Elucidation of the pathogenic mechanism of glomerulosclerosis by circulating factors

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390259
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Pediatrics
• Research Institution: The University of Tokyo
• Principal Investigator: HARITA Yutaka 東京大学, 医学部附属病院, 講師 (10451866)
• Co-Investigator(Kenkyū-buntansha): MIURA Kenichiro 東京大学, 医学部附属病院, 助教 (70408483) ; IGARASHI Takashi 独立行政法人国立成育医療センター, 総長室, 総長 (70151256) ; HATTORI Seisuke 北里大学, 薬学部, 教授 (50143508)
• Co-Investigator(Renkei-kenkyūsha): HATTORI Motoshi 東京女子医科大学, 医学部, 教授 (50192274)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: ネフローゼ症候群 / 巣状糸球体硬化症 / 糸球体上皮細胞

Outline of Final Research Achievements

Our objectives were to identify candidate circulating factor(s) of idiopathic nephrotic syndrome, and to elucidate the mechanism of impaired glomerular barrier function by nephrotic circulating factor(s). We found that soluble urokinase plasminogen receptor (suPAR) is not the primary factor of focal segmental glomerulosclerosis, and searched for novel candidate circulating factors of idiopathic nephrotic syndrome. We also identified the molecular mechanism of slit diaphragm maintenance crucial for prevention of proteinuria, and the molecular changes in podocytes in patients with various types of nephrotic syndrome. The present study revealed novel pathogenic mechanisms crucial for development of therapeutic targets of nephrotic syndrome.

Free Research Field

小児腎臓病学