Elucidation of mechanism for exercise-induced acute renal failure in urate transporter deficient mice
| Project/Area Number |
20590965
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
ICHIDA Kimiyoshi Tokyo University of Pharmacy and Life Science, 薬学部, 教授 (80183169)
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| Co-Investigator(Renkei-kenkyūsha) |
HOSOYA Tatsuo 東京慈恵会医科大学, 医学部, 教授 (10125031)
ANZAI Naohiko 杏林大学, 医学部, 准教授 (70276054)
HOSOYAMADA Makoto 慶應大学, 薬学部, 准教授 (00291659)
SHINOHARA Yoshihiko 東京薬科大学, 薬学部, 准教授 (00154229)
NAKAMURA Makiko 東京薬科大学, 薬学部, 助教 (80447557)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 腎臓学 / 尿酸輸送体 / URAT1 / 運動後急性腎不全 |
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| Research Abstract |
Exercise induced acute renal failure (EIARF) are significant complications of renal hypouricemia. Two mechanisms for EIARF were proposed. One hypothesis is that renal reperfusion injury due to vasoconstriction results from an exercise-induced increase in oxygen free radicals and a lack of urate, free radical scavengers. The other hypothesis is that urate nephropathy results from an increase in uric acid production by exercise induced ATP breakdown. We examined renal injury of mice deficient in urate reabsorption transporter, URAT1, fed with urate and oxonate. Renal reperfusion injury was acceptable from our results.
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Report
(4 results)
Research Products
(67 results)
