摘要
目的 1,2 5 (OH) 2 D3 、钙代谢紊乱是慢性肾衰继发性甲状旁腺功能亢进症 (SHPT)的主要原因 ,它们分别与维生素D受体 (VDR)、2 8ku钙结合蛋白 (CaBP D2 8k)结合而发挥作用 ,通过观察 5 / 6肾切除大鼠残余肾VDR、CaBP D2 8k表达 ,探讨其在早期SHPT中的作用。方法 采用免疫组化ABC法观察 5 / 6肾切除大鼠残余肾VDR、CaBP D2 8K蛋白阳性表达。结果 慢性肾功能衰竭 (CRF)大鼠血清全段甲状旁腺素水平增高 ,肾小管CaBP D2 8K阳性率明显增加 ,而VDR表达无明显改变。结论 早期CRF已有SHPT表现 ,残余肾CaBP D2 8K表达增强可能为纠正CRF钙、磷代谢紊乱的代偿机制之一。
Objective 1,25(OH)_2D_3 and Ca\+\{2+\} are criti ca l to the pathogenesis of secondary hyperparathyroidism (SHPT). Their actions are mediated through binding to vitamin D receptor (VDR) and Ca\+\{2+\}-binding pr otein (CaBP-D) of cells. Methods The expression of VDR and CaBP-D_ \{28K\} in the kidney tissue of subtotally nephrectomized rats (5/6) in experime ntal uremia with SHPT were detected by immunohistochemistry. Results Serum intact PTH levels in 5/6 NX rats were significantly higher than controls [(40.85±5.22)×10\+\{-9\} g/L vs (25.15±4.24)×10\+\{-9\} g/L, P <0.01)]. The expression of CaBP-D_\{28K\} was more increased in NX group than the control. However, the density of VDR in the kidney of NX rats was same as the sham-oper ated rats. Conclusion These results suggested that SHPT may occur in earlytage of renal failure and the increased expression of CaBP-D_\{28K\} m ay play a role to maintain metabolic balance of calcium, phosphorus.\;
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
2000年第5期344-346,共3页
Journal of Nanjing Medical University(Natural Sciences)
基金
江苏省教委科研基金资助项目!(No1 82FA970 7)
关键词
慢性肾功能衰竭
SHPT
维生素D受体
钙结合蛋白
chronic renal failure
hyperparathyroidism, secondary
vit amin D receptor
CaBP-D_(28K)