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Toxins
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Chronic Kidney Disease (CKD) Studies on Humans and Animals
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Chronic Kidney Disease (CKD) Studies on Humans and Animals

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

Deadline for manuscript submissions: closed (31 May 2021) | Viewed by 13253

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 noted increase in the number of patients with chronic kidney disease (CKD) is one of the biggest health problems in the world today. CKD is a risk factor not only for requirement of renal replacement therapy, but also for worse prognosis owing to CKD-related systemic disease. Kidney damage is induced by diabetes, hypertension, etc., and CKD-specific risk factors, including uremic toxins accelerate systemic disease, such as atherosclerosis, vascular calcification, and immunological disorders.

There are many studies aimed at understanding the pathophysiological aspect of CKD and the related systemic disorders, and recent findings suggest the impact of uremic toxins. Animal studies have shown the clear effect of uremic toxins on CKD and cardiovascular disease; however, recent clinical studies have produced controversial results on this topic. Thus, the next step is to fill the gap between basic and clinical research in CKD and its related diseases.

This Special Issue is titled ‘Chronic Kidney Disease (CKD) Studies on Humans and Animals’ focusing on understanding the pathophysiology of CKD and its related systemic disease. Both basic and clinical studies are welcomed, and we can discuss future tasks to prevent progression of CKD and its related systemic disease.

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

  • chronic kidney disease
  • uremic toxins
  • cardiovascular disease
  • diabetes
  • hypertension

Published Papers (5 papers)

