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8.3
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Biomolecules
Special Issues
Potential Use of Biomarkers in Acute Kidney Injury
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Potential Use of Biomarkers in Acute Kidney Injury

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 5045

Special Issue Editors

Prof. Dr. Vin-Cent Wu

E-Mail Website
Guest Editor
NSARF, Section of Nephrology, Department of Internal Medicine, National Taiwan University Hospital, Taipei 100, Taiwan
Interests: acute kidney injury; acute kidney disease; blood purification; biomarker
Special Issues, Collections and Topics in MDPI journals
Dr. Heng-Chih Pan

E-Mail Website
Guest Editor
Division of Nephrology, Department of Internal Medicine, Keelung Chang Gung Memorial Hospital, Keelung 204, Taiwan
Interests: acute kidney injury; prognostic scoring systems; liver cirrhosis with renal dysfunction

Special Issue Information

Dear Colleagues,

Acute kidney injury (AKI) is associated with higher risk of chronic kidney disease (CKD), end stage renal disease (ESRD), and long-term adverse cardiovascular effects. Owing to the lack of effective treatment for impaired renal function, the best strategy in clinical practice is to identify AKI as early as possible and reverse its cause. Emerging evidence has suggested the role of several biomarkers in the early prediction or risk assessment of AKI, including renal tubular damage markers (e.g., neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty-acid binding protein (L-FABP)), inflammation markers (e.g., Interleukin-18 (IL-18)), and stress markers (e.g., tissue inhibitor of metalloproteinases-2 and insulin-like growth factor-binding protein 7 (TIMP-2 x IGFBP7)). Previous investigations including patients with various clinical situations have suggested that these biomarkers hold promise as practical tools in the early prediction of AKI. However, considering the complex and multifactorial etiology of AKI, more kidney-tissue-specific markers might help to localize and quantify the severity of AKI, even with long-term outcomes. 

This Special Issue aims to investigate the role of the biomarkers in different clinical settings, signaling, and disease mechanisms and provide further insights into the underlying mechanisms of AKI. 

Prof. Dr. Vin-Cent Wu
Dr. Heng-Chih Pan
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. Biomolecules 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

  • biomarker
  • acute kidney injury
  • diagnosis
  • renal replacement therapy
  • critical care

Published Papers (3 papers)

