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Life
Special Issues
Pathogenesis and Novel Treatment for Kidney Diseases
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Pathogenesis and Novel Treatment for Kidney Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 25 September 2026 | Viewed by 1575

Editor

Dr. Nomy Levin-Iaina

E-Mail Website
Guest Editor
School of Medicine, Faculty of Health Sciences, Ben Gurion University of the Negev, Beer Sheva 8410501, Israel
Interests: kidney disease; hemodialysis

Special Issue Information

Dear Colleagues,

Kidney diseases represent a major global health burden, with increasing incidence and limited therapeutic options for many conditions. Significant advances in recent years have improved our understanding of the molecular, cellular, and immunological mechanisms underlying renal injury, disease progression, and repair. These insights have paved the way for the development of novel diagnostic tools and innovative therapeutic strategies.

This Special Issue aims to highlight recent progress in the pathogenesis of kidney diseases and emerging treatment approaches. Topics of interest include, but are not limited to, mechanisms of acute and chronic kidney injury, glomerular and tubular disorders, diabetic kidney disease, immune-mediated and genetic renal diseases, as well as the role of inflammation, fibrosis, metabolism, and cell signaling in disease progression. The Special Issue also welcomes studies on novel pharmacological agents, biologics, gene- and cell-based therapies, biomarkers, and translational or clinical research that bridge basic science and patient care.

By bringing together original research articles and comprehensive reviews, this Special Issue seeks to provide an updated and integrative perspective on kidney disease pathogenesis and to promote the development of more effective and personalized therapeutic strategies.

Dr. Nomy Levin-Iaina
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life 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 2600 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

  • molecular mechanisms of kidney disease
  • pathophysiology of renal injury
  • inflammation and fibrosis in kidney disease
  • novel therapeutic targets
  • precision medicine in nephrology
  • translational approaches in renal disease

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Published Papers (3 papers)