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Research

13 pages, 3659 KiB  
Article
Cyclophilin D Promotes Acute, but Not Chronic, Kidney Injury in a Mouse Model of Aristolochic Acid Toxicity
by Khai Gene Leong, Elyce Ozols, John Kanellis, Frank Y. Ma and David J. Nikolic-Paterson
Toxins 2021, 13(10), 700; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13100700 - 01 Oct 2021
Cited by 3 | Viewed by 2053
Abstract
The plant-derived toxin, aristolochic acid (AA), is the cause of Chinese Herb Nephropathy and Balkan Nephropathy. Ingestion of high dose AA induces acute kidney injury, while chronic low dose ingestion leads to progressive kidney disease. Ingested AA is taken up by tubular epithelial [...] Read more.
The plant-derived toxin, aristolochic acid (AA), is the cause of Chinese Herb Nephropathy and Balkan Nephropathy. Ingestion of high dose AA induces acute kidney injury, while chronic low dose ingestion leads to progressive kidney disease. Ingested AA is taken up by tubular epithelial cells of the kidney, leading to DNA damage and cell death. Cyclophilin D (CypD) participates in mitochondrial-dependent cell death, but whether this mechanism operates in acute or chronic AA-induced kidney injury is unknown. We addressed this question by exposing CypD-/- and wild type (WT) mice to acute high dose, or chronic low dose, AA. Administration of 5 mg/kg AA to WT mice induced acute kidney injury 3 days later, characterised by loss of kidney function, tubular cell damage and death, and neutrophil infiltration. All of these parameters were significantly reduced in CypD-/- mice. Chronic low dose (2 mg/kg AA) administration in WT mice resulted in chronic kidney disease with impaired renal function and renal fibrosis by day 28. However, CypD-/- mice were not protected from AA-induced chronic kidney disease. In conclusion, CypD facilitates AA-induced acute kidney damage, but CypD does not contribute to the transition of acute kidney injury to chronic kidney disease during ongoing AA exposure. Full article
(This article belongs to the Special Issue Chronic Kidney Disease (CKD) Studies on Humans and Animals)
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15 pages, 5249 KiB  
Article
Evaluation of the Therapeutic Effects of Protocatechuic Aldehyde in Diabetic Nephropathy
by Yu-Teng Chang, Mu-Chi Chung, Chang-Chi Hsieh, Jeng-Jer Shieh and Ming-Ju Wu
Toxins 2021, 13(8), 560; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13080560 - 10 Aug 2021
Cited by 7 | Viewed by 2932
Abstract
Diabetic nephropathy (DN) is one of the most severe chronic kidney diseases in diabetes and is the main cause of end-stage renal disease (ESRD). Protocatechuic aldehyde (PCA) is a natural product with a variety of effects on pulmonary fibrosis. In this study, we [...] Read more.
Diabetic nephropathy (DN) is one of the most severe chronic kidney diseases in diabetes and is the main cause of end-stage renal disease (ESRD). Protocatechuic aldehyde (PCA) is a natural product with a variety of effects on pulmonary fibrosis. In this study, we examined the effects of PCA in C57BL/KS db/db male mice. Kidney morphology, renal function indicators, and Western blot, immunohistochemistry, and hematoxylin and eosin (H&E) staining data were analyzed. The results revealed that treatment with PCA could reduce diabetic-induced renal dysfunction, as indicated by the urine albumin-to-creatinine ratio (db/m: 120.1 ± 46.1μg/mg, db/db: 453.8 ± 78.7 µg/mg, db/db + 30 mg/kg PCA: 196.6 ± 52.9 µg/mg, db/db + 60 mg/kg PCA: 163.3 ± 24.6 μg/mg, p < 0.001). However, PCA did not decrease body weight, fasting plasma glucose, or food and water intake in db/db mice. H&E staining data revealed that PCA reduced glomerular size in db/db mice (db/m: 3506.3 ± 789.3 μm2, db/db: 6538.5 ± 1818.6 μm2, db/db + 30 mg/kg PCA: 4916.9 ± 1149.6 μm2, db/db + 60 mg/kg PCA: 4160.4 ± 1186.5 μm2p < 0.001). Western blot and immunohistochemistry staining indicated that PCA restored the normal levels of diabetes-induced fibrosis markers, such as transforming growth factor-beta (TGF-β) and type IV collagen. Similar results were observed for epithelial–mesenchymal transition-related markers, including fibronectin, E-cadherin, and α-smooth muscle actin (α-SMA). PCA also decreased oxidative stress and inflammation in the kidney of db/db mice. This research provides a foundation for using PCA as an alternative therapy for DN in the future. Full article
(This article belongs to the Special Issue Chronic Kidney Disease (CKD) Studies on Humans and Animals)
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13 pages, 1909 KiB  
Article
The Protein-Independent Role of Phosphate in the Progression of Chronic Kidney Disease
by Irene Faria Duayer, Eduardo Jorge Duque, Clarice Kazue Fujihara, Ivone Braga de Oliveira, Luciene Machado dos Reis, Flavia Gomes Machado, Fabiana Giorgetti Graciolli, Vanda Jorgetti, Roberto Zatz, Rosilene Motta Elias and Rosa Maria Affonso Moysés
Toxins 2021, 13(7), 503; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13070503 - 19 Jul 2021
Cited by 6 | Viewed by 2728
Abstract
Several factors contribute to renal-function decline in CKD patients, and the role of phosphate content in the diet is still a matter of debate. This study aims to analyze the mechanism by which phosphate, independent of protein, is associated with the progression of [...] Read more.
