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Recent Insights in the Pathogenesis, Diagnosis, Prognosis and Treatment of...
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Recent Insights in the Pathogenesis, Diagnosis, Prognosis and Treatment of Glomerular Disorders

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

Deadline for manuscript submissions: 28 February 2026 | Viewed by 3065

Special Issue Editors

Prof. Dr. Adrian Constantin Covic

E-Mail Website
Guest Editor
1. “Dr. C.I. Parhon” University Hospital, Iasi, Romania
2. Faculty of Medicine, “Grigore T. Popa” University of Medicine, Iasi, Romania
Interests: immunology; renal transplantation; glomerular diseases; cardiovascular disease; dialysis; pathology
Prof. Dr. Gener Ismail

E-Mail Website
Guest Editor
1. Department of Nephrology, “Carol Davila” University of Medicine and Pharmacy, 020021 Bucharest, Romania
2. Department of Nephrology, Fundeni Clinical Institute, 022328 Bucharest, Romania
Interests: glomerular disorders; rare genetic kidney disorders; immunology; systemic autoimmune disorders with renal involvement; biomarkers; diabetic kidney disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Glomerular disorders are the third-leading cause of end-stage kidney disease worldwide. Significant progress has been made during the past decades in the understanding of the pathogenesis of glomerular disorders (e.g., IgA nephropathy, membranous nephropathy, lupus nephritis, ANCA-associated vasculitis, and C3 glomerulopathy), which has translated into better prognostication and development of targeted therapies with the potential to significantly alter the long-term patient and renal survival in such disorders. Nonetheless, despite these tremendous advances, the adequate diagnosis of the underlying glomerular disorders and the indications/availability of kidney biopsies still vary significantly across different regions of the world. Thus, there is still a need to better define the epidemiology of glomerular disorders across different regions and populations to further understand the contributing factors to glomerular disorders pathogenesis, evaluate the impact of genetic predisposition in these circumstances, better delineate the factors associated with treatment response and long-term renal survival, and refine treatment approaches in terms of minimizing the adverse effects of immunosuppressive therapy.

This Special Issue welcomes both original and review papers approaching the previously defined gaps in the knowledge of individual glomerular disorders. Nonetheless, studies evaluating glomerular disorders from kidney biopsy registries from individual clinics or geographic regions will also be considered, as there is an unmet need to better define the epidemiology and prognosis of these disorders in distinct parts of the world.

Prof. Dr. Adrian Constantin Covic
Prof. Dr. Gener Ismail
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. 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

  • glomerular disorders
  • pathology
  • kidney biopsy
  • immunology
  • immunosuppresion
  • vasculitis

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Published Papers (4 papers)

