Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid Stoffw Microb

Frauscher, B; Artinger, K; Kirsch, AH; Aringer, I; Moschovaki-Filippidou, F; Kétszeri, M; Schabhüttl, C; Rainer, PP; Schmidt, A; Stojakovic, T; Fahrleitner-Pammer, A; Rosenkranz, AR; Eller, P; Eller, K.
A New Murine Model of Chronic Kidney Disease-Mineral and Bone Disorder.
Int J Endocrinol. 2017; 2017(3):1659071-1659071 Doi: 10.1155/2017/1659071 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz

Eller Philipp

Frauscher Bianca

Co-Autor*innen der Med Uni Graz

Aringer Ida

Artinger Katharina

Eller Kathrin

Fahrleitner-Pammer Astrid

Ketszeri Mate Csaba

Kirsch Alexander

Rainer Peter

Rosenkranz Alexander

Schabhüttl Corinna

Schmidt Albrecht

Stojakovic Tatjana

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Abstract:

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.

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