Several factors contribute to renal-function decline in CKD patients, and the role of phosphate content in the diet is still a matter of debate. This study aims to analyze the mechanism by which phosphate, independent of protein, is associated with the progression of CKD. Adult Munich-Wistar rats were submitted to 5/6 nephrectomy (Nx), fed with a low-protein diet, and divided into two groups. Only phosphate content (low phosphate, LoP, 0.2%; high phosphate, HiP, 0.95%) differentiated diets. After sixty days, biochemical parameters and kidney histology were analyzed. The HiP group presented worse renal function, with higher levels of PTH, FGF-23, and fractional excretion of phosphate. In the histological analysis of the kidney tissue, they also showed a higher percentage of interstitial fibrosis, expression of α-actin, PCNA, and renal infiltration by macrophages. The LoP group presented higher expression of beclin-1 in renal tubule cells, a marker of autophagic flux, when compared to the HiP group. Our findings highlight the action of phosphate in the induction of kidney interstitial inflammation and fibrosis, contributing to the progression of renal disease. A possible effect of phosphate on the dysregulation of the renal cell autophagy mechanism needs further investigation with clinical studies. Full article
(This article belongs to the Special Issue Chronic Kidney Disease (CKD) Studies on Humans and Animals)
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10 pages, 692 KiB  
Article
A Novel Uremic Score Reflecting Accumulation of Specific Uremic Toxins More Precisely Predicts One-Year Mortality after Hemodialysis Commencement: A Retrospective Cohort Study
by Yohei Arai, Shingo Shioji, Hiroyuki Tanaka, Daisuke Katagiri and Fumihiko Hinoshita
Toxins 2020, 12(10), 634; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12100634 - 01 Oct 2020
Cited by 1 | Viewed by 1701
Abstract
Uremic toxins (UTs) generally accumulate in patients developing end-stage renal disease (ESRD). Although some kinds of UTs cause early death after starting hemodialysis (HD), it remains unknown whether the degree of excessive accumulation of various UTs is associated with worsening of prognosis. We [...] Read more.
Uremic toxins (UTs) generally accumulate in patients developing end-stage renal disease (ESRD). Although some kinds of UTs cause early death after starting hemodialysis (HD), it remains unknown whether the degree of excessive accumulation of various UTs is associated with worsening of prognosis. We retrospectively conducted this cohort study consisting of adult patients developing ESRD who initiated HD at the National Center for Global Health and Medicine from 2010 to 2019. We created a new uremic score, which was defined as the aggregate score of the following variables reflecting uremic state: elevated blood urea nitrogen, β2-microglobulin, and anion gap before starting HD. The primary outcome was early mortality within 1-year after HD commencement. The hazard ratio (HR) and 95% confidence interval (CI) for a one-point increase in uremic score was calculated with Cox proportional hazard models adjusted by baseline conditions. We included 230 participants, 16 of whom experienced the primary outcome of early mortality after HD commencement. Uremic score was significantly associated with the primary outcome (crude HR: 1.91, 95% CI 1.16–3.14; adjusted HR: 4.19, 95% CI 1.79–9.78). Our novel uremic score, reflecting accumulation of specific UTs, more precisely predicts early mortality after HD commencement. Full article
(This article belongs to the Special Issue Chronic Kidney Disease (CKD) Studies on Humans and Animals)
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11 pages, 4490 KiB  
Article
Endothelial Cell-Specific Molecule 1 Promotes Endothelial to Mesenchymal Transition in Renal Fibrosis
by Tung-Wei Hung, Chao-Yang Chu, Chen-Lin Yu, Chu-Che Lee, Li-Sung Hsu, Yong-Syuan Chen, Yi-Hsien Hsieh and Jen-Pi Tsai
Toxins 2020, 12(8), 506; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins12080506 - 06 Aug 2020
Cited by 12 | Viewed by 3137
Abstract
The endothelial-to-mesenchymal transition (EndoMT) is involved in the complex pathogenesis of renal fibrosis. The soluble proteoglycan endothelial cell-specific molecule 1 (ESM1) is significantly upregulated in many tumor cells and cirrhosis-related disease. The role of ESM1 in renal fibrosis is unknown. This study investigates [...] Read more.
The endothelial-to-mesenchymal transition (EndoMT) is involved in the complex pathogenesis of renal fibrosis. The soluble proteoglycan endothelial cell-specific molecule 1 (ESM1) is significantly upregulated in many tumor cells and cirrhosis-related disease. The role of ESM1 in renal fibrosis is unknown. This study investigates the role of ESM1 in renal fibrosis, using an in vivo unilateral ureteral obstruction (UUO) mouse model of renal fibrosis and in vitro mouse kidney MES 13 cells overexpressing ESM1. We observed that ESM1 overexpression significantly increased the motility and migration of MES 13 cells, independent of cell viability. In ESM1-overexpressing MES 13 cells, we also observed elevated expression of mesenchymal markers (N-cadherin, vimentin, matrix metallopeptidase 9 (MMP9)) and the fibrosis marker α-smooth muscle actin (α-SMA) and decreased expression of the endothelial marker vascular endothelial cadherin (VE-cadherin) and CD31. In a mouse model of fibrosis induced by unilateral ureter obstruction, we observed time-dependent increases in ESM1, α-SMA, and vimentin expression and renal interstitial collagen fibers in kidney tissue samples. These results suggest that ESM1 may serve as an EndoMT marker of renal fibrosis progression. Full article
(This article belongs to the Special Issue Chronic Kidney Disease (CKD) Studies on Humans and Animals)
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