Investigation of disease progression in difficult-to-treat nephrotic syndrome using urinary podocytes

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K07829
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 52050:Embryonic medicine and pediatrics-related
• Research Institution: Tokyo Women's Medical University
• Principal Investigator: Miura Kenichiro 東京女子医科大学, 医学部, 准教授 (70408483)
• Co-Investigator(Kenkyū-buntansha): 山本 俊至 東京女子医科大学, 医学部, 教授 (20252851) ; 服部 元史 東京女子医科大学, 医学部, 教授 (50192274) ; 栗原 秀剛 藍野大学, 医療保健学部, 副学長・教授 (80311976)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 巣状分節性糸球体硬化症 / ネフローゼ症候群 / 尿中ポドサイト / 細胞周期

Outline of Final Research Achievements

In this study, we performed morphological analyses of urinary podocytes in focal segmental glomerulosclerosis (FSGS), which causes difficult-to-treat nephrotic syndrome. The size of urinary podocytes was significantly larger in FSGS compared with minimal change nephrotic syndrome (MCNS) and glomerulonephritis. The proportion of urinary podocytes positive for cell cycle-associated proteins p21 and phospho-ribosomal protein S6 was significantly higher in FSGS than in MCNS. Our study suggested that hypertrophy associated with aberrant regulation of cell cycle and mitotic catastrophe are involved in the pathogenesis of an increased size of urinary podocytes in FSGS.

Free Research Field

小児腎臓病

Academic Significance and Societal Importance of the Research Achievements

本研究では、尿中ポドサイトの観察がFSGSとMCNSの非侵襲的な鑑別に有用であることが示唆された。また、FSGSの尿中ポドサイトのサイズの増大には細胞周期の制御に関わる分子が関与していることが示唆され、FSGSの腎機能障害進行の機序の一端が明らかとなった。