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Etiology and Research Progress of Chronic Kidney Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 4652

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Special Issue Editors

Dr. Silvia De Rosa

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Guest Editor

Centre for Medical Sciences—CISMed, University of Trento, Via S. Maria Maddalena 1, 38122 Trento, Italy
Interests: acute brain injury; acute kidney injury; blood purification in sepsis; airway management; infectious disease; extracorporeal organ support; nutrition and metabolism in critical care

Dr. Marco Fiorentino

E-Mail Website
Guest Editor

Department of Precision and Rigenerative Medicine and Ionian Area (DiMIPRE-J), University of Bari "Aldo Moro", 70124 Bari, Italy
Interests: AKI; CRRT; apheresis; diabetic nephropathy

Special Issue Information

Dear Colleagues,

We are delighted to present a Special Issue in the International Journal of Molecular Sciences: “Etiology and Research Progress of Chronic Kidney Disease”. Chronic kidney disease (CKD) is becoming an increasingly serious public health concern; the global burden is rising due to its high morbidity and mortality. Accurate progression monitoring and prognosis improvement of CKD are extremely significant with regard to improving the clinical treatment and management of the disease and reducing the social burden.

Several biomarkers reported in recent years could play important roles in accurate progression monitoring and prognosis improvement of CKD. Animal studies suggest that interstitial fibrosis could be reversed and could therefore be a therapeutic target in the prevention of CKD progression. We need to improve our understanding of early mechanisms of CKD, which will consequently enable early therapeutic intervention and delay the progression of CKD—or even reverse it.

International Journal of Molecular Sciences is proud to offer a platform to promote and highlight invaluable research on the Etiology and Research Progress of Chronic Kidney Disease.

Dr. Silvia De Rosa
Dr. Marco Fiorentino
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 single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

biomarkers
chronic kidney disease
imaging
end-stage renal disease
renal regeneration
fibrosis
inflammation
therapeutic targets

Published Papers (4 papers)

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Research

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14 pages, 746 KiB

Open AccessArticle

Measured and Estimated Glomerular Filtration Rate to Evaluate Rapid Progression and Changes over Time in Autosomal Polycystic Kidney Disease: Potential Impact on Therapeutic Decision-Making

by Rosa Miquel-Rodríguez, Beatriz González-Toledo, María-Vanessa Pérez-Gómez, María Ángeles Cobo-Caso, Patricia Delgado-Mallén, Sara Estupiñán, Coriolano Cruz-Perera, Laura Díaz-Martín, Federico González-Rinne, Alejandra González-Delgado, Armando Torres, Flavio Gaspari, Domingo Hernández-Marrero, Alberto Ortiz, Esteban Porrini and Sergio Luis-Lima

Int. J. Mol. Sci. 2024, 25(9), 5036; https://doi.org/10.3390/ijms25095036 - 5 May 2024

Viewed by 527

Abstract

Autosomal polycystic kidney disease (ADPKD) is the most common genetic form of kidney failure, reflecting unmet needs in management. Prescription of the only approved treatment (tolvaptan) is limited to persons with rapidly progressing ADPKD. Rapid progression may be diagnosed by assessing glomerular filtration rate (GFR) decline, usually estimated (eGFR) from equations based on serum creatinine (eGFRcr) or cystatin-C (eGFRcys). We have assessed the concordance between eGFR decline and identification of rapid progression (rapid eGFR loss), and measured GFR (mGFR) declines (rapid mGFR loss) using iohexol clearance in 140 adults with ADPKD with ≥3 mGFR and eGFRcr assessments, of which 97 also had eGFRcys assessments. The agreement between mGFR and eGFR decline was poor: mean concordance correlation coefficients (CCCs) between the method declines were low (0.661, range 0.628 to 0.713), and Bland and Altman limits of agreement between eGFR and mGFR declines were wide. CCC was lower for eGFRcys. From a practical point of view, creatinine-based formulas failed to detect rapid mGFR loss (−3 mL/min/y or faster) in around 37% of the cases. Moreover, formulas falsely indicated around 40% of the cases with moderate or stable decline as rapid progressors. The reliability of formulas in detecting real mGFR decline was lower in the non-rapid-progressors group with respect to that in rapid-progressor patients. The performance of eGFRcys and eGFRcr-cys equations was even worse. In conclusion, eGFR decline may misrepresent mGFR decline in ADPKD in a significant percentage of patients, potentially misclassifying them as progressors or non-progressors and impacting decisions of initiation of tolvaptan therapy. Full article

(This article belongs to the Special Issue Etiology and Research Progress of Chronic Kidney Disease)

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16 pages, 2018 KiB

Open AccessArticle

IL-6 and SAA—Strong Predictors for the Outcome in COVID-19 CKD Patients

by Rumen Filev, Mila Lyubomirova, Boris Bogov, Krassimir Kalinov, Julieta Hristova, Dobrin Svinarov and Lionel Rostaing

Int. J. Mol. Sci. 2024, 25(1), 311; https://doi.org/10.3390/ijms25010311 - 25 Dec 2023

