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Biomedicines
Special Issues
Nephrotic Syndrome: Pathomechanism, Diagnostics and Novel Treatment Options
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Nephrotic Syndrome: Pathomechanism, Diagnostics and Novel Treatment Options

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 4612

Special Issue Editor

Dr. Kan Katayama

E-Mail Website
Guest Editor
Department of Cardiology and Nephrology, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu 514-8507, Mie, Japan
Interests: nephrotic syndrome; interstitial nephritis; thin basement membrane nephropathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nephrotic syndrome (NS) is characterized by massive proteinuria, hypoproteinemia, and edema, and it is divided into steroid-sensitive NS (SSNS) and steroid-resistant NS (SRNS). While SSNS typically presents with minimal change NS, SRNS typically presents with focal segmental glomerulosclerosis (FSGS), which often leads to end-stage kidney failure. About 30% of cases of childhood-onset FSGS have been found to be hereditary FSGS caused by dozens of podocyte-related genes, and about 5-10% of cases of adult-onset FSGS have also been found to be hereditary FSGS.

The aim of this Special Issue is to gather original research articles and review articles that focus on NS. Articles focused on genetic forms of kidney disease are especially encouraged.

Dr. Kan Katayama
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 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

  • focal segmental glomerulosclerosis
  • genetic kidney disease
  • minimal change disease
  • nephrotic syndrome
  • podocyte

Published Papers (4 papers)

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Research

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11 pages, 864 KiB  
Article
Consequences of Nephrotic Proteinuria and Nephrotic Syndrome after Kidney Transplant
by María José Ortega, Miguel Martínez-Belotto, Cristina García-Majado, Lara Belmar, Covadonga López del Moral, Jose María Gómez-Ortega, Rosalía Valero, Juan Carlos Ruiz and Emilio Rodrigo
Biomedicines 2024, 12(4), 767; https://doi.org/10.3390/biomedicines12040767 - 30 Mar 2024
Viewed by 501
Abstract
Proteinuria is the main predictor of kidney graft loss. However, there is little information regarding the consequences of nephrotic proteinuria (NP) and nephrotic syndrome (NS) after a kidney transplant. We aimed to describe the clinical and histopathological characteristics of kidney recipients with nephrotic-range [...] Read more.
Proteinuria is the main predictor of kidney graft loss. However, there is little information regarding the consequences of nephrotic proteinuria (NP) and nephrotic syndrome (NS) after a kidney transplant. We aimed to describe the clinical and histopathological characteristics of kidney recipients with nephrotic-range proteinuria and compare the graft surveillance between those who developed NS and those who did not. A total of 204 patients (18.6% of kidney transplants in the study period) developed NP, and 68.1% of them had NS. Of the 110 patients who underwent a graft biopsy, 47.3% exhibited ABMR, 21.8% the recurrence of glomerulonephritis, 9.1% IFTA, and 7.3% de novo glomerulonephritis. After a median follow-up of 97.5 months, 64.1% experienced graft loss. The graft survival after the onset of NP declined from 75.8% at 12 months to 38% at 5 years, without significant differences between those with and those without NS. Patients who developed NS fewer than 3 months after the onset of NP exhibited a significantly higher risk of death-censored graft loss (HR: 1.711, 95% CI: 1.147–2.553) than those without NS or those with late NS. In conclusion, NP and NS are frequent conditions after a kidney transplant, and they imply extremely poor graft outcomes. The time from the onset of NP to the development of NS is related to graft survival. Full article
(This article belongs to the Special Issue Nephrotic Syndrome: Pathomechanism, Diagnostics and Novel Treatment Options)
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Review

