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Kidney Week

Abstract: TH-PO499

Disturbed Phosphate Metabolism Facilitates Kidney Damage in Dahl Salt-Sensitive Hypertensive Rats

Session Information

  • CKD: Mechanisms - I
    November 07, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms


  • Wang, Qin, Teikyo University, Tokyo, Japan
  • Ishizawa, Kenichi, Shinsen-Ikebukuro Clinic, TOKYO, Japan
  • Nemoto, Yoshikazu, Teikyo University hospital, Tokyo itabashi, Japan
  • Miura, Yutaka, Jichi Medical University,, Shimotsuke, Japan
  • Li, Jinping, Teikyo university, Tokyo, Japan
  • Kuro-o, Makoto, Jichi Medical University, Shimotsuke, Japan
  • Shibata, Shigeru, Teikyo University School of Medicine, Tokyo, Japan

Several lines of evidence indicate that hypertensive end-organ damage is associated with altered phosphate metabolism. Here, we evaluated the effects of intestinal phosphate binding by sucroferric oxyhydroxide (SF) on renal damage in Dahl salt-sensitive rats, a model of hypertensive kidney disease.


Control rats received a normal diet containing normal (0.3%) phosphate. High salt (HS) group received a diet containing 8% NaCl and 0.3% phosphate for four weeks. A subgroup of HS rats received SF (HS+SF). We also evaluated the effects of phosphate loading in NRK-52E, a proximal tubule cell line.


Compared with control, HS showed progressive increase in BP. Although urinary Na+and BP levels were similar between HS and HS+SF groups, albuminuria was significantly ameliorated in the latter. In PAS staining, SF attenuated glomerulosclerosis and tubulointerstitial injury in this model. Moreover, upregulation of inflammatory cytokines in renal tubules was significantly ameliorated by SF. Reduced inflammatory response in the tubulointerstitium of HS+SF rats were confirmed by quantitative evaluation of CD68 staining. In the heart, HS group showed myofiber hypertrophy and macrophage infiltration. However, only the latter was attenuated in HS+SF. We then evaluated phosphate metabolism in this model. Although plasma phosphate levels were not significantly different among three groups, fractional excretion of phosphate and plasma FGF23 levels were significantly elevated in HS group, which was attenuated by SF. In NRK-52E cells, phosphate loading significantly increased the expression of MCP-1. Removing calcium-phosphate crystals by centrifugation, but not the knockdown of sodium-dependent phosphate transporter Slc34a1, abolished the effect of phosphate.


Phosphate loading to renal tubules can aggravate renal inflammation likely through calcium-phosphate nanoparticle formation. These data support the pathological role of latent phosphate accumulation in hypertensive kidney damage.


  • Government Support - Non-U.S.