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Biomedicines
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Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel...
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Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 4237

Special Issue Editors

Dr. Vassilis Filiopoulos

E-Mail Website
Guest Editor
Department of Nephrology and Kidney Transplantation, School of Medicine, National and Kapodistrian University of Athens, General Hospital of Athens “Laiko”, 11527 Athens, Greece
Interests: polycystic kidney disease; glomerular disease; kidney transplantation; immunology
Dr. Chrysanthi Skalioti

E-Mail Website
Guest Editor
Department of Nephrology and Kidney Transplantation, School of Medicine, National and Kapodistrian University of Athens, General Hospital of Athens “Laiko”, 11527 Athens, Greece
Interests: glomerular disease; kidney transplantation; acute kidney injury

Special Issue Information

Dear Colleagues,

This Special issue aims to gather publications related to glomerular disease, both primary and secondary, and cystic kidney disease, especially polycystic kidney disease, the most common hereditary kidney disease. Glomerular disease describes a variety of relatively rare immune-mediated diseases characterized by damage to the glomerular compartment of the kidney. If not properly treated, glomerular disease can lead to chronic kidney disease and irreversible kidney failure. On the other hand, cystic kidney disease represents multisystemic disorders that can develop due to genetic or non-genetic causes in children and adults and may have serious renal and extrarenal complications. Both of these entities have to show notable progress in their complex pathophysiology and various potential therapeutic targets are available for which novel treatments are being developed or repurposed. The growing awareness of the immunopathogenesis of glomerular diseases and the improvements in immune phenotyping for the classification of patients have facilitated the choice of targeted immunotherapies. Regarding polycystic kidney disease, tolvaptan, a selective vasopressin V2 antagonist, has been proven to attenuate disease progression and several other disease-modifying therapies are currently being investigated in clinical trials. Furthermore, extended genetic testing, with next-generation sequencing, is another evolving diagnostic tool to ultimately define a molecular diagnosis and appears extremely useful in both of these entities.

This Special Issue welcomes original articles and reviews focused on pathogenesis and treatment of glomerular diseases and cystic kidney diseases.  

Dr. Vassilis Filiopoulos
Dr. Chrysanthi Skalioti
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. Biomedicines 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 disease
  • glomerulonephritis
  • glomerulopathy
  • podocytopathies
  • ciliopathies
  • cystic kidney disease
  • polycystic kidney disease
  • tolvaptan
  • vasopressin

Published Papers (4 papers)

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Research

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12 pages, 729 KiB  
Article
A Prospective Study of Eplerenone in the Treatment of Patients with Glomerulonephritis
by Marios Papasotiriou, Georgia Andrianna Georgopoulou, Adamantia Mpratsiakou, Theodoros Ntrinias, Georgios Lyras, Dimitrios S. Goumenos and Evangelos Papachristou
Biomedicines 2023, 11(12), 3340; https://doi.org/10.3390/biomedicines11123340 - 18 Dec 2023
Viewed by 1082
Abstract
Background: High aldosterone levels contribute to kidney disease progression, while spironolactone in combination with ACEi or ARBs can potentially reduce proteinuria and ameliorate kidney function deterioration. However, evidence on the impact of eplerenone in patients with glomerulonephritis is scarce. Methods: In this prospective [...] Read more.
Background: High aldosterone levels contribute to kidney disease progression, while spironolactone in combination with ACEi or ARBs can potentially reduce proteinuria and ameliorate kidney function deterioration. However, evidence on the impact of eplerenone in patients with glomerulonephritis is scarce. Methods: In this prospective observational study, we assessed the effects of eplerenone in patients with biopsy-proven glomerulonephritis who were already treated with ACEi or ARBs. Patients received either eplerenone (25 mg daily) on top of ACEi or ARBs or standard treatment alone. Proteinuria (24 h total protein excretion), kidney function, blood pressure and serum K+ levels were assessed at 3, 6 and 12 months after the initiation of treatment. Results: Sixty-six patients were included in the study. Eplerenone was administered in 30 patients, while 36 received only ACEi or ARB. Proteinuria decreased from 1768 to 1152 mg/24 h after 1 year of eplerenone treatment, while it remained stable in controls. Eplerenone showed significant impact on proteinuria in those with baseline proteinuria of >1000 mg/24 h. Patients who received eplerenone showed a reduction in systolic blood pressure, while eGFR and serum K+ levels remained stable. Conclusions: Addition of eplerenone has a beneficial effect on proteinuria in patients with glomerulonephritis and significant baseline proteinuria. Full article
(This article belongs to the Special Issue Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel Therapeutic Approaches)
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13 pages, 3151 KiB  
Article
Constitutive HO-1 and CD55 (DAF) Expression and Regulatory Interaction in Cultured Podocytes
by Elias A. Lianos, Kelsey Wilson, Katerina Goudevenou, Maria G. Detsika and Mukut Sharma
Biomedicines 2023, 11(12), 3297; https://doi.org/10.3390/biomedicines11123297 (registering DOI) - 13 Dec 2023
Viewed by 846
Abstract
Overexpression of the inducible heme oxygenase (HO-1) isoform in visceral renal glomerular epithelial cells (podocytes) using in vivo transgenesis methods was shown to increase glomerular expression of the complement regulatory protein decay-accelerating factor (DAF, CD55) and reduce complement activation/deposition in a rat model [...] Read more.
Overexpression of the inducible heme oxygenase (HO-1) isoform in visceral renal glomerular epithelial cells (podocytes) using in vivo transgenesis methods was shown to increase glomerular expression of the complement regulatory protein decay-accelerating factor (DAF, CD55) and reduce complement activation/deposition in a rat model of immune-mediated injury. In this preliminary study, we assessed whether constitutively expressed HO-1 regulates CD55 expression in cultured rat podocytes. We employed methods of flow cytometry, quantitative (q) RT-qPCR and post-transcriptional HO-1 gene silencing (HO-1 interfering RNA, RNAi), to assess changes in constitutive (basal) levels of podocyte HO-1 and CD55 mRNA in cultured rat podocytes. Additionally, the effect of the HO-1 inducer, heme, on HO-1 and CD55 expression was assessed. Results indicate that rat podocytes constitutively express HO-1 and DAF and that the HO-1 inducer, heme, increases both HO-1 and DAF expression. HO-1 gene silencing using RNA interference (RNAi) is feasible but the effect on constitutive CD55 transcription is inconsistent. These observations are relevant to conditions of podocyte exposure to heme that can activate the complementary cascade, as may occur in systemic or intraglomerular hemolysis. Full article
(This article belongs to the Special Issue Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel Therapeutic Approaches)
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Review

