【Animal Modeling】-Adenine-induced abnormal bone and mineral metabolism in a rat model of chronic kidney disease

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

  Methods: Twenty male SD rats were randomly divided into 2 groups: normal control group and CKD group? At the second weekend, serum biochemical markers were detected? At the sixth weekend, the rats were sacrificed, and serum biochemical markers were detected? Aortic vascular pathology Examination and determination of vascular calcium and phosphorus content, taking femur and fifth lumbar vertebra for bone mineral density (BMD) examination? Bone morphometric analysis?

  Results: At the end of the 2nd and 6th week, the serum creatinine, blood urea nitrogen, serum phosphorus and serum parathyroid hormone of the CKD group were significantly higher than those of the normal control group, and the serum calcium was significantly decreased? 50% of the rats in the CKD group Median vascular calcification occurred, and no vascular calcification occurred in the normal control group. The vascular calcium and phosphorus contents in the CKD group were significantly higher than those in the normal control group? The BMD of the trabecular bone and the fifth lumbar vertebra were significantly decreased? In terms of bone morphology, the bone resorption and bone formation of the trabecular bone in the CKD group were at a high level and were in a state of high conversion; the trabecular bone and cortical bone of the CKD group were The bone mass was significantly lower than that of the rats in the normal control group; there was no significant difference in the bone mineralization of the trabecular bone between the rats in the CKD group and the rats in the normal control group.

  Conclusion: Adenine-induced CKD rat model is characterized by hypocalcemia, hyperphosphatemia and high serum parathyroid hormone; vascular calcification is manifested as medial calcification; renal bone disease is manifested by high turnover of trabecular bone and normal mineralization. and low cortical bone and trabecular bone mass, also in line with the characteristics of osteitis fibrosus? Adenine-induced chronic kidney disease rat model can be used as a good carrier for future research on bone and mineral metabolism abnormalities in chronic kidney disease?