| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
Injury to the renal vasculature plays important roles in the pathogenesis of acute kidney injury (AKI). Asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhibitor, could enhance kidney injury during AKI by causing vascular damage. (Basic research) We investigated the roles of ADMA in AKI using ischemia/reperfusion (I/R)-induced renal injury model mice. I/R injury-induced oxidative stress may reduce DDAH, a degradading enzyme for ADMA, expression and cause ADMA accumulation, which may contribute to capillary loss and tubular necrosis in the kidney. (Clinical research) We next investigated whether ADMA could be a predictor for AKI in 55 patients undergoing elective coronary angiography (CAG). Although no cases of obvious AKI assessed by changes in creatinine levels were identified, administration of contrast medium caused significant increases in plasma ADMA levels. Further, eleveted ADMA was tended to correlated to annual eGFR loss in these subjects.
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