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Research

13 pages, 1433 KiB  
Article
Interleukin-18 and Gelsolin Are Associated with Acute Kidney Disease after Cardiac Catheterization
by Po-Yen Kuo, Kai-Fan Tsai, Po-Jung Wu, Pai-Chin Hsu, Chien-Hsing Wu, Wen-Chin Lee, Hsiu-Yu Fang, Chih-Yuan Fang, Sheng-Ying Chung, Yung-Lung Chen and Terry Ting-Yu Chiou
Biomolecules 2023, 13(3), 487; https://doi.org/10.3390/biom13030487 - 06 Mar 2023
Cited by 1 | Viewed by 1296
Abstract
Patients undergoing cardiac catheterization are at high risk of post-procedure acute kidney injury (AKI) and may experience persistent renal damage after an initial insult, a state known as acute kidney disease (AKD). However, the association between AKD and urinary renal biomarkers has not [...] Read more.
Patients undergoing cardiac catheterization are at high risk of post-procedure acute kidney injury (AKI) and may experience persistent renal damage after an initial insult, a state known as acute kidney disease (AKD). However, the association between AKD and urinary renal biomarkers has not yet been evaluated in this population. We enrolled 94 patients who underwent elective cardiac catheterization to investigate patterns of urinary renal biomarkers and their associations with post-procedure AKD. Serial urinary renal biomarker levels were measured during pre-procedure, early post-procedure (12–24 h), and late post-procedure (7–10 days) periods. In our investigation, 42.55% of the enrolled patients developed AKD during the late post-procedure period. While the liver-type free-fatty-acid-binding protein level increased sharply during the early post-procedure period, it returned to baseline during the late post-procedure period. In contrast, interleukin-18 (IL-18) levels increased steadily during the post-procedure period. Early post-procedure ratios of IL-18 and gelsolin (GSN) were independently associated with subsequent AKD (odds ratio (95% confidence interval), 4.742 (1.523–14.759) for IL-18 ratio, p = 0.007; 1.812 (1.027–3.198) for GSN ratio, p = 0.040). In conclusion, post-procedure AKD is common and associated with early changes in urinary IL-18 and GSN in patients undergoing cardiac catheterization. Full article
(This article belongs to the Special Issue Potential Use of Biomarkers in Acute Kidney Injury)
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12 pages, 1983 KiB  
Article
Assessment of Fibrinogen-like 2 (FGL2) in Human Chronic Kidney Disease through Transcriptomics Data Analysis
by Sara Denicolò, Viji Nair, Johannes Leierer, Michael Rudnicki, Matthias Kretzler, Gert Mayer, Wenjun Ju and Paul Perco
Biomolecules 2023, 13(1), 89; https://doi.org/10.3390/biom13010089 - 31 Dec 2022
Cited by 3 | Viewed by 1894
Abstract
Fibrinogen-like 2 (FGL2) was recently found to be associated with fibrosis in a mouse model of kidney damage and was proposed as a potential therapeutic target in chronic kidney disease (CKD). We assessed the association of renal FGL2 mRNA expression with the disease [...] Read more.
Fibrinogen-like 2 (FGL2) was recently found to be associated with fibrosis in a mouse model of kidney damage and was proposed as a potential therapeutic target in chronic kidney disease (CKD). We assessed the association of renal FGL2 mRNA expression with the disease outcome in two independent CKD cohorts (NEPTUNE and Innsbruck CKD cohort) using Kaplan Meier survival analysis. The regulation of FGL2 in kidney biopsies of CKD patients as compared to healthy controls was further assessed in 13 human CKD transcriptomics datasets. The FGL2 protein expression in human renal tissue sections was determined via immunohistochemistry. The regulators of FGL2 mRNA expression in renal tissue were identified in the co-expression and upstream regulator analysis of FGL2-positive renal cells via the use of single-cell RNA sequencing data from the kidney precision medicine project (KPMP). Higher renal FGL2 mRNA expression was positively associated with kidney fibrosis and negatively associated with eGFR. Renal FGL2 mRNA expression was upregulated in CKD as compared with healthy controls and associated with CKD progression in the Innsbruck CKD cohort (p-value = 0.0036) and NEPTUNE cohort (p-value = 0.0048). The highest abundance of FGL2 protein in renal tissue was detected in the thick ascending limb of the loop of Henle and macula densa, proximal tubular cells, as well as in glomerular endothelial cells. The upstream regulator analysis identified TNF, IL1B, IFNG, NFKB1, and SP1 as factors potentially inducing FGL2-co-expressed genes, whereas factors counterbalancing FGL2-co-expressed genes included GLI1, HNF1B, or PPARGC1A. In conclusion, renal FGL2 mRNA expression is elevated in human CKD, and higher FGL2 levels are associated with fibrosis and worse outcomes. Full article
(This article belongs to the Special Issue Potential Use of Biomarkers in Acute Kidney Injury)
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16 pages, 2447 KiB  
Article
Circulating Fibroblast Growth Factor-23 Levels Can Predict Rapid Kidney Function Decline in a Healthy Population: A Community-Based Study
by Hsing-Yu Chen, Wei-Ching Fang, Shao-Chi Chu, Po-Hsi Wang, Chin-Chan Lee, I-Wen Wu, Chiao-Yin Sun, Heng-Jung Hsu, Chun-Yu Chen, Yung-Chang Chen, Vin-Cent Wu and Heng-Chih Pan
Biomolecules 2023, 13(1), 31; https://doi.org/10.3390/biom13010031 - 24 Dec 2022
Viewed by 1213
Abstract
Background: Fibroblast growth factor-23 (FGF-23) associates with decreased kidney function in patients with chronic kidney disease (CKD). However, the correlation between circulating FGF-23 levels and the rate of renal function decline in healthy individuals is largely unknown. We aimed to evaluate the predictive [...] Read more.
Background: Fibroblast growth factor-23 (FGF-23) associates with decreased kidney function in patients with chronic kidney disease (CKD). However, the correlation between circulating FGF-23 levels and the rate of renal function decline in healthy individuals is largely unknown. We aimed to evaluate the predictive performance of FGF-23 for rapid kidney function decline (RKFD) in a community-based study. Methods: A total of 2963 people residing in northern Taiwan were enrolled from August 2013 to May 2018 for an annual assessment of kidney function for five years. The baseline estimated glomerular filtration rates (eGFR) were calculated using the 2009 and 2021 Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation, which aggregates the values of serum creatinine and cystatin C (eGFRcr-cys). The outcome was RKFD—a 15% decrease in estimated glomerular filtration rate (eGFR) within the first four years, and a reduction in eGFR without improvement in the 5th year. A generalized additive model (GAM) was used to determine the cut-off value of FGF-23 to predict RKFD. Results: The incidence of RKFD was 18.0% (114/634). After matching for age and sex at a 1:1 ratio, a total of 220 subjects were analyzed. eGFRcr-cys was negatively correlated with total vitamin D level but seemed irrelevant to FGF-23. Multivariable logistic regression analysis showed that FGF-23, eGFRcr-cys, and urine albumin-to-creatinine ratio (UACR) were independent predictors of the possibility of RKFD. FGF-23 showed the best predictive performance for RKFD (AUROC: 0.803), followed by baseline eGFRcr-cys (AUROC: 0.639) and UACR (AUROC: 0.591). From the GAM, 32 pg/mL was the most appropriate cut-off value of FGF-23 with which to predict RKFD. The subgroup and sensitivity analyses showed consistent results that high-FGF-23 subjects had higher risks of RKFD. Conclusions: Circulating FGF-23 level could be a helpful predictor for RKFD in this community-based population. Full article
(This article belongs to the Special Issue Potential Use of Biomarkers in Acute Kidney Injury)
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