Pathogenesis and control of renal osteodystrophy

肾性骨营养不良的发病机制和控制

• 批准号: 14571030
• 负责人: AKIZAWA Tadao
• 金额: $ 2.18万
• 依托单位: Wakayama Medical University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571030/
• 关键词: RENAL OSTEODYSTROPHY; SECONDARY HYPERPARATHYROIDISM; PARATHYROID HORMONE; ACTIVE VITAMIN D; CALCIUM SENSING RECEPTOR; VITAMIN D RECEPTOR; CALCIMIMETICS; APOPTOSIS; 活性型ビタミンDアナログ; Calcium sensing receptor; vitamin D receptro; calciumimetics

In uremic rats with secondary hyperparathyroidism, following results were observed.1.Gene expression and protein content of vitamin D receptor (VDR) and calcium sensing receptor (CaR) in parathyroid cell were decreased according to the progression of parathyroid proliferation.2.Cell proliferation preceded the decrease in CaR.3.Direct injection of vitamin D analogue in parathyroid gland upregulated decreased CaR and VDR, and suppressed the proliferation of parathyroid cells and induced apoptosis of cells.4.In advanced secondary hyperparathyroidism, CaR agonist (calcimimetics) suppressed proliferation of cells and upregulated VDR and CaR in parathyroid gland.5.CaR agonist decreased weight of parathyroid gland.6.Same findings were also observed by direct injection of vitamin D analogue.These results elucidated the mechanism by which direct injection of vitamin D analogue into parathyroid and CaR agonist regress the advanced secondary hyperparathyroidism.

In uremic rats with secondary hyperparathyroidism, following results were observed.1.Gene expression and protein content of vitamin D receptor (VDR) and calcium sensing receptor (CaR) in parathyroid cell were decreased according to the progression of parathyroid proliferation.2.Cell proliferation preceded the decrease in CaR.3.Direct injection of vitamin D analogue in parathyroid gland upregulated decreased CaR and VDR, and suppressed the proliferation of parathyroid cells and induced apoptosis of cells.4.In advanced secondary hyperparathyroidism, CaR agonist (calcimimetics) suppressed proliferation of cells and upregulated VDR and CaR in parathyroid gland.5.CaR agonist decreased weight of parathyroid gland.6.Same findings were also observed by direct injection of vitamin D类似物。这些结果阐明了将维生素D模拟直接注射到甲状旁腺和汽车激动剂中的机制，从而回归晚期的继发性甲状旁腺功能亢进症。

项目成果

Akizawa T, Ogata H, et al.: "Management of secondary hyperparathyroidism of dialysis patients."Nephrology. 8・S-2. 53-57 (2003)

Akizawa T、Ogata H 等：“透析患者继发性甲状旁腺功能亢进症的治疗”，8・S-2（2003 年）。

Shiizaki K, Akizawa T, et al.: "Effect of percutaneous calcitol injection therapy on secondary Hyperparathyroidism in uraemic patients"Nephrol Dial Transplant. 18・s-3. 42-46 (2003)

Shiizaki K、Akizawa T 等：“经皮骨化醇注射疗法对尿毒症患者继发性甲状旁腺功能亢进症的影响”Nephrol Dial Transplant 18・s-3 (2003)。

Akizawa T, Kamimura M, et al.: "Management of secondary hyperparathyroidism of dialysis patients."Nephrology (Carlton). 8・S-2. 53-57 (2003)

Akizawa T、Kamimura M 等人：“透析患者继发性甲状旁腺功能亢进症的治疗”（Carlton） 8·S-2（2003 年）。

Kinugasa E, Akizawa T, et al.: "Effects of maxacalcitol on parathyroid gland function in haemodialysis patients"Nephrol Dial Transplant. 17・S-10. 20-27 (2002)

Kinugasa E、Akizawa T 等：“马沙骨化醇对血液透析患者甲状旁腺功能的影响”Nephrol Dial Transplant 17・S-10 (2002)。

Akizawa T, Kamimura M, et al.: "Management of secondary hyperparathyroidism of dialysis Patients"Nephrology (Carlton). 8・s-2. 53-57 (2003)

Akizawa T、Kamimura M 等：“透析患者继发性甲状旁腺功能亢进症的管理”《肾病学》8·s-2 (2003)。