Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2023 Mar 10;24(6):5325.
doi: 10.3390/ijms24065325.

Mouse Models of Mineral Bone Disorders Associated with Chronic Kidney Disease

Affiliations
Review

Mouse Models of Mineral Bone Disorders Associated with Chronic Kidney Disease

Ariane Zaloszyc et al. Int J Mol Sci. .

Abstract

Patients with chronic kidney disease (CKD) inevitably develop mineral and bone disorders (CKD-MBD), which negatively impact their survival and quality of life. For a better understanding of underlying pathophysiology and identification of novel therapeutic approaches, mouse models are essential. CKD can be induced by surgical reduction of a functional kidney mass, by nephrotoxic compounds and by genetic engineering specifically interfering with kidney development. These models develop a large range of bone diseases, recapitulating different types of human CKD-MBD and associated sequelae, including vascular calcifications. Bones are usually studied by quantitative histomorphometry, immunohistochemistry and micro-CT, but alternative strategies have emerged, such as longitudinal in vivo osteoblast activity quantification by tracer scintigraphy. The results gained from the CKD-MBD mouse models are consistent with clinical observations and have provided significant knowledge on specific pathomechanisms, bone properties and potential novel therapeutic strategies. This review discusses available mouse models to study bone disease in CKD.

Keywords: CKD; CKD–MBD; mice; renal osteodystrophy.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Similar articles

Cited by

References

    1. Ziolkowska H., Paniczyk-Tomaszewska M., Debinski A., Polowiec Z., Sawicki A., Sieniawska M. Bone biopsy results and serum bone turnover parameters in uremic children. Acta Paediatr. 2000;89:666–671. doi: 10.1111/j.1651-2227.2000.tb00361.x. - DOI - PubMed
    1. Drueke T.B., Massy Z.A. Changing bone patterns with progression of chronic kidney disease. Kidney Int. 2016;89:289–302. doi: 10.1016/j.kint.2015.12.004. - DOI - PubMed
    1. Drueke T.B. In: Hyperparathyroidism in Chronic Kidney Disease. De Groot L.J., Chrousos G., Dungan K., Feingold K.R., Grossman A., Hershman J.M., Koch C., Korbonits M., McLachlan R., New M., et al., editors. Endotext; South Dartmouth, MA, USA: 2000.
    1. Foley R.N., Parfrey P.S., Sarnak M.J. Epidemiology of cardiovascular disease in chronic renal disease. J. Am. Soc. Nephrol. 1998;9((Suppl. S12)):S16–S23. doi: 10.1053/ajkd.1998.v32.pm9820470. - DOI - PubMed
    1. Hruska K.A., Choi E.T., Memon I., Davis T.K., Mathew S. Cardiovascular risk in chronic kidney disease (CKD): The CKD-mineral bone disorder (CKD-MBD) Pediatr. Nephrol. 2010;25:769–778. doi: 10.1007/s00467-009-1337-0. - DOI - PMC - PubMed

Grants and funding

This research received no external funding.