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Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model.
Sci Rep 2019; 9(1):1732SR

Abstract

Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal phosphate binding by sucroferric oxyhydroxide (SF) ameliorates renal injury in the rat remnant kidney model. Sprague-Dawley rats received 5/6 nephrectomy (RK) and had a normal chow or the same diet containing SF (RK + SF). RK rats showed increased plasma FGF23 and phosphate levels, which were suppressed by SF administration. Of note, albuminuria in RK rats was significantly ameliorated by SF at both 4 and 8 weeks. SF also attenuated glomerulosclerosis and tubulointerstitial injury. Moreover, several different approaches confirmed the protective effects on podocytes, explaining the attenuation of glomerulosclerosis and albuminuria observed in this study. As a possible mechanism, we found that SF attenuated renal inflammation and fibrosis in RK rats. Interestingly, von Kossa staining of the kidney revealed calcium phosphate deposition in neither RK nor RK + SF rats; however, plasma levels of calciprotein particles were significantly reduced by SF. These data indicate that latent positive phosphate balance accelerates CKD progression from early stages, even when overt ectopic calcification is absent.

Authors+Show Affiliations

Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Department of Cell Biology, Kidney Research Center, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.Division of Anti-aging Medicine, Center for Molecular Medicine, Jichi Medical University, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan.Division of Nephrology, Department of Internal Medicine, Teikyo University School of Medicine, Tokyo, Japan. shigeru.shibata@med.teikyo-u.ac.jp. Division of Clinical Epigenetics, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan. shigeru.shibata@med.teikyo-u.ac.jp.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30741979

Citation

Nemoto, Yoshikazu, et al. "Phosphate Binding By Sucroferric Oxyhydroxide Ameliorates Renal Injury in the Remnant Kidney Model." Scientific Reports, vol. 9, no. 1, 2019, p. 1732.
Nemoto Y, Kumagai T, Ishizawa K, et al. Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model. Sci Rep. 2019;9(1):1732.
Nemoto, Y., Kumagai, T., Ishizawa, K., Miura, Y., Shiraishi, T., Morimoto, C., ... Shibata, S. (2019). Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model. Scientific Reports, 9(1), p. 1732. doi:10.1038/s41598-018-38389-3.
Nemoto Y, et al. Phosphate Binding By Sucroferric Oxyhydroxide Ameliorates Renal Injury in the Remnant Kidney Model. Sci Rep. 2019 Feb 11;9(1):1732. PubMed PMID: 30741979.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Phosphate binding by sucroferric oxyhydroxide ameliorates renal injury in the remnant kidney model. AU - Nemoto,Yoshikazu, AU - Kumagai,Takanori, AU - Ishizawa,Kenichi, AU - Miura,Yutaka, AU - Shiraishi,Takeshi, AU - Morimoto,Chikayuki, AU - Sakai,Kazuhiro, AU - Omizo,Hiroki, AU - Yamazaki,Osamu, AU - Tamura,Yoshifuru, AU - Fujigaki,Yoshihide, AU - Kawachi,Hiroshi, AU - Kuro-O,Makoto, AU - Uchida,Shunya, AU - Shibata,Shigeru, Y1 - 2019/02/11/ PY - 2018/09/03/received PY - 2018/12/27/accepted PY - 2019/2/12/entrez PY - 2019/2/12/pubmed PY - 2019/2/12/medline SP - 1732 EP - 1732 JF - Scientific reports JO - Sci Rep VL - 9 IS - 1 N2 - Recent clinical studies indicate that the disturbed phosphate metabolism in chronic kidney disease (CKD) may facilitate kidney injury; nonetheless, the causal role of phosphate in CKD progression remains to be elucidated. Here, we show that intestinal phosphate binding by sucroferric oxyhydroxide (SF) ameliorates renal injury in the rat remnant kidney model. Sprague-Dawley rats received 5/6 nephrectomy (RK) and had a normal chow or the same diet containing SF (RK + SF). RK rats showed increased plasma FGF23 and phosphate levels, which were suppressed by SF administration. Of note, albuminuria in RK rats was significantly ameliorated by SF at both 4 and 8 weeks. SF also attenuated glomerulosclerosis and tubulointerstitial injury. Moreover, several different approaches confirmed the protective effects on podocytes, explaining the attenuation of glomerulosclerosis and albuminuria observed in this study. As a possible mechanism, we found that SF attenuated renal inflammation and fibrosis in RK rats. Interestingly, von Kossa staining of the kidney revealed calcium phosphate deposition in neither RK nor RK + SF rats; however, plasma levels of calciprotein particles were significantly reduced by SF. These data indicate that latent positive phosphate balance accelerates CKD progression from early stages, even when overt ectopic calcification is absent. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/30741979/Phosphate_binding_by_sucroferric_oxyhydroxide_ameliorates_renal_injury_in_the_remnant_kidney_model L2 - http://dx.doi.org/10.1038/s41598-018-38389-3 DB - PRIME DP - Unbound Medicine ER -