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New Insights into the Pathogenesis and Therapies of IgA Nephropathy—Second...
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New Insights into the Pathogenesis and Therapies of IgA Nephropathy—Second Volume

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Nephrology & Urology".

Deadline for manuscript submissions: 20 June 2024 | Viewed by 6380

Special Issue Editors

Prof. Dr. Hitoshi Suzuki

E-Mail Website
Guest Editor
Department of Nephrology, Juntendo University Urayasu Hospital, Chiba, Japan
Interests: IgA nephropathy; immune complex; chronic kidney disease; hypertension
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jan Novak

E-Mail Website
Guest Editor
Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
Interests: glycosylation in health and disease; chronic inflammatory diseases; glomerular diseases; IgA nephropathy; gly-comics; infectious diseases; HIV-1 glycomics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and a frequent cause of kidney failure. Up to 20–40% of IgAN patients progress to kidney failure within 20 years after diagnosis. Moreover, life expectancy is reduced in patients with IgAN by a decade. Thus, IgAN is an important public health problem. A better understanding of the pathogenesis of IgAN and the related genetic, immunological and cellular susceptibility factors is needed to allow for the development of an effective disease-specific therapy.

The pathologic assessment of a renal biopsy specimen is the current “gold standard” for the diagnosis of IgAN, as well as an assessment of disease severity and prognosis. However, the findings may be impacted in the time between disease onset and diagnostic renal biopsy, as well as by prior medications. Thus, renal biopsy provides a snapshot in time as the inherent risks associated with renal biopsy discourage from repeat biopsy. Minimally invasive approaches, such as those based on liquid biopsy biomarkers (e.g., blood and urine), are needed for the monitoring of disease progression, responses to treatments and the selection of IgAN patients who would benefit from participation in novel clinical trials.

Although the understanding of IgAN pathogenesis has expanded significantly since the initial disease description in 1968, disease-specific therapy to slow or prevent the progression of IgAN to kidney failure is still not available now. To develop a curative treatment, novel strategies for the early diagnosis, disease-specific targets and methods for the assessment of responses in clinical trials need to be identified and developed.

After the success of the Special Issue “New Insights into the Pathogenesis and Therapies of IgA Nephropathy”, a second volume is in production to continue seeking clinical and experimental studies with emphasis on early diagnosis, prognosis, disease pathogenesis, the determination of disease activity and novel strategies for the treatment of IgAN. Both original research and comprehensive review papers are welcome.

Prof. Dr. Hitoshi Suzuki
Prof. Dr. Jan Novak
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly 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

  • IgA nephropathy
  • immune complex
  • galactose-deficient IgA1
  • autoantibodies
  • complement
  • biomarker
  • B cell
  • renal pathology
  • genetic factor
  • corticosteroid
  • immunosuppressant
  • natural product
  • clinical trial

Related Special Issue

Published Papers (3 papers)

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Research

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11 pages, 2155 KiB  
Article
Colocalization of IgG and IgA Heavy Chains with Kappa and Lambda Light Chains in Glomerular Deposits of IgA Nephropathy Patients Using High-Resolution Confocal Microscopy and Correlation with Oxford MEST-C Scores
by Dana V. Rizk, Lea Novak, Stacy D. Hall, Zina Moldoveanu, Bruce A. Julian, Jan Novak and Mark Haas
J. Clin. Med. 2023, 12(23), 7361; https://doi.org/10.3390/jcm12237361 - 28 Nov 2023
Viewed by 877
Abstract
Routine immunofluorescence microscopy of glomerular immunodeposits in IgA nephropathy shows IgA, C3, and lambda light chains, and sometimes IgG, IgM, and kappa light chains. However, a previous study using high-resolution confocal microscopy showed IgG in all IgA nephropathy cases, likely representing autoantibodies specific [...] Read more.
Routine immunofluorescence microscopy of glomerular immunodeposits in IgA nephropathy shows IgA, C3, and lambda light chains, and sometimes IgG, IgM, and kappa light chains. However, a previous study using high-resolution confocal microscopy showed IgG in all IgA nephropathy cases, likely representing autoantibodies specific for galactose-deficient IgA1. Here, we used high-resolution confocal microscopy to examine the composition of glomerular immunodeposits and colocalization of kappa and lambda light chains with IgA or IgG heavy chains in kidney-biopsy samples from twenty patients with IgA nephropathy, seventeen without IgG, and nine with no or trace kappa light chains by routine immunofluorescence microscopy. IgG was detected in all biopsies by high-resolution confocal microscopy. Single-optical-plane images showed similar colocalization of IgG heavy chains with kappa and lambda light chains. Colocalization of IgA heavy chains was greater with lambda light chains than with kappa light chains. Colocalization of IgG heavy chain with kappa light chains was higher than with lambda light chains in biopsies with endocapillary hypercellularity and crescents, i.e., biopsies with active lesions. We confirmed the utility of high-resolution confocal microscopy to detect components of glomerular immunodeposits not apparent on routine immunofluorescence microscopy and for colocalization of different components, potentially clarifying the pathogenesis of IgA nephropathy. Full article
(This article belongs to the Special Issue New Insights into the Pathogenesis and Therapies of IgA Nephropathy—Second Volume)
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Review

