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Cells
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Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology
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Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Tissues and Organs".

Deadline for manuscript submissions: 28 February 2026 | Viewed by 211

Special Issue Editor

Dr. Jinu Kim

E-Mail Website
Guest Editor
1. Department of Anatomy, Jeju National University College of Medicine, Jeju 63243, Republic of Korea
2. Interdisciplinary Graduate Program in Advanced Convergence Technology & Science, Jeju National University, Jeju 63243, Republic of Korea
Interests: kidney fibrosis; acute kidney injury; renal denervation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The growing incidence of kidney diseases, including chronic kidney disease (CKD) and acute kidney injury (AKI), poses significant challenges to global health. Cellular mechanisms play a crucial role in the development and progression of these conditions. Understanding the cellular dynamics within the kidney, such as epithelial-to-mesenchymal transition (EMT), fibrosis, and inflammation, is vital for improving diagnosis and therapeutic strategies. This Special Issue will explore the molecular and cellular mechanisms that underlie renal pathology, with a particular focus on kidney fibrosis, cell death, repair processes, and regeneration.

Key topics will include the identification of key renal cell populations involved in injury and repair, the role of stem and progenitor cells in kidney regeneration, and the impact of metabolic and environmental factors on renal health. In addition, we will highlight advancements in cell-based models for studying kidney disease, innovative therapeutic approaches targeting cellular pathways, and in vivo models used to assess novel treatments for kidney injury and fibrosis. This Special Issue aims at providing a comprehensive overview of the cellular mechanisms driving kidney diseases, offering new insights into potential therapeutic interventions and clinical applications.

Dr. Jinu Kim
Guest Editor

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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

  • kidney fibrosis
  • acute kidney injury (AKI)
  • chronic kidney disease (CKD)
  • epithelial-to-mesenchymal transition (EMT)
  • renal cell populations
  • stem cell therapy
  • renal regeneration
  • inflammation in kidney disease
  • cell-based models
  • renal repair mechanisms

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Published Papers (1 paper)

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Research

25 pages, 3625 KB  
Article
Checkpoint Imbalance in Primary Glomerulopathies: Comparative Insights into IgA Nephropathy and Membranoproliferative Glomerulonephritis
by Sebastian Mertowski, Paulina Mertowska, Milena Czosnek, Iwona Smarz-Widelska, Wojciech Załuska and Ewelina Grywalska
Cells 2025, 14(19), 1551; https://doi.org/10.3390/cells14191551 - 3 Oct 2025
Abstract
Introduction: Primary glomerulopathies are immune-driven kidney diseases. IgA nephropathy (IgAN) and membranoproliferative glomerulonephritis (MPGN) are prevalent entities with a risk of chronic progression. Immune checkpoints, such as PD-1/PD-L1, CTLA-4/CD86, and CD200R/CD200, regulate activation and tolerance in T, B, and NK cells, and also [...] Read more.
Introduction: Primary glomerulopathies are immune-driven kidney diseases. IgA nephropathy (IgAN) and membranoproliferative glomerulonephritis (MPGN) are prevalent entities with a risk of chronic progression. Immune checkpoints, such as PD-1/PD-L1, CTLA-4/CD86, and CD200R/CD200, regulate activation and tolerance in T, B, and NK cells, and also exist in soluble forms, reflecting systemic immune balance. Objective: To compare immune checkpoint profiles in IgAN and MPGN versus healthy volunteers (HV) through surface expression, soluble serum levels, and PBMC transcripts, with attention to sex-related differences and diagnostic value assessed by ROC curves. Materials and Methods: Ninety age-matched subjects were studied: IgAN (n = 30), MPGN (n = 30), HV (n = 30). Flow cytometry evaluated checkpoint expression on CD4+/CD8+ T cells, CD19+ B cells, and NK cells. ELISA quantified sPD-1, sPD-L1, sCTLA-4, sCD86, sCD200, sCD200R; PBMC transcript levels were assessed. Group comparisons, sex stratification, and ROC analyses were performed. Results: Lymphocyte distributions were preserved, but IgAN patients showed anemia and impaired renal function, while MPGN patients had greater proteinuria and dyslipidemia. GN patients displayed increased PD-1/PD-L1 and CD200R/CD200, with reduced CTLA-4/CD86, compared to HV. Serum analysis revealed elevated sPD-1, sPD-L1, sCD200, sCD200R and decreased sCTLA-4, sCD86. PBMC transcripts paralleled these trends, with PD-1/PD-L1 mainly increased in MPGN. Sex had minimal impact. ROC analyses showed strong GN vs. HV discrimination by CD19+CTLA-4+, PD-1/PD-L1, and CD200/CD200R, but limited ability to separate IgAN from MPGN. Conclusions: IgAN and MPGN share a sex-independent checkpoint signature: PD-1/PD-L1 and CD200R/CD200 upregulation with CTLA-4/CD86 downregulation. CD19+, CTLA-4+, and soluble PD-1/PD-L1/CD200(R) emerge as promising biomarkers requiring further validation. Full article
(This article belongs to the Special Issue Kidney Disease: The Role of Cellular Mechanisms in Renal Pathology)
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