| Project/Area Number |
18K08224
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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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| Review Section |
Basic Section 53040:Nephrology-related
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| Research Institution | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2020: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | CKD / ABCG2 / 腎機能 / 尿酸トランスポーター / 尿酸 / 一塩基多型 / 慢性腎臓病 / 腎不全 |
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| Outline of Final Research Achievements |
Hyperuricemia is a risk factor for the development of renal disease or a facilitator of renal impairment, and to clarify the effect of ABCG2 function on the renal function decline, we evaluated the single nucleotide polymorphisms Q126X and Q141K in the ABCG2 gene. In a study of 276 CKD patients, there was a trend toward accelerated eGFR decline with presumed ABCG2 functional decline in the CKD stage G3 group. A retrospective cohort study of 1885 healthy subjects (eGFR >60 mL/min/1.73m2) also showed that estimated ABCG2 functional decline significantly reduced renal function over a longer time course of 9-10 years. Furthermore, the results were similar when matched by propensity score for age, gender (males only), eGFR, BMI, and serum uric acid level, indicating the involvement of ABCG2 in renal function independent of serum uric acid level.
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| Academic Significance and Societal Importance of the Research Achievements |
ABCG2の機能低下が高尿酸血症を引き起こすと同時に、高尿酸血症を介さずにも腎障害の進行を促進することが明らかになった。さらに高尿酸血症に著しいABCG2機能低下を合併すると、腎障害の進行は促進されることも明らかになった。ABCG2の機能低下を来す一塩基多型Q126XとQ141Kの頻度は高いことから、将来的には高尿酸血症患者のABCG2の一塩基多型を調べることにより、より腎障害の進行のリスクの高い患者に絞って、その他のリスクの管理や生活指導を行えるようになることが期待される。
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