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17 pages, 11177 KiB  
Article
Pathogenesis of Focal Segmental Glomerulosclerosis and Minimal Change Disease: Insights from Glomerular Proteomics
by Yuriy Maslyennikov, Ioana-Ecaterina Pralea, Andrada Alina Bărar, Crina Claudia Rusu, Diana Tania Moldovan, Alina Ramona Potra, Dacian Tirinescu, Maria Țicală, Alexandra Urs, Paula Zamfir, Emil Boțan, Ximena-Maria Mureșan, Simina Pîrv, Andreea Nuțu, Ioana Berindan-Neagoe, Cristina-Adela Iuga and Ina Maria Kacso
Life 2025, 15(4), 527; https://doi.org/10.3390/life15040527 - 23 Mar 2025
Viewed by 334
Abstract
Podocyte injury is a hallmark of both focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD), ultimately reflected in foot process effacement and proteinuria. Triggers and pathogenic pathways leading to podocyte cytoskeleton rearrangements are, however, incompletely explained. Here, we aimed to contribute to [...] Read more.
Podocyte injury is a hallmark of both focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD), ultimately reflected in foot process effacement and proteinuria. Triggers and pathogenic pathways leading to podocyte cytoskeleton rearrangements are, however, incompletely explained. Here, we aimed to contribute to the understanding of these pathways using tissue bottom-up proteomic profiling of laser-capture microdissected glomeruli from MCD and FSGS. Forty-six differentially expressed proteins were identified between the two groups (p < 0.05, |FC| ≥ 1.2). Pathway analysis showed that 16 out of 46 proteins were associated with the immune system, with E2 ubiquitin-conjugating enzyme (UBE2K) and complement factor H-related protein-1 (CFHR1) yielding the highest fold change in FSGS compared to MCD. The two target proteins were further validated through immunohistochemistry, confirming the podocyte localization of UBE2K and endothelial staining of CFHR. Additionally, several other differentially expressed proteins were linked to the cytoskeleton structure and its regulation. Our results point to the possibility that complement dysregulation may be the source of cytoskeleton rearrangement in FSGS. Full article
(This article belongs to the Special Issue Recent Insights in the Pathogenesis, Diagnosis, Prognosis and Treatment of Glomerular Disorders)
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14 pages, 635 KiB  
Article
Candidate Genetic Modifiers in Alport Syndrome: A Case Series
by Ștefan Nicolaie Lujinschi, Bogdan Marian Sorohan, Bogdan Obrișcă, Alexandra Vrabie, Elena Rusu, Diana Zilișteanu, Camelia Achim, Andreea Gabriella Andronesi and Gener Ismail
Life 2025, 15(2), 298; https://doi.org/10.3390/life15020298 - 14 Feb 2025
Viewed by 540
Abstract
Background: Alport syndrome (AS) is one of the most common monogenic kidney disorders. Recent studies have highlighted the modifier effect of variants involving podocyte and non-collagenous extracellular matrix (ECM) proteins in AS. Methods: We report a case series of eight patients with genetically [...] Read more.
Background: Alport syndrome (AS) is one of the most common monogenic kidney disorders. Recent studies have highlighted the modifier effect of variants involving podocyte and non-collagenous extracellular matrix (ECM) proteins in AS. Methods: We report a case series of eight patients with genetically proven AS and simultaneous variants involving podocyte and non-collagenous ECM proteins. Our aim is to describe the influence of such variants on the phenotype of patients with AS. Results: We identified 10 different type IV collagen variants. Patients were diagnosed with autosomal dominant (3/8), autosomal recessive (2/8), digenic (2/8) and X-linked AS (1/8). There were eight different variants involving podocyte and non-collagenous ECM proteins. The genes involved were CRB2, LAMA5, LAMB2, NUP107, MYO1E and PLCE1. Four patients (LAMB2, LAMA5 and PLCE1 variants) presented with nephrotic syndrome or nephrotic range proteinuria. Two patients had hearing loss. Most patients (7/8) had a family history of kidney disease. Two patients (LAMB2 and LAMA5 variants) were diagnosed with focal segmental glomerulosclerosis. Two patients developed end-stage kidney disease (LAMA5, MYO1E and NUP107 variants). Conclusions: Although mutations of podocyte and ECM proteins do not have phenotypic expression in monoallelic form, the presence of such variants could explain the phenotypic variability of AS. Full article
(This article belongs to the Special Issue Recent Insights in the Pathogenesis, Diagnosis, Prognosis and Treatment of Glomerular Disorders)
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12 pages, 965 KiB  
Article
Comparing Long-Term Outcomes in Glomerular Disease Patients Presenting with Nephrotic Syndrome Versus Nephrotic Range Proteinuria