Cited by 1 | Viewed by 807

Abstract

In this prospective study, we assessed biomarkers of inflammation (IL-6 and SAA) from the serum of 120 COVID-19 patients, of whom 70 had chronic kidney disease. All the samples were taken at emergency-department (ED) admission. Our goal was to relate the biomarkers to the results of death and acute kidney injury. All the patients underwent chest computer tomography to estimate the severity score (0–5), which was performed at hospital admission. Finally, biomarkers were also evaluated in a healthy control group and in non-COVID-19-CKD patients. IL-6 and SAA were statistically different between the subgroups, i.e., they were significantly increased in patients with COVID-19. Both of the biomarkers (IL-6 and SAA) were independently associated with mortality, AKI and a higher grade of pathological changes in the lung’s parenchyma. Both high baseline levels of IL-6 and SAA on hospital admission were highly correlated with a later ventilatory requirement and mortality, independent of hospital stay. Mortality was found to be significantly higher when the chest CT severity score was 3–4, compared with a severity score of 0–2 (p < 0.0001). Conclusions: at the admission stage, IL-6 and SAA are useful markers for COVID-19 patients with CKD. Full article

(This article belongs to the Special Issue Etiology and Research Progress of Chronic Kidney Disease)

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12 pages, 3181 KiB

Open AccessArticle

Gold Nanoparticles for Monitoring of Mesenchymal Stem-Cell-Loaded Bioresorbable Polymeric Wraps for Arteriovenous Fistula Maturation

by Allan John R. Barcena, Joy Vanessa D. Perez, Jossana A. Damasco, Marvin R. Bernardino, Erin Marie D. San Valentin, Carleigh Klusman, Benjamin Martin, Andrea Cortes, Gino Martin Canlas, Huckie C. Del Mundo, Francisco M. Heralde III, Rony Avritscher, Natalie Fowlkes, Richard R. Bouchard, Jizhong Cheng, Steven Y. Huang and Marites P. Melancon

Int. J. Mol. Sci. 2023, 24(14), 11754; https://doi.org/10.3390/ijms241411754 - 21 Jul 2023

Cited by 1 | Viewed by 1381

Abstract

Mesenchymal stem cell (MSC)-seeded polymeric perivascular wraps have been shown to enhance arteriovenous fistula (AVF) maturation. However, the wraps’ radiolucency makes their placement and integrity difficult to monitor. Through electrospinning, we infused gold nanoparticles (AuNPs) into polycaprolactone (PCL) wraps to improve their radiopacity and tested whether infusion affects the previously reported beneficial effects of the wraps on the AVF’s outflow vein. Sprague Dawley rat MSCs were seeded on the surface of the wraps. We then compared the effects of five AVF treatments—no perivascular wrap (i.e., control), PCL wrap, PCL + MSC wrap, PCL-Au wrap, and PCL-Au + MSC wrap—on AVF maturation in a Sprague Dawley rat model of chronic kidney disease (n = 3 per group). Via micro-CT, AuNP-infused wraps demonstrated a significantly higher radiopacity compared to that of the wraps without AuNPs. Wraps with and without AuNPs equally reduced vascular stenoses, as seen via ultrasonography and histomorphometry. In the immunofluorescence analysis, representative MSC-seeded wraps demonstrated reduced neointimal staining for markers of infiltration with smooth muscle cells (α-SMA), inflammatory cells (CD45), and fibroblasts (vimentin) compared to that of the control and wraps without MSCs. In conclusion, AuNP infusion allows in vivo monitoring via micro-CT of MSC-seeded polymeric wraps over time, without compromising the benefits of the wrap for AVF maturation. Full article

(This article belongs to the Special Issue Etiology and Research Progress of Chronic Kidney Disease)

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Review

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28 pages, 1767 KiB

Open AccessReview

Unravelling the Link between the Gut Microbiome and Autoimmune Kidney Diseases: A Potential New Therapeutic Approach

by Diana Shu Yee Tan, Yibeltal Akelew, Matthew Snelson, Jenny Nguyen and Kim Maree O’Sullivan

Int. J. Mol. Sci. 2024, 25(9), 4817; https://doi.org/10.3390/ijms25094817 - 28 Apr 2024

Viewed by 996

Abstract

The gut microbiota and short chain fatty acids (SCFA) have been associated with immune regulation and autoimmune diseases. Autoimmune kidney diseases arise from a loss of tolerance to antigens, often with unclear triggers. In this review, we explore the role of the gut microbiome and how disease, diet, and therapy can alter the gut microbiota consortium. Perturbations in the gut microbiota may systemically induce the translocation of microbiota-derived inflammatory molecules such as liposaccharide (LPS) and other toxins by penetrating the gut epithelial barrier. Once in the blood stream, these pro-inflammatory mediators activate immune cells, which release pro-inflammatory molecules, many of which are antigens in autoimmune diseases. The ratio of gut bacteria Bacteroidetes/Firmicutes is associated with worse outcomes in multiple autoimmune kidney diseases including lupus nephritis, MPO-ANCA vasculitis, and Goodpasture’s syndrome. Therapies that enhance SCFA-producing bacteria in the gut have powerful therapeutic potential. Dietary fiber is fermented by gut bacteria which in turn release SCFAs that protect the gut barrier, as well as modulating immune responses towards a tolerogenic anti-inflammatory state. Herein, we describe where the current field of research is and the strategies to harness the gut microbiome as potential therapy. Full article

(This article belongs to the Special Issue Etiology and Research Progress of Chronic Kidney Disease)

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