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Nephrectomy Does not Exacerbate Cancellous Bone loss in Thalassemic Mice
Sutada Lotinun1,2, Korakot Atjanasuppat3, Jutatip Limsuvech3
1Department of Physiology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand. sutada.l@chula.ac.th.
Scientific Reports
|May 10, 2020
Summary
Beta-thalassemia (BKO) mice showed resistance to kidney disease-induced bone loss. Lower erythropoietin levels in these mice may prevent bone density reduction.
Area of Science:
- Nephrology
- Hematology
- Bone Biology
Background:
- Beta-thalassemia is linked to chronic kidney disease (CKD), osteoporosis, and periodontitis.
- Understanding bone changes in beta-thalassemia patients with CKD is crucial.
Purpose of the Study:
- To investigate mandibular and femoral bone alterations in heterozygous beta-globin knockout (BKO) mice after 5/6 nephrectomy (Nx).
- To explore the role of anemia and related factors in CKD-induced bone changes.
Main Methods:
- Evaluated bone morphology, serum biochemistry, and gene expression in BKO and wild-type (WT) mice post-nephrectomy.
- Measured serum levels of urea nitrogen, creatinine, calcium, phosphorus, FGF23, and erythropoietin.
Main Results:
- BKO mice exhibited anemia but were resistant to Nx-induced cancellous bone loss.
- Nx induced renal fibrosis comparably in BKO and WT mice.
- Nx reduced cancellous bone volume and cortical thickness in WT mice, but BKO mice showed resistance, except for reduced cortical thickness and bone mineral density in males.
- Serum erythropoietin levels were lower in Nx BKO mice, potentially preventing bone loss.
Conclusions:
- Heterozygous BKO mice are protected against certain kidney disease-induced bone changes, particularly cancellous bone loss.
- Erythropoietin levels may play a key role in mediating bone loss in the context of CKD and beta-thalassemia.
