Acute kidney injury-induced mineral and bone disorder: concept and characterization

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K08618
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 53040:Nephrology-related
• Research Institution: Tokai University
• Principal Investigator: Komaba Hirotaka 東海大学, 医学部, 准教授 (60437481)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 急性腎障害 / 骨ミネラル代謝異常

Outline of Final Research Achievements

Acute kidney injury (AKI) is known to induce alterations in mineral metabolism, but the detailed mechanisms remain to be determined. To address this, we used a rat model of renal ischemia-reperfusion injury and demonstrated that AKI induces a transient but marked increase of osteoid formation in association with alterations in mineral metabolism, which could be explained by increased levels of PTH after AKI. We also found that high phosphate diet exacerbates alterations in mineral metabolism after AKI and delays the recovery of renal function through induction of mineralization in the tubular lumen.

Free Research Field

腎臓内科学

Academic Significance and Societal Importance of the Research Achievements

今回の検討結果より，急性腎障害（AKI）がミネラル代謝の変化のみならず，骨病変や腎障害の回復過程に大きな影響を及ぼすことが明らかとなった。実臨床ではAKI発症後に腎機能が改善せずそのまま腎不全に至る場合が多く，合併症により死亡することも稀ではない。本研究成果は，骨ミネラル代謝への介入がAKI発症後の予後改善につながる可能性を示すものであり，新たな治療薬の開発につながると期待される。