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Molecular Mechanisms of Kidney Disease: From Neonates to Adolescents
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Molecular Mechanisms of Kidney Disease: From Neonates to Adolescents

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 (30 May 2023) | Viewed by 4813

Special Issue Editors

Prof. Dr. Danuta Zwolińska

E-Mail Website
Guest Editor
Department of Pediatric Nephrology, Wroclaw Medical University, 50-556 Wroclaw, Poland
Interests: pediatric nephrologuy
Prof. Dr. Kinga Musiał

E-Mail Website
Guest Editor
Department of Pediatric Nephrology, Wroclaw Medical University, Wybrzeże L. Pasteura 1, 50-367 Wrocław, Poland
Interests: acute kidney injury; biomarkers in nephrology; CAKUT; obstructive uropathy; vesicoureteral reflux; hemolytic uremic syndrome; idiopathic/congenital/infantile nephrotic syndrome; primary glomerulopathies; chronic kidney disease; hemodialysis; peritoneal dialysis; transition medicine; hypertension
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The ongoing progress on understanding the background of kidney pathology is based on insight into its molecular mechanisms. The variability of immune reactions has shaped primary and secondary glomerulopathies, vasculitides, and acute rejection, whereas the genetic background and molecular architecture of the glomerular filtration barrier have reshaped idiopathic nephrotic syndrome. Inflammatory processes and fibrosis have added to chronic kidney disease and hypertension. Complement system anomalies have redefined the background of hemolytic uremic syndrome. Even urinary tract infections have revealed a new side through microbiotic impact.

These advances have always been analyzed in the context of age-related changes, from neonatal kidney immaturity into adolescent transition, making pediatric nephrology a fascinating compilation of microscale discoveries extended along the time dimension.

Therefore, this Special Issue is an invitation to share molecular experience and navigate the new perspectives that nephrology offers to its enthusiasts.

Prof. Dr. Danuta Zwolińska
Prof. Dr. Kinga Musiał
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.

Published Papers (3 papers)

