Risk factors for the development of sclerosing renal lesions after the onset of hemolytic uremic syndrome.

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K17305
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 52050:Embryonic medicine and pediatrics-related
• Research Institution: Fukushima Medical University
• Principal Investigator: Kume Yohei 福島県立医科大学, 医学部, 助手 (20835988)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 溶血性尿毒症症候群 / リポポリサッカライド / 志賀毒素 / 尿細管

Outline of Final Research Achievements

In a hemolytic uremic syndrome-like mouse model treated with Shiga toxin and lipopolysaccharide, glomerular mesangiolysis in glomeruli and dilation and vacuolar degeneration in renal tubule were observed at 72 hours post-treatment in the acute phase. Molecular analysis by microarray revealed a strong decrease in gene expression in the distal nephron, which was considered to be the main site of damage in this mouse model. In addition, some of the chronic phase model mice 6 months after administration were observed an increase in mesangial matrix and cells and amyloid-like deposits in glomeruli.

Free Research Field

小児科

Academic Significance and Societal Importance of the Research Achievements

溶血性尿毒症症候群(HUS)の尿細管障害のメカニズムや慢性腎不全進展への影響については未だ不明な点が多い。本モデルマウスでの経過をさらに詳細に検討することでHUS発症後の尿細管を含めた腎障害の回復過程や慢性腎不全進展のメカニズムが明らかになる可能性がある。