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World J Nephrol. Sep 25, 2021; 10(5): 88-100
Published online Sep 25, 2021. doi: 10.5527/wjn.v10.i5.88
Trends in pediatric nephrotic syndrome
Hiroshi Tamura
Hiroshi Tamura, Department of Pediatrics, Kumamoto University, Kumamoto 8608556, Japan
Author contributions: Tamura H wrote the paper and collected the data.
Conflict-of-interest statement: The author declare that this manuscript has no conflict of interest.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Hiroshi Tamura, MD, PhD, Assistant Professor, Department of Pediatrics, Kumamoto University, 1-1-1 Honjo, Chuo-ku, Kumamoto 8608556, Japan. bohm1905ht@kuh.kumamoto-u.ac.jp
Received: March 21, 2021
Peer-review started: March 21, 2021
First decision: May 6, 2021
Revised: May 15, 2021
Accepted: August 10, 2021
Article in press: August 10, 2021
Published online: September 25, 2021
Core Tip

Core Tip: There is no doubt that some vascular hyperpermeability factor is involved in the incidence of proteinuria in idiopathic nephrotic syndrome (INS). However, no etiological molecule has been identified in INS as a factor for increasing the permeability of renal glomerular capillaries with reproducibility and clinical consistency. In addition, since the onset is sometimes observed in the family, there is high incidence of INS in East Asian children and there is the association of steroid-sensitive NS in childhood in Japan with the HLA-DR/DQ region, it is highly possible that some genetic factors are involved in the onset of NS. In our opinion, INS is a multifactorial disease in which immunological stimuli, trigger the production of substances that impair podocytes, resulting in dysfunction of the slit membrane and cause proteinuria.