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Advances in the Pathogenesis of Diabetic Kidney Disease: Second Edition
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Advances in the Pathogenesis of Diabetic Kidney Disease: Second Edition

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 (20 September 2024) | Viewed by 5055

Special Issue Editor

Dr. Konstantinos Tziomalos

E-Mail Website
Guest Editor
First Propedeutic Department of Internal Medicine, Medical School, Aristotle University of Thessaloniki, AHEPA Hospital, 54636 Thessaloniki, Greece
Interests: dyslipidemia; stroke; diabetes; non-alcoholic fatty liver disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetic kidney disease is the leading cause of chronic kidney disease and end-stage renal disease in high-income countries. Recent research has identified the novel molecular pathways that are implicated in the pathogenesis of this disease. In addition, emerging molecular markers are also being developed that might be useful in the timely diagnosis of diabetic kidney disease and monitoring of its progression. Furthermore, translational research has led to the identification of new molecular targets for its treatment.

This Special Issue, ‘Advances in the Pathogenesis of Diabetic Kidney Disease: Second Edition’, invites submissions of original papers as well as reviews that underscore the recent research progress in the pathogenesis, diagnosis, and management of diabetic kidney disease, with a focus on the molecular mechanisms underpinning these aspects.

For information on the first edition of this Special Issue: https://www.mdpi.com/journal/ijms/special_issues/H6WLKG3244

Dr. Konstantinos Tziomalos
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 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

  • diabetic kidney disease
  • diagnosis
  • pathogenesis
  • treatment
  • molecular mechanisms
  • chronic kidney disease
  • end-stage renal disease
  • inflammation
  • oxidative stress
  • glycemia

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Related Special Issue

Published Papers (3 papers)

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Research

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18 pages, 5191 KiB  
Article
Complement Cascade Proteins Correlate with Fibrosis and Inflammation in Early-Stage Type 1 Diabetic Kidney Disease in the Ins2Akita Mouse Model
by Aggeliki Tserga, Jean Sébastien Saulnier-Blache, Kostantinos Palamaris, Despoina Pouloudi, Harikleia Gakiopoulou, Jerome Zoidakis, Joost Peter Schanstra, Antonia Vlahou and Manousos Makridakis
Int. J. Mol. Sci. 2024, 25(3), 1387; https://doi.org/10.3390/ijms25031387 - 23 Jan 2024
Cited by 2 | Viewed by 1823
Abstract
Diabetic kidney disease (DKD) is characterized by histological changes including fibrosis and inflammation. Evidence supports that DKD is mediated by the innate immune system and more specifically by the complement system. Using Ins2Akita T1D diabetic mice, we studied the connection between the complement [...] Read more.
Diabetic kidney disease (DKD) is characterized by histological changes including fibrosis and inflammation. Evidence supports that DKD is mediated by the innate immune system and more specifically by the complement system. Using Ins2Akita T1D diabetic mice, we studied the connection between the complement cascade, inflammation, and fibrosis in early DKD. Data were extracted from a previously published quantitative-mass-spectrometry-based proteomics analysis of kidney glomeruli of 2 (early DKD) and 4 months (moderately advanced DKD)-old Ins2Akita mice and their controls A Spearman rho correlation analysis of complement- versus inflammation- and fibrosis-related protein expression was performed. A cross-omics validation of the correlation analyses’ results was performed using public-domain transcriptomics datasets (Nephroseq). Tissue sections from 43 patients with DKD were analyzed using immunofluorescence. Among the differentially expressed proteins, the complement cascade proteins C3, C4B, and IGHM were significantly increased in both early and later stages of DKD. Inflammation-related proteins were mainly upregulated in early DKD, and fibrotic proteins were induced in moderately advanced stages of DKD. The abundance of complement proteins with fibrosis- and inflammation-related proteins was mostly positively correlated in early stages of DKD. This was confirmed in seven additional human and mouse transcriptomics DKD datasets. Moreover, C3 and IGHM mRNA levels were found to be negatively correlated with the estimated glomerular filtration rate (range for C3 rs = −0.58 to −0.842 and range for IGHM rs = −0.6 to −0.74) in these datasets. Immunohistology of human kidney biopsies revealed that C3, C1q, and IGM proteins were induced in patients with DKD and were correlated with fibrosis and inflammation. Our study shows for the first time the potential activation of the complement cascade associated with inflammation-mediated kidney fibrosis in the Ins2Akita T1D mouse model. Our findings could provide new perspectives for the treatment of early DKD as well as support the use of Ins2Akita T1D in pre-clinical studies. Full article
(This article belongs to the Special Issue Advances in the Pathogenesis of Diabetic Kidney Disease: Second Edition)
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8 pages, 249 KiB  
Communication
Presence of Non-Diabetic Kidney Diseases in Biopsy Specimens of Diabetic Patients’ Single Center Experience
by Aleksandar Janković, Nada Dimković, Verica Todorov-Sakić, Ana Bulatović, Nikola Simović, Petar Đurić and Radomir Naumović
Int. J. Mol. Sci. 2023, 24(19), 14759; https://doi.org/10.3390/ijms241914759 - 29 Sep 2023
Cited by 1 | Viewed by 1121
Abstract
The complications of type 2 diabetes mellitus (T2DM) are well known and one of them is diabetic chronic kidney disease (DCKD). Over time, it has become clear that patients with T2DM can have nondiabetic chronic kidney diseases (NDCKD), especially those that affect the [...] Read more.
The complications of type 2 diabetes mellitus (T2DM) are well known and one of them is diabetic chronic kidney disease (DCKD). Over time, it has become clear that patients with T2DM can have nondiabetic chronic kidney diseases (NDCKD), especially those that affect the glomeruli. Clinical indicators for identifying DCKD from NDCKD with high sensitivity and specificity have not yet been identified. Therefore, kidney biopsy remains the golden standard for DCKD diagnosis in patients with T2DM. Despite some indications for kidney biopsy, criteria for a biopsy differ between countries, regions, and doctors. The aim of the study was to analyze the biopsy findings in our T2DM population and the justification of the biopsy according to widely accepted criteria. This single center retrospective study analyzed data from 74 patients with T2DM who underwent kidney biopsy from January 2014 to January 2021. According to the biopsy data, we categorized31 patients in the DN group, patients with typical diabetic glomerulopathy, 11 patients in the mixed group, patients who had pathohistological elements for both DN and non-DN glomerulopathy, and 32 patients in the non-DN group, patients with primary glomerulopathy not linked with DM. In the non-DN and mixed groups, the most frequent glomerulopathy was mesangioproliferative glomerulonephritis, including IgA and non-IgA forms, found in 10 patients, and membranous nephropathy (MN) in 10 patients. We analyzed several parameters and only the amount of proteinuria was found to be significantly linked to biopsy findings related to DN. With the existing criteria for kidney biopsy, we managed to detect changes in the kidneys in about half of our patients with T2DM. These patients required specific treatment, different from that which we use for DCKD patients. Full article
(This article belongs to the Special Issue Advances in the Pathogenesis of Diabetic Kidney Disease: Second Edition)

