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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Sci+Rep
2017 ; 7
(1
): 2233
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Development of a novel chronic kidney disease mouse model to evaluate the
progression of hyperphosphatemia and associated mineral bone disease
#MMPMID28533541
Tani T
; Orimo H
; Shimizu A
; Tsuruoka S
Sci Rep
2017[May]; 7
(1
): 2233
PMID28533541
show ga
Medial arterial calcification (MAC) and renal osteodystrophy are complications of
mineral bone disease (MBD) associated with chronic kidney disease (CKD). Our aim
was to develop a novel mouse model to investigate the clinical course of CKD-MBD.
Eight-week-old C57BL/6?J male mice were assigned to the following groups: the
control group, fed a standard chow for 6 or 12 weeks; the CKD-normal phosphorus
(NP) group, fed a chow containing 0.2% adenine, with normal (0.8%) phosphorus,
for 6 or 12 weeks; and the CKD-high phosphorus (HP) group, fed 6 weeks with the
0.2% adenine/0.8% phosphorus diet, followed by a chow with 1.8% phosphorus for 2
weeks, 4 weeks or 6 weeks. Serum phosphorus was significantly increased in the
CKD-HP group, and associated with MAC formation; the volume of calcification
increased with longer exposure to the high phosphorus feed. MAC was associated
with upregulated expression of runt-related transcription factor 2, alkaline
phosphatase, and osteopontin, indicative of osteoblastic trans-differentiation of
vascular smooth muscle cells. A significant mineral density depletion of cortical
bone was observed. We describe the feasibility of developing a model of CKD-MBD
and provide findings of a direct association between elevated serum phosphorus
and the formation of MAC and renal osteodystrophy.
|Animals
[MESH]
|Biomarkers
[MESH]
|Chronic Kidney Disease-Mineral and Bone Disorder/*etiology/*metabolism/pathology
[MESH]
free
free
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