Renal anemia treatment increase frataxin Level in patients with chronic kidney disease
| Project/Area Number |
16K09635
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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 | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
中西 健 兵庫医科大学, 医学部, 教授 (70217769)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥130,000 (Direct Cost: ¥100,000、Indirect Cost: ¥30,000)
Fiscal Year 2017: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2016: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
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| Keywords | 酸化ストレス / フラタキシン / 鉄代謝 / 腎臓内科学 |
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| Outline of Final Research Achievements |
During 6 month treatment with erythropoiesis-stimulating agents (ESA) in patients whose ferritin levels were >250 ng/ml, ESA administration had been maintained, without iron administration.
Hemoglobin levels did not change significantly. ESA dose and ESA resistant index were significantly decreased at 3 month. Serum hepcidin levels decreased significantly in pararell with serum ferritin levels. Frataxin protein levels were significantly increased, and correlated with ferritin levels at the start and 3 month. Pentosidine and TNF-α levels were significantly decreased at 3 month.
Treatment for renal anemia with ESA, aiming for lowering ferritin levels, may increase frataxin, and decrease oxidative stress in patients on hemodialysis.
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| Academic Significance and Societal Importance of the Research Achievements |
慢性腎臓病の患者では心血管疾患の合併が多く，合併症の治療に要する医療費は膨大となっている．合併症の原因となる酸化ストレスは鉄代謝の異常から発生するが，腎臓病患者では鉄代謝の調節蛋白であるフラタキシンが減少し酸化ストレスが亢進することをわれわれは報告しtてきた．
本研究では，腎臓病患者におけるフラタキシン減少とそれに伴う酸化ストレス亢進を明らかにし，フラタキシンを増加させる治療を探究した．この治療により酸化ストレスを軽減して，合併症の発症を未然に防ぐ新しい戦略が可能となる．
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Report
(4 results)
Research Products
(1 results)
