Pathogenesis and control of renal osteodystrophy

在继发性甲状旁腺功能亢进的尿毒症大鼠中，观察到以下结果：甲状旁腺细胞中维生素D受体（VDR）和钙敏感受体（CaR）的基因表达和蛋白含量随甲状旁腺增生的进展而降低。细胞增殖先于car - 3的降低。3 .在甲状旁腺直接注射维生素D类似物可上调CaR和VDR水平，抑制甲状旁腺细胞增殖，诱导细胞凋亡。在晚期继发性甲状旁腺功能亢进症中，CaR激动剂（钙化剂）抑制细胞增殖并上调甲状旁腺的VDR和CaR。5 . CaR激动剂降低甲状旁腺重量。直接注射维生素D类似物也观察到同样的结果。这些结果阐明了维生素D类似物直接注射甲状旁腺和CaR激动剂治疗晚期继发性甲状旁腺功能亢进的机制。

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.