| Project/Area Number |
18590909
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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 | Showa University |
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Principal Investigator |
AKIZAWA Tadao Showa University, School of Medicine, Professor (40102339)
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| Co-Investigator(Kenkyū-buntansha) |
OGATA Hiroaki Showa University, School of Medicine, Assistant Professor (30296959)
SHIIZKI Kazuhiro Wakayama Medical University, 医学部, Assistant Professor (10423930)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Renal osteodystrophy / Secondary hyperparathyroidism / Ectopic vascular calcification / Phosphorus / Vitamin D / Calcium / Parathyroid hormone / Osteitis fibrosa / 活性型ビタミンD / 異所性石灰化 / 副甲状腺ホルモン / カルシウム受容体 / カルシウム受容体作動薬 / アポトーシス / 2次性副甲状腺機能亢進症 / 無形成骨 / 副甲状腺機能低下症 |
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| Research Abstract |
Representative outcomes of disturbed Ca and phosphate metabolism are renal osteodystrophy, secondary hyperparathyroidism and ectopic vascular calcification. These abnormalities result in systemic pathological changes in dialysis patients, and shorten the survival or deteriorate the health related quality of life. To understand the mechanisms to progress these systemic abnormalities, cross-talk between renal osteodystrophy, secondary hyperparathyroidism and ectopic vascular calcification was investigated. In uremic rats that develop severe secondary hyperparathyroidism with vascular calcification, advanced osteitis fibrosa has been developed, and the strong association among these progressions was observed. By the intervention of direct injection of vitamin D into hyperplastic parathyroid grand recovered the hyperplasia of parathyroid grand as well as the osteitis fibrosa. However this intervention failed to decrease the ectopic vascular calcification. These results suggest that the presence of cross talk in the developing stage between renal osteodystrophy, secondary hyperparathyroidism and ectopic vascular calcification, but this cross talk disappear at the regression process. The precise process of the cross talk should be further evaluated.
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