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Molecular Mechanisms in Glomerular and Renal Diseases

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: 31 March 2027 | Viewed by 469

Editors


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Guest Editor
1. Department of Nephrology, University General Hospital of Ioannina, 451 10 Ioannina, Greece
2. Department of Nephrology and Clinical Immunology, RWTH Aachen University Hospital, 52074 Aachen, Germany
Interests: acute kidney injury; tubular regeneration; glomerulonephritis; FSGS; IgAN
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Nephrology, University Hospital Ioannina, Ioannina, Greece
Interests: chronic kidney disease; kidney transplant; cardiovascular disease; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, “Molecular Mechanisms in Glomerular and Renal Diseases,” aims to bring together original research, reviews and insightful commentaries addressing the molecular basis of kidney disease, with a particular focus on glomerular disorders. The goal is to provide an updated and integrated overview of current advances that deepen our understanding of disease mechanisms and inform clinical practice.

Glomerular and kidney diseases constitute a growing global health burden, affecting more than 10% of the population worldwide and frequently progressing to end-stage renal disease (ESRD). In recent years, the nephrology landscape has undergone a profound transformation with the emergence of new therapies. These advances underscore the urgent need to align molecular understanding with individualized therapeutic strategies.

The primary aim of this Special Issue is to assemble contributions that elucidate the molecular drivers of glomerular and kidney disease pathogenesis and progression, while showcasing how these discoveries pave the way for personalized diagnostics and next-generation therapies. This Special Issue also seeks to bridge basic molecular research and clinical nephrology by highlighting novel insights into signaling pathways, immune and inflammatory mechanisms, genetic and epigenetic regulation, and cellular crosstalk underlying kidney injury and repair.

Dr. Eleni Stamellou
Dr. Evangelia Dounousi
Guest Editors

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Keywords

  • glomerulonephritis (GN)
  • podocytopathies
  • IgA (IgAN)
  • chronic kindey disease (CKD)
  • membra-nous nephropathy
  • focal segmental glomerulosclerosis (FSGS)

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Published Papers (1 paper)

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Review

30 pages, 1783 KB  
Review
Emerging Immune Cell Biomarkers in Primary Membranous Nephropathy: Immune Cell Profiling During Anti-CD20 B Cell-Targeted Therapy
by Christos Georgopoulos, Eleni Stamellou, Anila Duni, Lefkothea Dova, Georgios Vartholomatos, Ekaterini Siomou, Haralampos Milionis and Evangelia Dounousi
Int. J. Mol. Sci. 2026, 27(16), 7233; https://doi.org/10.3390/ijms27167233 - 13 Aug 2026
Viewed by 165
Abstract
Primary membranous nephropathy (pMN) is an antibody-mediated podocytopathy, most commonly caused by autoantibodies against the M-type phospholipase A2 receptor (PLA2R1). Rituximab (RTX), an anti-CD20 monoclonal antibody, is a first-line treatment for moderate-to-high-risk pMN, inducing partial or complete remission in about 60% of patients [...] Read more.
Primary membranous nephropathy (pMN) is an antibody-mediated podocytopathy, most commonly caused by autoantibodies against the M-type phospholipase A2 receptor (PLA2R1). Rituximab (RTX), an anti-CD20 monoclonal antibody, is a first-line treatment for moderate-to-high-risk pMN, inducing partial or complete remission in about 60% of patients within 24 months. However, treatment response varies considerably, and current biomarkers, including anti-PLA2R1 titers and peripheral B cell counts, have limited predictive value for non-response or relapse. Beyond B cell depletion, RTX exerts broader immunomodulatory effects by influencing T cell subsets, monocytes, and natural killer (NK) cells involved in antibody-dependent cellular cytotoxicity. This review examines the peripheral immune cell changes that accompany anti-CD20 therapy and their value as candidate biomarkers. Total CD19+ B cell depletion is the standard pharmacodynamic measure of drug effect but correlates only loosely with clinical outcome. A specific B cell reconstitution profile was associated with pending relapse. Class-switched memory B cells remain depleted during sustained remission, and their premature re-expansion has been associated with subsequent relapse. Regulatory T cells are reduced in active disease and rise within days of infusion in patients who later respond. The systemic inflammation response index, derived from the routine differential count, has been associated with both 6- and 12-month remission. These observations derive from small, mostly single-center cohorts using heterogeneous panels and different RTX regimens. On the available evidence, immune cell profiling cannot yet be recommended for routine disease monitoring, and larger prospective studies with standardized panels are required. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Glomerular and Renal Diseases)
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