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14 pages, 2013 KiB  
Review
The Han:SPRD Rat: A Preclinical Model of Polycystic Kidney Disease
by Ioannis Kofotolios, Michael J. Bonios, Markos Adamopoulos, Iordanis Mourouzis, Gerasimos Filippatos, John N. Boletis, Smaragdi Marinaki and Manolis Mavroidis
Biomedicines 2024, 12(2), 362; https://doi.org/10.3390/biomedicines12020362 - 3 Feb 2024
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Abstract
Autosomal Dominant Polycystic Kidney Disease (ADPKD) stands as the most prevalent hereditary renal disorder in humans, ultimately culminating in end-stage kidney disease. Animal models carrying mutations associated with polycystic kidney disease have played an important role in the advancement of ADPKD research. The [...] Read more.
Autosomal Dominant Polycystic Kidney Disease (ADPKD) stands as the most prevalent hereditary renal disorder in humans, ultimately culminating in end-stage kidney disease. Animal models carrying mutations associated with polycystic kidney disease have played an important role in the advancement of ADPKD research. The Han:SPRD rat model, carrying an R823W mutation in the Anks6 gene, is characterized by cyst formation and kidney enlargement. The mutated protein, named Samcystin, is localized in cilia of tubular epithelial cells and seems to be involved in cystogenesis. The homozygous Anks6 mutation leads to end-stage renal disease and death, making it a critical factor in kidney development and function. This review explores the utility of the Han:SPRD rat model, highlighting its phenotypic similarity to human ADPKD. Specifically, we discuss its role in preclinical trials and its importance for investigating the pathogenesis of the disease and developing new therapeutic approaches. Full article
(This article belongs to the Special Issue Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel Therapeutic Approaches)
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Other

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13 pages, 8042 KiB  
Systematic Review
Recurrence of Idiopathic Membranous Nephropathy in the Kidney Allograft: A Systematic Review
by Anastasios Panagakis, Ioannis Bellos, Konstantinos Grigorakos, Stylianos Panagoutsos, Ploumis Passadakis and Smaragdi Marinaki
Biomedicines 2024, 12(4), 739; https://doi.org/10.3390/biomedicines12040739 - 26 Mar 2024
Viewed by 641
Abstract
Introduction: The recurrence of idiopathic membranous nephropathy (iMN) after kidney transplantation is common, although its exact clinical significance remains unclear. This systematic review aims to elucidate the effects of iMN recurrence on graft survival. Materials and methods: A literature search was performed by [...] Read more.
Introduction: The recurrence of idiopathic membranous nephropathy (iMN) after kidney transplantation is common, although its exact clinical significance remains unclear. This systematic review aims to elucidate the effects of iMN recurrence on graft survival. Materials and methods: A literature search was performed by systematically searching Medline, Scopus, Web of Science, and Google Scholar from inception. Cohort studies examining iMN recurrence after kidney transplantation were deemed eligible. Meta-analysis was performed by fitting random-effects models. Results: Twelve (12) articles published from 1995 to 2016 reporting on 139 transplant patients with recurrent iMN were included. The median time of the diagnosis of recurrent iMN was 18 months during follow-up from 35 to 120 months. Risk factors for iMN recurrence in the renal allograft are a positive serum test for anti-PLA2R antibodies pretransplant, female sex, younger age, high proteinuria pretransplant, the longest interval from initial disease to end-stage chronic kidney disease, and the combination of alleles HLA DQA1 05:01 and HLA DQB1 02:01. In the pretransplant period, 37 (26.61%) patients had a positive serum test and 18 (12.94%) patients had a positive biopsy stain for anti-PLA2R antibodies. The sensitivity of the pretransplant positive serum test for these antibodies ranges from 57% to 85.30% and the specificity is 85.10–100%. A total of 81.80% of patients who received rituximab as treatment for iMN recurrence achieved complete and partial remission, while 18.20% had no response to treatment. iMN recurrence was not associated with significantly different rates of graft loss (odds ratio = 1.03, 95% CI: 0.52–2.04, p = 0.524, I2 = 0.00%). Recurrence of iMN was not associated with increased risk of graft loss independently of whether patients were treated with rituximab (OR: 0.98, 95% CI: 0.39–2.50, I2: 0%) or not (OR: 1.22, 95% CI: 0.58–2.59, I2: 3.8%). Patients with iMN recurrence who achieved remission had significantly reduced risk of graft loss (OR: 0.14, 95% CI: 0.03 to 0.73). Conclusion: The main outcome from this systematic review is that there is no statistically significant difference in graft survival in patients with iMN recurrence compared to those without recurrence in long-term follow-up. The achievement of remission is associated with significantly reduced risk of graft loss. Full article
(This article belongs to the Special Issue Glomerular Disease and Cystic Kidney Disease: From Pathogenesis to Novel Therapeutic Approaches)
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