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New Insights into the Pathogenesis and Therapies of IgA Nephropathy

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 end-stage renal disease (ESRD). Up to 20%–40% of IgAN patients progress to ESRD 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. Better understanding of the pathogenesis of IgAN and the related genetic, immunological, and cellular susceptibility factors is needed to enable development of effective disease-specific therapy.

Pathologic assessment of a renal-biopsy specimen is the current “gold standard” for diagnosis of IgAN as well as assessment of disease severity and prognosis. However, the findings may be impacted by 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, urine), are needed for monitoring of disease progression, responses to treatments, and selection of IgAN patients who would benefit from participation in new 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 ESRD is still available now. To develop a curative treatment, new strategies for early diagnosis, disease-specific targets, and methods for assessment of clinical responses in clinical trials need to be identified and developed.

In this Special Issue on ‘New Insights into the Pathogenesis and Therapies of IgA Nephropathy’, we seek clinical and experimental studies with emphasis on early diagnosis, prognosis, disease pathogenesis, determination of disease activity, and new strategies for treatment for IgAN. Both original research papers and comprehensive review papers are welcome.

Dr. Hitoshi Suzuki
Dr. Jan Novak
Guest Editors

Manuscript Submission Information

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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
  • complement
  • biomarker
  • B cell
  • renal pathology
  • genetic factor
  • corticosteroid
  • immunosuppressant

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J. Clin. Med. - ISSN 2077-0383