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Research

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30 pages, 7083 KB  
Article
Network Pharmacology and Molecular Docking-Based Investigation of Empagliflozin’s Therapeutic Potential in Chronic Kidney Disease
by Aman Tedasen, Moragot Chatatikun, Ratana Netphakdee, Jason C. Huang and Atthaphong Phongphithakchai
Life 2026, 16(5), 719; https://doi.org/10.3390/life16050719 - 23 Apr 2026
Viewed by 676
Abstract
Chronic kidney disease (CKD) is a progressive global health challenge. While empagliflozin, a selective SGLT2 inhibitor, is known to attenuate CKD progression through mechanisms beyond glycemic control, the precise molecular pathways remain incompletely characterized and warrant further investigation. This study employed an integrated [...] Read more.
Chronic kidney disease (CKD) is a progressive global health challenge. While empagliflozin, a selective SGLT2 inhibitor, is known to attenuate CKD progression through mechanisms beyond glycemic control, the precise molecular pathways remain incompletely characterized and warrant further investigation. This study employed an integrated network pharmacology and molecular docking approach to elucidate the multi-target mechanisms of empagliflozin in CKD. Initial evaluation demonstrated that empagliflozin exhibits favorable physicochemical properties, drug-likeness, and ADMET profiles, supporting its potential as an effective orally administered therapeutic option for CKD management. Network analysis identified 221 shared molecular targets between empagliflozin and CKD-associated genes. Topological analysis of the protein–protein interaction (PPI) network revealed ten critical hub proteins—GAPDH, IL6, EGFR, HSP90AA1, NFKB1, HSP90AB1, MTOR, MAPK3, IL2, and PIK3CA—which serve as key regulators in CKD pathophysiology. Gene Ontology and KEGG pathway enrichment analyses indicated that these shared targets are significantly involved in phosphorylation, signal transduction, and central signaling cascades associated with CKD progression, including the PI3K-Akt, FoxO, HIF-1, and AGE-RAGE pathways. Molecular docking simulations corroborated empagliflozin’s multi-target affinity, demonstrating particularly strong binding energies toward HSP90AB1 (−10.85 kcal/mol), MAPK3 (−9.46 kcal/mol), and EGFR (−9.38 kcal/mol). Empagliflozin maintained stable hydrogen bonding throughout the 200-ns molecular dynamics simulation, primarily with GLN18, GLU42, SER45, ASN46, ASN101, GLY130, and TYR134, underscoring its persistent and well-anchored interaction with HSP90AB1. Collectively, these findings provide crucial mechanistic insights, suggesting that empagliflozin might exerts therapeutic effects by modulating interconnected pathways regulating inflammation, oxidative stress, and metabolic homeostasis, thereby reinforcing its role as a comprehensive, multi-target therapeutic strategy for CKD management. Nonetheless, validation through in vitro experiments remains necessary. Full article
(This article belongs to the Special Issue Pathogenesis and Novel Treatment for Kidney Diseases)
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15 pages, 5938 KB  
Case Report
Phenotypic Variability of Kidney Involvement in Fabry Disease—Lessons from a Family Study
by Elena-Emanuela Rusu, Ruxandra-Oana Jurcut, Mihaela Gherghiceanu, Filip Muresan, Gheona Altarescu, Bogdan Stanciulescu, Robert Adam, Alexandru Procop, Cristina Stoica, Bogdan Marian Sorohan, Vlad Stefanescu and Gener Ismail
Life 2026, 16(6), 866; https://doi.org/10.3390/life16060866 - 22 May 2026
Viewed by 247
Abstract
Fabry disease is an X-linked lysosomal storage disease that leads to the intracellular accumulation of glycosphingolipids in many tissues and fluids, including the kidneys. We report a single family with Fabry disease that includes seven patients carrying the pathogenic variant c.797A>C in the [...] Read more.
Fabry disease is an X-linked lysosomal storage disease that leads to the intracellular accumulation of glycosphingolipids in many tissues and fluids, including the kidneys. We report a single family with Fabry disease that includes seven patients carrying the pathogenic variant c.797A>C in the GLA gene, with remarkable variability in kidney involvement, assessed based on clinical, biological, and histological data. The patients were monitored for 2–9 years, and all received enzyme replacement therapy. Kidney involvement was variable and included severely decreased GFR with significant proteinuria, mildly to moderately decreased GFR with proteinuria, mildly decreased GFR with microalbuminuria or normoalbuminuria, hyperfiltration with normoalbuminuria, and preserved kidney function. All patients who underwent kidney biopsy presented with Fabry-specific lesions and, in some cases, chronic histological damage. This study provides valuable insights into kidney involvement evaluated through kidney biopsy, personalized management strategies for family members according to their phenotype, and long-term follow-up of kidney function. We underscore the importance of molecular screening of the GLA gene in all family members for early identification of the disease and early initiation of specific treatments that can prevent or delay the progression of this disease. Full article
(This article belongs to the Special Issue Pathogenesis and Novel Treatment for Kidney Diseases)
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17 pages, 472 KB  
Protocol
Protocol for Developing and Validating a Multimarker-Clinical Prediction Model of SGLT2 Inhibitor-Induced Acute eGFR Dip in CKD Stages 3–4: A Three-Stage Urinary Proteomics Study
by Zhiyu Duan, Youhe Gao, Mengjie Huang, Yanjun Liang, Jing Hao, Jie Wang and Guangyan Cai
Life 2026, 16(6), 865; https://doi.org/10.3390/life16060865 - 22 May 2026
Viewed by 369
Abstract
Introduction: SGLT2 inhibitors reduce renal composite endpoints and proteinuria, yet RCTs uniformly show an acute eGFR dip within 2 weeks to 2 months after initiation. However, demographic and clinical predictors of an acute eGFR dip demonstrate considerable heterogeneity across studies. This study aims [...] Read more.
Introduction: SGLT2 inhibitors reduce renal composite endpoints and proteinuria, yet RCTs uniformly show an acute eGFR dip within 2 weeks to 2 months after initiation. However, demographic and clinical predictors of an acute eGFR dip demonstrate considerable heterogeneity across studies. This study aims to identify urinary protein biomarkers of this early eGFR dip and integrate them with routine variables to build a clinically actionable prediction model. Methods and analysis: This three-stage proteomics study includes retrospective discovery, prospective internal validation, and external validation cohorts (total n ≈ 600–700). DIA mass spectrometry will screen for urinary proteins associated with ≥10% eGFR decline at 1 month post-SGLT2i initiation in CKD stages 3–4. Top candidates (FDR < 10%, FC > 1.5, ion intensity > 1 × 104, unique gene families) will be validated by ELISA. A LASSO-logistic regression model will integrate the top three proteins with seven routinely available clinical variables: age, BMI, diabetes status, heart failure, systolic blood pressure, baseline eGFR, and diuretic use. Model performance will be assessed using the C-statistic, NRI, IDI, and calibration metrics. Adaptive stopping rules are pre-specified. Ethics and dissemination: Approved by the Ethics Review Committee at Chinese PLA General Hospital (S2025-859-02, 2025KY126-KS002), all participants will provide written informed consent prior to enrollment, and the study will adhere to the Declaration of Helsinki. Data will be pseudonymized and stored securely according to institutional regulations. Findings will be published in peer-reviewed journals and presented at international nephrology conferences. Trial Registration: Registered Report Identifier: ChiCTR2600119772. Date of registration: 3 March 2026. Full article
(This article belongs to the Special Issue Pathogenesis and Novel Treatment for Kidney Diseases)
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