动物造模,慢性肾脏病 zi-bio 2024-03-19 528

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

　　Method: 20 male SD rats were randomly divided into two groups: a normal control group and a CKD group? On the second weekend, will serum biochemical markers be tested? On the 6th weekend, the rats were euthanized and serum biochemical markers were tested? Aortic vascular pathological examination and determination of vascular calcium and phosphorus content, taking femur and fifth lumbar vertebrae for bone density (BMD) examination? Bone morphometric analysis?

　　Result: On the 2nd and 6th weekends, did the CKD group rats have blood creatinine? Urea nitrogen? Blood phosphorus? The serum parathyroid hormone levels were significantly increased compared to the normal control group, while blood calcium levels were significantly decreased? 50% of rats in the CKD group developed medial vascular calcification, while no vascular calcification occurred in the normal control group? Vascular calcium in the CKD group? Is the phosphorus content significantly higher than that of the normal control group? BMD examination, compared with the normal control group, the total femur of the CKD group? Femoral cortical bone? Is the BMD of the femoral trabecular bone and the fifth lumbar vertebra significantly reduced? In terms of bone morphometry, the trabecular bone resorption and formation in the CKD group rats were at high levels and in a high transition state; The bone mass of trabecular bone and cortical bone in CKD group rats was significantly lower than that in normal control group rats; Is there no significant difference in trabecular bone mineralization between CKD group rats and normal control group rats?

　　Conclusion: Does the adenine induced CKD rat model exhibit hypocalcemia? High blood phosphorus and high serum parathyroid hormone; Vascular calcification manifests as medial calcification; Is renal bone disease characterized by trabecular bone height transition? Is normal mineralization and low cortical bone and trabecular bone mass also consistent with the characteristics of fibrous osteoarthritis? Can the adenine induced chronic kidney disease rat model serve as a good carrier for future research on abnormal bone and mineral metabolism in chronic kidney disease?