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

This special issue belongs to the section “Nephrology & Urology“.

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.

All papers submitted to this Special Issue are reviewed by independent referees, and the final decision is made by a JCM Editorial Board Member who does not have any conflict of interest with the submission.

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 250 words) can be sent to the Editorial Office for assessment.

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

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J. Clin. Med. - ISSN 2077-0383