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Research

14 pages, 2146 KiB  
Article
KIM-1, IL-18, and NGAL, in the Machine Learning Prediction of Kidney Injury among Children Undergoing Hematopoietic Stem Cell Transplantation—A Pilot Study
by Kinga Musiał, Jakub Stojanowski, Justyna Miśkiewicz-Bujna, Krzysztof Kałwak and Marek Ussowicz
Int. J. Mol. Sci. 2023, 24(21), 15791; https://doi.org/10.3390/ijms242115791 - 31 Oct 2023
Cited by 1 | Viewed by 991
Abstract
Children undergoing allogeneic hematopoietic stem cell transplantation (HSCT) are prone to developing acute kidney injury (AKI). Markers of kidney damage: kidney injury molecule (KIM)-1, interleukin (IL)-18, and neutrophil gelatinase-associated lipocalin (NGAL) may ease early diagnosis of AKI. The aim of this study was [...] Read more.
Children undergoing allogeneic hematopoietic stem cell transplantation (HSCT) are prone to developing acute kidney injury (AKI). Markers of kidney damage: kidney injury molecule (KIM)-1, interleukin (IL)-18, and neutrophil gelatinase-associated lipocalin (NGAL) may ease early diagnosis of AKI. The aim of this study was to assess serum concentrations of KIM-1, IL-18, and NGAL in children undergoing HSCT in relation to classical markers of kidney function (creatinine, cystatin C, estimated glomerular filtration rate (eGFR)) and to analyze their usefulness as predictors of kidney damage with the use of artificial intelligence tools. Serum concentrations of KIM-1, IL-18, NGAL, and cystatin C were assessed by ELISA in 27 children undergoing HSCT before transplantation and up to 4 weeks after the procedure. The data was used to build a Random Forest Classifier (RFC) model of renal injury prediction. The RFC model established on the basis of 3 input variables, KIM-1, IL-18, and NGAL concentrations in the serum of children before HSCT, was able to effectively assess the rate of patients with hyperfiltration, a surrogate marker of kidney injury 4 weeks after the procedure. With the use of the RFC model, serum KIM-1, IL-18, and NGAL may serve as markers of incipient renal dysfunction in children after HSCT. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Kidney Disease: From Neonates to Adolescents)
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11 pages, 1829 KiB  
Article
Assessment of Brain-Derived Neurotrophic Factor (BDNF) Concentration in Children with Idiopathic Nephrotic Syndrome
by Andrzej Badeński, Marta Badeńska, Elżbieta Świętochowska, Agnieszka Didyk, Aurelia Morawiec-Knysak and Maria Szczepańska
Int. J. Mol. Sci. 2022, 23(20), 12312; https://doi.org/10.3390/ijms232012312 - 14 Oct 2022
Cited by 1 | Viewed by 1464
Abstract
Idiopathic nephrotic syndrome (INS) is a chronic disease affecting children in early childhood. It is characterized by proteinuria, hypoalbuminemia, edema and hyperlipidemia. To date, the diagnosis is usually established at an advanced stage of proteinuria. Therefore, new methods of early INS detection are [...] Read more.
Idiopathic nephrotic syndrome (INS) is a chronic disease affecting children in early childhood. It is characterized by proteinuria, hypoalbuminemia, edema and hyperlipidemia. To date, the diagnosis is usually established at an advanced stage of proteinuria. Therefore, new methods of early INS detection are desired. This study was designed to assess brain-derived neurotrophic factor (BDNF) as a potential marker in the early diagnosis of INS. The study group included patients with a diagnosis of idiopathic nephrotic syndrome (n = 30) hospitalized in Clinical Hospital No. 1 in Zabrze, from December 2019 to December 2021. Our study shows that serum BDNF concentration decreased and urine BDNF concentration increased in a group of patients with INS, compared with healthy controls. Such outcomes might be related to loss of the BDNF contribution in podocyte structure maintenance. Moreover, we anticipate the role of BDNF in urine protein concentration increase, which could be used as a direct predictor of urine protein fluctuations in clinical practice. Moreover, the ROC curve has also shown that serum BDNF and urine BDNF levels might be useful as an INS marker. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Kidney Disease: From Neonates to Adolescents)
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22 pages, 4725 KiB  
Article
Decreased Expression of the Slc31a1 Gene and Cytoplasmic Relocalization of Membrane CTR1 Protein in Renal Epithelial Cells: A Potent Protective Mechanism against Copper Nephrotoxicity in a Mouse Model of Menkes Disease
by Olga Haberkiewicz, Paweł Lipiński, Rafał R. Starzyński, Aneta Jończy, Patrycja Kurowska, Mateusz Ogórek, Aleksandra Bednarz, Sylwia Herman, Dawid Hatala, Paweł Grzmil, Zenon Rajfur, Zbigniew Baster and Małgorzata Lenartowicz
Int. J. Mol. Sci. 2022, 23(19), 11441; https://doi.org/10.3390/ijms231911441 - 28 Sep 2022
Cited by 1 | Viewed by 1754
Abstract
Kidneys play an especial role in copper redistribution in the organism. The epithelial cells of proximal tubules perform the functions of both copper uptake from the primary urine and release to the blood. These cells are equipped on their apical and basal membrane [...] Read more.
Kidneys play an especial role in copper redistribution in the organism. The epithelial cells of proximal tubules perform the functions of both copper uptake from the primary urine and release to the blood. These cells are equipped on their apical and basal membrane with copper transporters CTR1 and ATP7A. Mosaic mutant mice displaying a functional dysfunction of ATP7A are an established model of Menkes disease. These mice exhibit systemic copper deficiency despite renal copper overload, enhanced by copper therapy, which is indispensable for their life span extension. The aim of this study was to analyze the expression of Slc31a1 and Slc31a2 genes (encoding CTR1/CTR2 proteins) and the cellular localization of the CTR1 protein in suckling, young and adult mosaic mutants. Our results indicate that in the kidney of both intact and copper-injected 14-day-old mutants showing high renal copper content, CTR1 mRNA level is not up-regulated compared to wild-type mice given a copper injection. The expression of the Slc31a1 gene in 45-day-old mice is even reduced compared with intact wild-type animals. In suckling and young copper-injected mutants, the CTR1 protein is relocalized from the apical membrane to the cytoplasm of epithelial cells of proximal tubules, the process which prevents copper transport from the primary urine and, thus, protects cells against copper toxicity. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Kidney Disease: From Neonates to Adolescents)
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