Review

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24 pages, 969 KiB  
Review
Novel Insights into Diabetic Kidney Disease
by Ewelina Młynarska, Dominika Buławska, Witold Czarnik, Joanna Hajdys, Gabriela Majchrowicz, Filip Prusinowski, Magdalena Stabrawa, Jacek Rysz and Beata Franczyk
Int. J. Mol. Sci. 2024, 25(18), 10222; https://doi.org/10.3390/ijms251810222 - 23 Sep 2024
Viewed by 1624
Abstract
Diabetic kidney disease (DKD) is a major complication of diabetes mellitus (DM), affecting over one-third of type 1 and nearly half of type 2 diabetes patients. As the leading cause of end-stage renal disease (ESRD) globally, DKD develops through a complex interplay of [...] Read more.
Diabetic kidney disease (DKD) is a major complication of diabetes mellitus (DM), affecting over one-third of type 1 and nearly half of type 2 diabetes patients. As the leading cause of end-stage renal disease (ESRD) globally, DKD develops through a complex interplay of chronic hyperglycemia, oxidative stress, and inflammation. Early detection is crucial, with diagnosis based on persistent albuminuria and reduced estimated glomerular filtration rate (eGFR). Treatment strategies emphasize comprehensive management, including glycemic control, blood pressure regulation, and the use of nephroprotective agents such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), sodium-glucose cotransporter-2 (SGLT2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists. Ongoing research explores novel therapies targeting molecular pathways and non-coding RNAs. Preventive measures focus on rigorous control of hyperglycemia and hypertension, aiming to mitigate disease progression. Despite therapeutic advances, DKD remains a leading cause of ESRD, highlighting the need for continued research to identify new biomarkers and innovative treatments. Full article
(This article belongs to the Special Issue Advances in the Pathogenesis of Diabetic Kidney Disease: Second Edition)
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