中国比较医学杂志2018，Vol.28Issue(1)：8-15,8.DOI:10.3969/j.issn.1671-7856.2018.01.002
腺嘌呤诱导慢性肾脏病大鼠模型的骨与矿物质代谢异常
Mineral and bone metabolism disorder in an adenine-induced rat model of chronic kidney disease
摘要
Abstract
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 fed with 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 2nd week, serum biochemical markers were detected. At the end of the 6th 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 2nd and 6th 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).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Key words
chronic kidney disease/CKD/chronic kidney disease-mineral and bone disorder/CKD-MBD/renal osteodystrophy/vascular calcification/osteitis fibrosa/rats分类
医药卫生引用本文复制引用
孟彦,张豪,贺宁,石东英,李青南,赵建荣,左力..腺嘌呤诱导慢性肾脏病大鼠模型的骨与矿物质代谢异常[J].中国比较医学杂志,2018,28(1):8-15,8.基金项目
内蒙古自然科学基金(编号: 2014BS0807) （编号: 2014BS0807）
内蒙古医科大学附属医院科研启动基金 (编号: NYFYBS2015013) （编号: NYFYBS2015013）
北京自然科学基金(编号: 7162193) （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. （）