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15 pages, 1515 KiB  
Review
Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome
by Maria E. Kovalik, Monique A. Dacanay, Steven D. Crowley and Gentzon Hall
Biomedicines 2024, 12(4), 738; https://doi.org/10.3390/biomedicines12040738 - 26 Mar 2024
Viewed by 656
Abstract
Interleukins are a family of 40 bioactive peptides that act through cell surface receptors to induce a variety of intracellular responses. While interleukins are most commonly associated with destructive, pro-inflammatory signaling in cells, some also play a role in promoting cellular resilience and [...] Read more.
Interleukins are a family of 40 bioactive peptides that act through cell surface receptors to induce a variety of intracellular responses. While interleukins are most commonly associated with destructive, pro-inflammatory signaling in cells, some also play a role in promoting cellular resilience and survival. This review will highlight recent evidence of the cytoprotective actions of the interleukin 1 receptor (IL-1R)- and common gamma chain receptor (IL-Rγc)-signaling cytokines in nephrotic syndrome (NS). NS results from the injury or loss of glomerular visceral epithelial cells (i.e., podocytes). Although the causes of podocyte dysfunction vary, it is clear that pro-inflammatory cytokines play a significant role in regulating the propagation, duration and severity of disease. Pro-inflammatory cytokines signaling through IL-1R and IL-Rγc have been shown to exert anti-apoptotic effects in podocytes through the phosphoinositol-3-kinase (PI-3K)/AKT pathway, highlighting the potential utility of IL-1R- and IL-Rγc-signaling interleukins for the treatment of podocytopathy in NS. The paradoxical role of interleukins as drivers and mitigators of podocyte injury is complex and ill-defined. Emerging evidence of the cytoprotective role of some interleukins in NS highlights the urgent need for a nuanced understanding of their pro-survival benefits and reveals their potential as podocyte-sparing therapeutics for NS. Full article
(This article belongs to the Special Issue Nephrotic Syndrome: Pathomechanism, Diagnostics and Novel Treatment Options)
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16 pages, 618 KiB  
Review
Complement Activation in Nephrotic Glomerular Diseases
by Dominik Nell, Robert Wolf, Przemyslaw Marek Podgorny, Tobias Kuschnereit, Rieke Kuschnereit, Thomas Dabers, Sylvia Stracke and Tilman Schmidt
Biomedicines 2024, 12(2), 455; https://doi.org/10.3390/biomedicines12020455 - 18 Feb 2024
Viewed by 1050
Abstract
The nephrotic syndrome holds significant clinical importance and is characterized by a substantial protein loss in the urine. Damage to the glomerular basement membrane or podocytes frequently underlies renal protein loss. There is an increasing belief in the involvement of the complement system, [...] Read more.
The nephrotic syndrome holds significant clinical importance and is characterized by a substantial protein loss in the urine. Damage to the glomerular basement membrane or podocytes frequently underlies renal protein loss. There is an increasing belief in the involvement of the complement system, a part of the innate immune system, in these conditions. Understanding the interactions between the complement system and glomerular structures continually evolves, challenging the traditional view of the blood–urine barrier as a passive filter. Clinical studies suggest that a precise inhibition of the complement system at various points may soon become feasible. However, a thorough understanding of current knowledge is imperative for planning future therapies in nephrotic glomerular diseases such as membranous glomerulopathy, membranoproliferative glomerulonephritis, lupus nephritis, focal segmental glomerulosclerosis, and minimal change disease. This review provides an overview of the complement system, its interactions with glomerular structures, and insights into specific glomerular diseases exhibiting a nephrotic course. Additionally, we explore new diagnostic tools and future therapeutic approaches. Full article
(This article belongs to the Special Issue Nephrotic Syndrome: Pathomechanism, Diagnostics and Novel Treatment Options)
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16 pages, 798 KiB  
Review
Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models
by Ryosuke Saiki, Kan Katayama and Kaoru Dohi
Biomedicines 2023, 11(7), 1803; https://doi.org/10.3390/biomedicines11071803 - 23 Jun 2023
Viewed by 1772
Abstract
Proteinuria is known to be associated with all-cause and cardiovascular mortality, and nephrotic syndrome is defined by the level of proteinuria and hypoalbuminemia. With advances in medicine, new causative genes for genetic kidney diseases are being discovered increasingly frequently. We reviewed articles on [...] Read more.
Proteinuria is known to be associated with all-cause and cardiovascular mortality, and nephrotic syndrome is defined by the level of proteinuria and hypoalbuminemia. With advances in medicine, new causative genes for genetic kidney diseases are being discovered increasingly frequently. We reviewed articles on proteinuria/nephrotic syndrome, focal segmental glomerulosclerosis, membranous nephropathy, diabetic kidney disease/nephropathy, hypertension/nephrosclerosis, Alport syndrome, and rare diseases, which have been studied in mouse models. Significant progress has been made in understanding the genetics and pathophysiology of kidney diseases thanks to advances in science, but research in this area is ongoing. In the future, genetic analyses of patients with proteinuric kidney disease/nephrotic syndrome may ultimately lead to personalized treatment options. Full article
(This article belongs to the Special Issue Nephrotic Syndrome: Pathomechanism, Diagnostics and Novel Treatment Options)
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