Risedronate Attenuates Podocyte Injury in Phosphate Transporter-Overexpressing Rats

Yohei Asada, Takeshi Takayanagi, Tsukasa Kawakami, Eisuke Tomatsu, Atsushi Masuda, Yasumasa Yoshino, Sahoko Sekiguchi-Ueda, Megumi Shibata, Tomihiko Ide, Hajime Niimi, Eishin Yaoita, Yusuke Seino, Yoshihisa Sugimura, Atsushi Suzuki

研究成果: ジャーナルへの寄稿学術論文査読

3 被引用数 (Scopus)


Osteoporosis patients with chronic kidney disease (CKD) are becoming common in our superaging society. Renal dysfunction causes phosphorus accumulation in the circulating plasma and leads to the development of CKD-mineral bone disorder (MBD). We have previously reported that type III Pi transporter-overexpressing transgenic (Pit-1 TG) rats manifest phosphate (Pi)-dependent podocyte injury. In the present study, we explored the effect of risedronate on Pi-induced podocyte injury in vivo. Pit-1 TG rats and wild-type rats at 5 weeks old were divided into a risedronate-treated group and an untreated group. We subcutaneously administered 5 μg/kg body weight of risedronate or saline twice a week during the experimental period. Risedronate did not alter serum creatinine levels at 5, 8, and 12 weeks of age. However, electron microscopy images showed that thickening of the glomerular basement membrane was improved in the risedronate treatment group. Furthermore, immunostaining for podocyte injury markers revealed that both desmin- and connexin43-positive areas were smaller in the risedronate-treated group than in the untreated group, suggesting that bisphosphonates could rescue Pi-induced podocyte injury. In conclusion, our findings suggest that risedronate could maintain glomerular barrier function by rescuing Pi-induced podocyte injury.

ジャーナルInternational Journal of Endocrinology
出版ステータス出版済み - 2019

All Science Journal Classification (ASJC) codes

  • 内分泌学、糖尿病および代謝内科学
  • 内分泌学
  • 内分泌系および自律システム


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