by Gabriel Ștefan, Simona Stancu, Adrian Zugravu and Nicoleta Petre
Life 2024, 14(12), 1674; https://doi.org/10.3390/life14121674 - 18 Dec 2024
Viewed by 761
Abstract
Background: Despite extensive research on proteinuria’s impact on chronic kidney disease progression, there is no direct comparison of outcomes in biopsy-diagnosed glomerular disease (GD) patients with nephrotic syndrome (NS) or nephrotic range proteinuria (NRP). Our study addresses this gap, comparing long-term outcomes between [...] Read more.
Background: Despite extensive research on proteinuria’s impact on chronic kidney disease progression, there is no direct comparison of outcomes in biopsy-diagnosed glomerular disease (GD) patients with nephrotic syndrome (NS) or nephrotic range proteinuria (NRP). Our study addresses this gap, comparing long-term outcomes between NS and NRP. Methods: We conducted a retrospective study on 240 kidney biopsy-proven GD patients, tracked from 2010 to 2015 until end-stage kidney disease (ESKD), death, or the study end in January 2022. Results: The median follow-up was 8.8 years. Diagnoses were predominantly nonproliferative (53%), proliferative (25%) nephropathies, diabetic nephropathy (12%), and paraprotein diseases (10%). NS was observed in 141 (59%) patients, presenting more frequently with arterial hypertension, higher eGFR, increased proteinuria, and dyslipidemia than NRP patients. NRP patients often had proliferative GD and diabetic nephropathy; their renal chronicity score was higher. The ESKD endpoint occurred in 35% NS and 39% NRP patients (p 0.4). The cohort’s mean kidney survival time was 8.2 years. In a multivariate analysis, NS, lower eGFR, a higher renal chronicity score, and diabetic nephropathy were associated with ESKD. A total of 64 patients (27%) died, 73% post-kidney replacement therapy initiation, and mostly from cardiovascular disease (63%). Mortality between proteinuria forms showed no difference. The multivariate analysis found lower eGFR, a higher Charlson comorbidity score, and diabetic nephropathy associated with mortality. Conclusions: Our study found no difference in all-cause mortality between NS and NRP in glomerular diseases. However, an adjusted analysis revealed poorer kidney survival for NS patients, emphasizing the need for personalized management to improve renal prognoses. Full article
(This article belongs to the Special Issue Recent Insights in the Pathogenesis, Diagnosis, Prognosis and Treatment of Glomerular Disorders)
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12 pages, 1037 KiB  
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Advances in Multitarget Therapeutic Approaches for Immune-Mediated Glomerular Diseases
by Luminita Voroneanu, Andreea Covic, Vladimir Tesar, Mehmet Kanbay and Adrian Covic
Life 2025, 15(2), 243; https://doi.org/10.3390/life15020243 - 6 Feb 2025
Viewed by 842
Abstract
Glomerulonephritis (GN) encompasses a diverse group of immune-mediated diseases that damage the glomerular component of the nephron. While kidney biopsy remains the gold standard for diagnosis, it often fails to provide adequate insight into the underlying etiology of GN. Current classification systems have [...] Read more.
Glomerulonephritis (GN) encompasses a diverse group of immune-mediated diseases that damage the glomerular component of the nephron. While kidney biopsy remains the gold standard for diagnosis, it often fails to provide adequate insight into the underlying etiology of GN. Current classification systems have limited our understanding of the disease’s pathophysiology and hinder the development of targeted therapies. Immunosuppressive treatments, such as glucocorticoids, calcineurin inhibitors, cyclophosphamide, and rituximab, remain the mainstay of therapy, though many patients fail to achieve remission or experience significant adverse effects. Moreover, the complex and multifactorial nature of GN pathogenesis calls for more refined therapeutic approaches. In recent years, multitarget therapies—combining different immunosuppressive agents targeting distinct immune pathways—have emerged as promising alternatives. Evidence suggests that multitarget therapy may offer superior outcomes compared to standard treatments. Despite early success, further studies are needed to optimize these regimens, reduce toxicity, and extend benefits to a broader range of GN patients. The development of personalized, biomarker-driven treatments, potentially leveraging innovative drug delivery systems and targeted biologics, holds promise for transforming GN care in the future. Full article
(This article belongs to the Special Issue Recent Insights in the Pathogenesis, Diagnosis, Prognosis and Treatment of Glomerular Disorders)
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