Table of Contents Author Guidelines Submit a Manuscript
International Journal of Endocrinology
Volume 2017, Article ID 1659071, 8 pages
Research Article

A New Murine Model of Chronic Kidney Disease-Mineral and Bone Disorder

1Clinical Division of Nephrology, Medical University of Graz, Graz, Austria
2Clinical Division of Cardiology, Medical University of Graz, Graz, Austria
3Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University of Graz, Graz, Austria
4Clinical Division of Endocrinology and Diabetes, Medical University of Graz, Graz, Austria
5Intensive Care Unit, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Correspondence should be addressed to Philipp Eller; ta.zarginudem@relle.ppilihp

Received 5 June 2017; Revised 31 August 2017; Accepted 11 September 2017; Published 14 December 2017

Academic Editor: Rosaria Meccariello

Copyright © 2017 Bianca Frauscher et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Chronic kidney disease (CKD) is associated with mineral and bone disorder (MBD), which is the main cause of the extensively increased cardiovascular mortality in the CKD population. We now aimed to establish a new murine experimental CKD-MBD model. Dilute brown non-Agouti (DBA/2) mice were fed with high-phosphate diet for 4 (HPD4) or 7 (HPD7) days, then with standard chow diet (SCD) and subsequently followed until day 84. They were compared to DBA/2 mice maintained on SCD during the whole study period. Both 4 and 7 days HPD-fed mice developed phosphate nephropathy with tubular atrophy, interstitial fibrosis, decreased glomerular filtration rate, and increased serum urea levels. The abdominal aorta of HPD-treated mice showed signs of media calcification. Histomorphometric analysis of HPD-treated mice showed decreased bone volume/tissue volume, low mineral apposition rate, and low bone formation rate as compared to SCD-fed mice, despite increased parathyroid hormone levels. Overall, the observed phenotype was more pronounced in the HPD7 group. In summary, we established a new, noninvasive, and therefore easy to perform reproducible CKD-MBD model, which showed media calcification, secondary hyperparathyroidism, and low-turnover bone disease.