10.6084/m9.figshare.5455117.v1
Yokote S.
Yokote
S.
Yokoo T.
Yokoo
T.
Matsumoto K.
Matsumoto
K.
Ohkido I.
Ohkido
I.
Utsunomiya Y.
Utsunomiya
Y.
Kawamura T.
Kawamura
T.
Hosoya T.
Hosoya
T.
Supplementary Material for: Metanephros Transplantation Inhibits the Progression of Vascular Calcification in Rats with Adenine-Induced Renal Failure
Karger Publishers
2017
Adenine
Chronic renal failure
Metanephros
Nephrogenesis
Transplantation
Vascular calcification
2017-09-29 10:17:30
Dataset
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Metanephros_Transplantation_Inhibits_the_Progression_of_Vascular_Calcification_in_Rats_with_Adenine-Induced_Renal_Failure/5455117
<p><i>Background/Aim:</i> Recent research has shown that transplanted
metanephroi form primitive vascularized kidneys with histologically
recognizable renal features. The aim of the present study was to
determine the metabolic function of transplanted metanephroi in rats
with chronic renal failure (CRF), with particular reference to secondary
hyperparathyroidism and vascular calcification. <i>Methods:</i> CRF was
induced in 11-week-old male Wistar rats by maintaining them on a 0.75%
adenine diet for 4 weeks, followed by normal diet for an additional 2
weeks. At the end of adenine loading, whole metanephroi from embryonic
day 15 rats were transplanted into the omentum and epididymis of the
transplantation group. Vascular calcification was evaluated 2 weeks
after metanephroi transplantation. <i>Results:</i> Metanephros
transplantation significantly reduced vascular calcium and phosphorus
content and suppressed the progression of vascular calcification as
indicated by von Kossa staining of the media of the thoracic aorta.
However, no significant differences between the adenine-fed control and
transplantation groups were found regarding the serum levels of 1,25(OH)<sub>2</sub>D<sub>3</sub>, calcium or phosphorus or the calcium × phosphorus product. <i>Conclusion:</i>
The present study has shown that transplantation of metanephroi
suppresses the progression of vascular calcification via a mechanism
that is independent of calcium-phosphorus dynamics.</p>