| Project/Area Number |
26462427
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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 |
Urology
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| Research Institution | Saitama Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
城武 卓 埼玉医科大学, 医学部, 講師 (10528805)
井上 勉 埼玉医科大学, 医学部, 准教授 (30406475)
岡田 浩一 埼玉医科大学, 医学部, 教授 (60233342)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 腎癌 / 蛋白尿 / 分子標的治療薬 / チロシンキナーゼ阻害薬 / 進行性腎癌 / 転移性腎癌 / 分子標的薬 |
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| Outline of Final Research Achievements |
A side effect of tyrosine kinase inhibitor (TKI) use for advanced renal cell carcinoma is proteinuria.We evaluated urinary biomarkers for their ability to predict an increase in urine protein.We measured urinary nephrin, an indicator of glomerular epithelial cell damage, and urinary beta-2 microglobulin (β2-MG), N-acetyl-β-D-glucosaminidase (NAG), and liver-type fatty acid binding protein (L-FABP), which are indicators of renal tubular damage, using semiquantitative methods before and after TKI treatment. But, urinary biomarkers cannot predict an increase in urine protein.Proteinuria is thought to result from TKI-induced vascular endothelial growth factor inhibition in the glomerular capillary wall. In this study, biomarkers of both renal tubular damage and glomerular epithelial cell damage were significantly increased. Proteinuria caused by TKI treatment may also be associated with tubular impairment. we could identify that proteinuria for TKI concerned renal tubular damage.
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