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Advances in Primary Nephropathies: Pathogenesis, Inflammatory Response and Advanced Treatments

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 30 December 2024 | Viewed by 1104

Special Issue Editors


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Guest Editor
Nephrology and Transplantation Group (2017 SGR189), Institut d’Investigació Biomèdica (IDIBELL), Hospital Universitari de Bellvitge, 08907 Barcelona, Spain
Interests: microscopic vasculitis; primary glomerular diseases; membranous nephropathy; IgA nephropathy; clinical nephrology; interstitial nephritis; immune checkpoint inhibitors; autoimmune diseases; renal transplantation; clinical immunosuppression; experimental models; alloreactivity, autoimmunity; lupus nephritis; renal models; gene therapy; cell therapy; transplantation; ischemia–reperfusion

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Guest Editor
1. Nephrology Department, Bellvitge University Hospital, 08907 L’Hospitalet de Llobregat, Spain
2. Experimental Nephrology Laboratory, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), 08907 L’Hospitalet de Llobregat, Spain
Interests: microscopic vasculitis; primary glomerular diseases; membranous nephropathy; IgA nephropathy; clinical nephrology; interstitial nephritis; immune checkpoint inhibitors; autoimmune diseases

Special Issue Information

Dear Colleagues,

IgA and membranous nephropathies are the most prevalent primary glomerular diseases and constitute a frequent etiology of end-stage renal failure. Recent advances in our knowledge of the pathogenesis of both nephropathies have highlighted new variables that will allow us to better understand the complex mechanisms involved in their development and pathogenesis.

A myriad of new protein markers in membranous nephropathy have been described that warrant further research to understand the pathways and mechanisms of this disease. Moreover, the “four hit” hypothesis in IgA nephropathy, with a central role in galactose-deficient IgA1, needs a better description, and new essential research items must be established, to develop a clear understanding of this disease.

The pharmaceutic industry is making considerable efforts to better understand both of these diseases, investigating alternative complement pathways, as well as B-cell blocking with anti-CD20 or anti-APRIL antibodies. This topic constitutes a hot spot in clinical nephrology.

This Special Issue entitled “Advances in Primary Nephropathies: Pathogenesis, Inflammatory Response and Advanced Treatments” will include papers investigating the pathological mechanisms involved in primary nephropathies, as well as diagnostics using new biomarkers. Furthermore, it will present experimental in vitro and in vivo studies and clinical studies examining potential new approaches to attenuating kidney dysfunction.

This Special Issue welcomes original research and review papers, with potential topics including, but not limited to, the keywords below.

Prof. Dr. Joan Torras-Ambròs
Dr. Juliana Bordignon-Draibe
Guest Editors

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Keywords

  • primary glomerular diseases
  • membranous nephropathy
  • IgA nephropathy
  • glomerular inflammatory mechanisms
  • aberrantly glycosylated IgA1
  • galactose-deficient IgA1 (Gd-IgA1)
  • alternative complement pathway
  • C5
  • factor B
  • factor D
  • APRIL
  • BAFF
  • phospholipase A2 receptor (PLA2R)
  • thrombospondin type I domain-containing 7A (THSD7A)
  • exostosins 1 and 2 (EXT1/2)
  • neural epidermal growth factor-like 1 protein (NELL-1)
  • semaphorin 3B (Sema3B)
  • neural cell adhesion molecule 1 (NCAM1)

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Published Papers (1 paper)

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11 pages, 3096 KiB  
Article
Soluble Epoxide Hydrolase Inhibition Attenuates Proteinuria by Alleviating Renal Inflammation and Podocyte Injuries in Adriamycin-Induced Nephropathy
by Qingyu Niu, Ziyu Guo, Yaoxian Liang and Li Zuo
Int. J. Mol. Sci. 2024, 25(19), 10629; https://doi.org/10.3390/ijms251910629 - 2 Oct 2024
Viewed by 829
Abstract
Soluble epoxide hydrolase (sEH) has previously been demonstrated to play an important part in kidney diseases by hydrolyzing renoprotective epoxyeicosatrienoic acids to their less active diols. However, little is known about the role of sEH in primary glomerular diseases. Here, we investigated the [...] Read more.
Soluble epoxide hydrolase (sEH) has previously been demonstrated to play an important part in kidney diseases by hydrolyzing renoprotective epoxyeicosatrienoic acids to their less active diols. However, little is known about the role of sEH in primary glomerular diseases. Here, we investigated the effects of sEH inhibition on proteinuria in primary glomerular diseases and the underlying mechanism. The expression of sEH in the renal tubules of patients with minimal change disease, IgA nephropathy, and membranous nephropathy was significantly increased. Renal sEH expression level was positively correlated with the 24 h urine protein excretion and negatively correlated with serum albumin. In the animal model of Adriamycin (ADR)-induced nephropathy, renal sEH mRNA and protein expression increased significantly. Pharmacological inhibition of sEH with AUDA effectively reduced urine protein excretion and attenuated renal pathological damage. Furthermore, sEH inhibition markedly abrogated the abnormal expressions of nephrin and desmin in glomerular podocytes induced by ADR. More importantly, AUDA treatment inhibited renal NF-κB activation and reduced TNF-α levels in rats with ADR-induced nephropathy. Overall, our findings suggest that sEH inhibition ameliorates renal inflammation and podocyte injury, thus reducing proteinuria and exerting renoprotective effects. Targeting sEH might be a potential strategy for the treatment of proteinuria in primary glomerular diseases. Full article
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