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The pathophysiological role of FGF23 in disordered mineral metabolism after acute kidney injury

Research Project

Project/Area Number 16K21384
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Kidney internal medicine
Metabolomics
Research InstitutionTokai University

Principal Investigator

KOMABA Hirotaka  東海大学, 医学部, 講師 (60437481)

Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords急性腎障害 / 骨ミネラル代謝異常 / FGF23 / 急性腎傷害
Outline of Final Research Achievements

FGF23 levels increase rapidly after acute kidney injury (AKI), but the role of FGF23 is largely unknown. We investigated the longitudinal changes in mineral metabolism and FGF23 using a rat ischemia-reperfusion injury (IRI) model, which involved unilateral nephrectomy and 35-min contralateral IRI. Rats with IRI exhibited acute hyperphosphatemia and progressively increasing FGF23 levels, which was accompanied by decreased biosynthesis of 1,25-dihydroxyvitamin D. During renal recovery, the elevated FGF23 levels declined progressively and finally normalized, with the occurrence of hypophosphatemia and increased 1,25-dihydroxyvitamin D levels. Administration of the pan-FGFR inhibitor (PD173074) led to persistent hyperphosphatemia and increased production of 1,25-dihydroxyvitamin D. These results suggest that elevated FGF23 after AKI represents a compensatory response to maintain neutral phosphate balance in a similar, but more rapid and dynamic, manner to that in chronic kidney disease.

Academic Significance and Societal Importance of the Research Achievements

今回の検討結果より,慢性腎臓病のみならず,急性腎障害においても骨ミネラル代謝異常が出現することが示され,さらにこの病態においてFGF23が重要な役割を担っていることが明らかとなった。急性腎障害はさまざまな疾患を背景に発症し,予後に重大な影響を及ぼし,その対策は喫緊の課題である。急性腎障害に伴う骨ミネラル代謝異常は,急性腎障害後の予後悪化にも関与し得る病態であり,本研究成果は急性腎障害後の予後改善を図る上で重要な基盤的理解を提供するものと考えられる。

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (3 results)

All 2018

All Presentation (3 results) (of which Int'l Joint Research: 1 results)

  • [Presentation] FGF23 mitigates hyperphosphatemia and causes low 1,25-dihydroxyvitamin D levels after acute kidney injury in rats.2018

    • Author(s)
      Komaba H, Ishida H, Hamano N, Sawada K, Wada T, Nakamura M, Fukagawa M.
    • Organizer
      55th ERA-EDTA Congress
    • Related Report
      2018 Annual Research Report
    • Int'l Joint Research
  • [Presentation] 急性腎障害後のミネラル代謝異常におけるFGF23の病態生理学的役割2018

    • Author(s)
      駒場大峰,石田寛明,濱野直人,澤田佳一郎,和田健彦,中村道郎,深川雅史
    • Organizer
      第61回日本腎臓学会学術総会
    • Related Report
      2018 Annual Research Report
  • [Presentation] 急性腎障害後のミネラル代謝異常におけるFGF23の病態生理学的役割2018

    • Author(s)
      駒場大峰,石田寛明,濱野直人,澤田佳一郎,和田健彦,中村道郎,深川雅史
    • Organizer
      第36回日本骨代謝学会学術総会
    • Related Report
      2018 Annual Research Report

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Published: 2016-04-21   Modified: 2020-03-30  

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