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18 pages, 993 KiB  
Review
An Update on Current Therapeutic Options in IgA Nephropathy
by Regina Shaoying Lim, See Cheng Yeo, Jonathan Barratt and Dana V. Rizk
J. Clin. Med. 2024, 13(4), 947; https://doi.org/10.3390/jcm13040947 - 7 Feb 2024
Cited by 1 | Viewed by 2946
Abstract
Immunoglobulin A nephropathy (IgAN) remains the leading cause of primary glomerular disease worldwide. Outcomes are poor with high rates of progressive chronic kidney disease and kidney failure, which contributes to global healthcare costs. Although this disease entity has been described, there were no [...] Read more.
Immunoglobulin A nephropathy (IgAN) remains the leading cause of primary glomerular disease worldwide. Outcomes are poor with high rates of progressive chronic kidney disease and kidney failure, which contributes to global healthcare costs. Although this disease entity has been described, there were no disease-specific treatments until recently, with the current standard of care focusing on optimal supportive measures including lifestyle modifications and optimization of the renin-angiotensin-aldosterone blockade. However, with significant advances in the understanding of the pathogenesis of IgAN in the past decade, and the acceptance of surrogate outcomes for accelerated drug approval, there have been many new investigational agents tested to target this disease. As these agents become available, we envision a multi-pronged treatment strategy that simultaneously targets the consequences of ongoing nephron loss, stopping any glomerular inflammation, inhibiting pro-fibrotic signals in the glomerulus and tubulo-interstitium, and inhibiting the production of pathogenic IgA molecules. This review is an update on a previous review published in 2021, and we aim to summarize the developments and updates in therapeutic strategies in IgAN and highlight the promising discoveries that are likely to add to our armamentarium. Full article
(This article belongs to the Special Issue New Insights into the Pathogenesis and Therapies of IgA Nephropathy—Second Volume)
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15 pages, 1244 KiB  
Review
An Update on the Genetics of IgA Nephropathy
by Lin-Lin Xu, Xu-Jie Zhou and Hong Zhang
J. Clin. Med. 2024, 13(1), 123; https://doi.org/10.3390/jcm13010123 - 25 Dec 2023
Viewed by 1903
Abstract
Immunoglobulin A (IgA) nephropathy (IgAN), the most common form of glomerulonephritis, is one of the leading causes of end-stage kidney disease (ESKD). It is widely believed that genetic factors play a significant role in the development of IgAN. Previous studies of IgAN have [...] Read more.
Immunoglobulin A (IgA) nephropathy (IgAN), the most common form of glomerulonephritis, is one of the leading causes of end-stage kidney disease (ESKD). It is widely believed that genetic factors play a significant role in the development of IgAN. Previous studies of IgAN have provided important insights to unravel the genetic architecture of IgAN and its potential pathogenic mechanisms. The genome-wide association studies (GWASs) together have identified over 30 risk loci for IgAN, which emphasizes the importance of IgA production and regulation in the pathogenesis of IgAN. Follow-up fine-mapping studies help to elucidate the candidate causal variant and the potential pathogenic molecular pathway and provide new potential therapeutic targets. With the rapid development of next-generation sequencing technologies, linkage studies based on whole-genome sequencing (WGS)/whole-exome sequencing (WES) also identify rare variants associated with IgAN, accounting for some of the missing heritability. The complexity of pathogenesis and phenotypic variability may be better understood by integrating genetics, epigenetics, and environment. We have compiled a review summarizing the latest advancements in genetic studies on IgAN. We similarly summarized relevant studies examining the involvement of epigenetics in the pathogenesis of IgAN. Future directions and challenges in this field are also proposed. Full article
(This article belongs to the Special Issue New Insights into the Pathogenesis and Therapies of IgA Nephropathy—Second Volume)
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