Elucidation and therapeutic intervention of the mechanism of CKD onset and aggravation due to repeated and accumulated mild renal damages
| Project/Area Number |
17K09714
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Women's Medical University |
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Principal Investigator |
Tsuchiya Ken 東京女子医科大学, 医学部, 教授 (00246472)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | Klotho / 慢性腎臓病 / リン / 急性腎障害 / 虚血 / FGF23 / 繊維化 / CKD / AKI |
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| Outline of Final Research Achievements |
The essential pathological condition of chronic kidney disease (CKD) is assumed to be due to a chronic failure of maintaining homeostasis of the body such as water / electrolyte, metabolic abnormality, anemia due to renal tubular function / interstitial region disorder. It is proposed that the onset, progression, and aggravation of CKD are caused by the accumulation of various degrees of frequent renal injury (including AKI: acute kidney injury). Researchers have traditionally focused on the Klotho protein, which is a phosphorus regulator and has physiological activities such as anti-aging and anti-fibrosis, and has hypothesized that it is greatly involved in the pathophysiology of CKD. As an experimental model, we established a model in which CKD develops and progress in mice with low expression of the klotho with frequent and minimally invasive disorders, and examined the significance of various disease exacerbating factors.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性腎臓病(CKD)の本質的な病態は、腎尿細管機能・間質部の障害による水・電解質、代謝異常、貧血などの生体の恒常性維持の慢性的な破綻が、全身的な臓器障害、特に循環・血管系の動脈硬化病変、石灰化などを引き起こし、心腎連関などと総称される、全体的な病態像を形成すると考えられている。最近、CKDの発症・進展・重症化には、種々の程度の頻回な腎障害(AKI: acute kidney injuryを含む)が集積することにより生じうることが注目されている。それは、特定の原因疾患によらず、CKDが発症もしくは増悪する可能性を示唆し、特に高齢化社会では末期腎不全・透析の患者が増加する結果となる。
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Report
(4 results)
Research Products
(16 results)
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[Journal Article] High Serum Phosphate Level as a Risk Factor to Determine Renal Prognosis in Autosomal Dominant Polycystic Kidney Disease: A Retrospective Study.2020
Author(s)
Sato M, Kataoka H, Ushio Y, Manabe S, Watanabe S, Akihisa T, Makabe S, Yoshida R, Iwasa N, Mitobe M, Hanafusa N, Tsuchiya K, Nitta K, Mochizuki T.
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Journal Title
Medicines (Basel).
Volume: 7
Issue: 3
Pages: 13-13
DOI
Related Report
Peer Reviewed
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[Journal Article] The Importance of Biologically Active Vitamin D for Mineralization by Osteocytes After Parathyroidectomy for Renal Hyperparathyroidism.2019
Author(s)
Yajima A, Tsuchiya K, Burr DB, Wallace JM, Damrath JD, Inaba M, Tominaga Y, Satoh S, Nakayama T, Tanizawa T, Ogawa H, Ito A, Nitta K.
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Journal Title
JBMR Plus.
Volume: 3
Issue: 11
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Osteocytic perilacunar/canalicular turnover in hemodialysis patients with high and low serum PTH levels.2018
Author(s)
Yajima A, Tsuchiya K, Burr DB, Minner DE, Condon KW, Miller CA, Satoh S, Inaba M, Nakayama T, Tanizawa T, Ito A, Nitta K.
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Journal Title
Bone
Volume: 113
Pages: 68-76
DOI
Related Report
Peer Reviewed / Open Access
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