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Newly Developed Rat Model of Chronic Kidney Disease-Mineral Bone Disorder
Kentaro Watanabe1, Hideki Fujii1, Shunsuke Goto1
1Division of Nephrology and Kidney Center, Kobe University Graduate School of Medicine.
Insights
This study introduces a new rat model for chronic kidney disease-mineral bone disorder (CKD-MBD). The model showed increased aortic calcification, highlighting CKD-MBD progression and potential therapeutic targets.
Area of Science:
- Nephrology
- Endocrinology
- Pathophysiology
Background:
- Chronic kidney disease-mineral bone disorder (CKD-MBD) significantly increases morbidity and mortality in CKD patients.
- Understanding CKD-MBD's mechanisms is crucial for improving patient outcomes.
- A novel rat model was developed to investigate CKD-MBD characteristics.
Purpose of the Study:
- To evaluate the characteristics of CKD-MBD in a newly developed rat model.
- To assess the impact of paricalcitol on CKD-MBD markers in this model.
- To establish a relevant preclinical model for CKD-MBD research.
Main Methods:
- Male Sprague-Dawley (SD) and spontaneously diabetic Torii (SDT) rats underwent 5/6 nephrectomy (Nx) to induce CKD.
- Rats were treated with vehicle or paricalcitol (low/high dose) for 10 weeks.
- Biochemical and histological analyses of serum, urine, and aorta were performed at 20 weeks.
Main Results:
- SDT-Nx rats exhibited higher serum calcium, phosphate, and urinary calcium/phosphate excretion compared to SD-Nx rats.
- Paricalcitol administration increased serum parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) in SDT-Nx rats.
- SDT-Nx rats showed significantly more severe aortic calcification and higher aortic calcium content.
Conclusions:
- The novel SDT rat model effectively represents CKD-MBD.
- Paricalcitol administration significantly influenced CKD-MBD parameters in this model.
- Further research is warranted to elucidate the detailed pathophysiological mechanisms.
Aim:
Chronic kidney disease-mineral bone disorder (CKD-MBD) is associated with all-cause and cardiovascular morbidity and mortality in patients with CKD. Thus, elucidating its pathophysiological mechanisms is essential for improving the prognosis. We evaluated characteristics of CKD-MBD in a newly developed CKD rat model.
Methods:
We used male Sprague-Dawley (SD) rats and spontaneously diabetic Torii (SDT) rats, which are used as models for nonobese type 2 diabetes. CKD was induced by 5/6 nephrectomy (Nx). At 10 weeks, the rats were classified into six groups and administered with a vehicle or a low- or high-dose paricalcitol thrice a week. At 20 weeks, the rats were sacrificed; blood and urinary biochemical analyses and histological analysis of the aorta were performed.
Results:
At 20 weeks, hemoglobin A1c (HbA1c) levels, blood pressure, and renal function were not significantly different among the six groups. Serum calcium and phosphate levels tended to be higher in SDT-Nx rats than in SD-Nx rats. The urinary excretion of calcium and phosphate was significantly greater in SDT-Nx rats than in SD-Nx rats. After administering paricalcitol, serum parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) levels were significantly higher in SDT-Nx rats than in SD-Nx rats. The degree of aortic calcification was significantly more severe and the aortic calcium content was significantly greater in SDT-Nx rats than in SD-Nx rats.
Conclusions:
We suggest that our new CKD rat model using SDT rats represents a useful CKD-MBD model, and this model was greatly influenced by paricalcitol administration. Further studies are needed to clarify the detailed mechanisms underlying this model.
