摘要
目的观察腺嘌呤诱导的慢性肾脏病(CKD)大鼠模型矿物质代谢生化标志物、血管钙化和肾性骨病改变的特点。方法 20只雄性SD大鼠随机分2组:正常对照组和CKD组。第2周末,行血清生化标志物检测。第6周末处死大鼠,行血清生化标志物检测、主动脉血管病理学检查和血管钙磷含量测定,取股骨和第五腰椎做骨密度(BMD)检查、骨形态计量学分析。结果在第2和第6周末,CKD组大鼠血肌酐、尿素氮、血磷、血清甲状旁腺激素较正常对照组均明显升高,血钙明显下降。CKD组有50%的大鼠发生中膜血管钙化,正常对照组无血管钙化发生。CKD组的血管钙、磷含量均明显大于正常对照组。BMD检查,与正常对照组比较,CKD组的全股骨、股骨皮质骨、股骨小梁骨和第五腰椎BMD均明显降低。骨形态计量学方面,CKD组大鼠的小梁骨骨吸收和骨形成均处于高水平,处于高转换状态;CKD组大鼠小梁骨和皮质骨骨量明显低于正常对照组大鼠;CKD组大鼠小梁骨骨矿化与正常对照组大鼠比较无明显差别。结论腺嘌呤诱导的CKD大鼠模型表现为低血钙、高血磷和高血清甲状旁腺激素;血管钙化表现为中膜钙化;肾性骨病表现为小梁骨高转换、正常矿化和低皮质骨和小梁骨骨量,也符合纤维性骨炎的特点。腺嘌呤诱导的慢性肾脏病大鼠模型可以作为未来开展慢性肾脏病骨及矿物质代谢异常研究的良好载体。
Objective To investigate the characteristic changes of biochemical markers of mineral metabolism,vascular calcification,and renal osteodystrophy in an adenine-induced rat model of chronic kidney disease（ CKD）.Methods A total of 20 male Sprague Dawley rats（ SD rats） were randomly divided into two groups： the normal group fedwith a diet without adenine,and the CKD group fed with an adenine-containing diet（ 7. 5 g/kg） for the first 4 weeks and then a diet without adenine for the following 2 weeks. At the end of the 2 nd week,serum biochemical markers were detected. At the end of the 6 th week,the SD rats were sacrificed and serum biochemical markers were detected once again.The aortas were collected for pathological examination and detection of vascular calcium and phosphorus contents. Femurs and the fifth lumbar vertebrae were taken for bone mineral density（ BMD） measurement and bone histomorphometric analysis. Results At the end of the 2 nd and 6 th weeks,compared with the normal control group,the levels of serum creatinine,urea nitrogen,phosphorus and parathyroid hormone（ PTH） in the CKD group were significantly increased（ P〈0. 05 or P〈0. 01）,and the level of serum calcium was significantly decreased（ P〈0. 05 or P〈0. 01）. Medial layer vascular calcification of the aorta occurred in 50% of the rats in the CKD group,but was not observed in the normal control group. Vascular calcium and phosphorus contents were significantly higher in the CKD group compared with the normal control group（ P〈0. 05）. The BMD of total femur,cortical and trabecular bone tissues of the femur,and the fifth lumbar vertebra was significantly decreased in the CKD group（ P〈0. 05 or P〈0. 01）. The histomorphometric analysis showed that both bone resorption and bone formation of the trabecular bone in the CKD group were increased,indicating a high bone turnover status. The volumes of both trabecular and cortical bones of rats in the CKD group were significantly lower than that of the normal control group（ P〈0. 05 or P〈0. 01）. However,the trabecular bone mineralization was not significantly different between the two groups. Conclusions The adenine-induced rat model of chronic kidney disease（ CKD） established in this study shows reduced serum calcium and increased serum phosphorus and PTH,and medial layer vascular calcification of the aorta. With respect to renal osteodystrophy,this model shows a high trabecular bone turnover,normal trabecular bone mineralization,and low bone volume of cortical and trabecular bone,which meets the characteristics of osteitis fibrosa. This model may become a useful tool for future study of chronic kidney disease-mineral and bone disorder（ CKD-MBD）.
出处
《中国比较医学杂志》
CAS
北大核心
2018年第1期8-15,共8页
Chinese Journal of Comparative Medicine
基金
内蒙古自然科学基金(编号:2014BS0807)
内蒙古医科大学附属医院科研启动基金(编号:NYFYBS2015013)
北京自然科学基金(编号:7162193)
第五批内蒙古"草原英才"基金内蒙古医科大学附属医院肾内科创新人才团队基金
关键词
慢性肾脏病
慢性肾脏病骨及矿物质代谢异常
肾性骨病
血管钙化
纤维性骨炎
大鼠
chronic kidney disease, CKD
chronic kidney disease-mineral and bone disorder, CKD-MBD
renal osteodystrophy
vascular calcification
osteitis fibrosa
rats
