动物造模,慢性肾脏病大鼠模型 z-bo 2021-11-01 519

　　Objective: To observe the characteristics of biochemical markers of mineral metabolism in a rat model of adenine-induced chronic kidney disease, vascular calcification and renal bone disease?

　　 Method: 20 male SD rats were randomly divided into two groups: normal control group and CKD group? Did you test the serum biochemical indicators on the second weekend? Did you sacrifice the rats and test the serum biochemical indicators in the 6th week? Perform aortic vascular pathology and measurement of vascular calcium and phosphorus content. Collect the femur and the fifth lumbar vertebra. Is there a bone mineral density (BMD) test? Bone morphology analysis?

　　Result: At the end of the 2nd and 6th weeks, the blood creatinine, urea nitrogen, blood phosphorus and serum parathyroid hormone of the CKD group were more obvious than those of the normal control group. Is the increase in blood calcium significantly reduced? In the CKD group, 50% of the rats developed median vascular calcification, while in the normal control group there was no vascular calcification. The vascular calcium and phosphorus levels of the CKD group were significantly higher than those of the normal control group. Compared with the control group, the bone mineral density of total femur, femoral cortical bone, femoral trabecular bone and fifth lumbar vertebra in the CKD group was significantly reduced. Regarding bone morphology, the trabecular bone resorption and bone formation of the CKD group rats were both at a high level. In the high conversion state, the bone mass of trabecular bone and cortical bone in the CKD group was significantly lower than that in the normal control group; is there no significant difference in trabecular bone calcification in the CKD group and the normal control group?

　　 Conclusion: The adenine-induced CKD rat model shows hypocalcemia, hyperphosphatemia and high serum parathyroid hormone; vascular calcification shows medial calcification; renal bone disease shows high trabecular bone metabolism, do you show rotation? Normal calcification. In addition, is the low bone mass of cortex and trabecular bone consistent with the characteristics of fibrous osteitis? Can the rat model of adenine-induced chronic kidney disease be a good vehicle for future studies of abnormal bone and mineral metabolism in chronic kidney disease?