022, 14(4), 287; https://doi.org/10.3390/toxins14040287 - 16 Apr 2022
Viewed by 2205
Abstract
p-Cresyl sulfate (PCS) is a uremic toxin that causes cardiovascular injury and progression in patients with chronic kidney disease (CKD). Peripheral arterial stiffness (PAS) as measured using the brachial-ankle pulse wave velocity (baPWV) is considered a valuable predictor of cardiovascular event risk [...] Read more.
p-Cresyl sulfate (PCS) is a uremic toxin that causes cardiovascular injury and progression in patients with chronic kidney disease (CKD). Peripheral arterial stiffness (PAS) as measured using the brachial-ankle pulse wave velocity (baPWV) is considered a valuable predictor of cardiovascular event risk in the general population. The study investigated the correlation between serum PCS levels and PAS (baPWV > 18.0 m/s) in 160 patients with stage 3–5 CKD. Liquid chromatography–mass spectrometry was used to assay serum PCS levels. PAS was detected in 54 patients (33.8%), and it was linked to older age, a higher prevalence of hypertension, higher systolic and diastolic blood pressure, higher serum calcium–phosphorus product and PCS levels, and lower height and body weight. Multivariable logistic regression analysis for independent factors associated with PAS illustrated that, in addition to age and diastolic blood pressure, serum PCS levels exhibited an odds ratio (OR) of 1.098 (95% confidence interval = 1.029–1.171, p = 0.005). These findings demonstrated that serum PCS levels were associated with PAS among patients with stage 3–5 CKD. Full article
(This article belongs to the Special Issue Uremic Toxins and Organ Damage)
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Review

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14 pages, 582 KiB  
Review
The Role of Gut-Derived, Protein-Bound Uremic Toxins in the Cardiovascular Complications of Acute Kidney Injury
by Pauline Caillard, Youssef Bennis, Isabelle Six, Sandra Bodeau, Saïd Kamel, Gabriel Choukroun, Julien Maizel and Dimitri Titeca-Beauport
Toxins 2022, 14(5), 336; https://doi.org/10.3390/toxins14050336 - 11 May 2022
Cited by 6 | Viewed by 2988
Abstract
Acute kidney injury (AKI) is a frequent disease encountered in the hospital, with a higher incidence in intensive care units. Despite progress in renal replacement therapy, AKI is still associated with early and late complications, especially cardiovascular events and mortality. The role of [...] Read more.
Acute kidney injury (AKI) is a frequent disease encountered in the hospital, with a higher incidence in intensive care units. Despite progress in renal replacement therapy, AKI is still associated with early and late complications, especially cardiovascular events and mortality. The role of gut-derived protein-bound uremic toxins (PBUTs) in vascular and cardiac dysfunction has been extensively studied during chronic kidney disease (CKD), in particular, that of indoxyl sulfate (IS), para-cresyl sulfate (PCS), and indole-3-acetic acid (IAA), resulting in both experimental and clinical evidence. PBUTs, which accumulate when the excretory function of the kidneys is impaired, have a deleterious effect on and cause damage to cardiovascular tissues. However, the link between PBUTs and the cardiovascular complications of AKI and the pathophysiological mechanisms potentially involved are unclear. This review aims to summarize available data concerning the participation of PBUTs in the early and late cardiovascular complications of AKI. Full article
(This article belongs to the Special Issue Uremic Toxins and Organ Damage)
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