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Abstract: FR-PO086

Preceding High-Phosphate Diet Exacerbates AKI in Rats

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Nakagawa, Yosuke, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
  • Komaba, Hirotaka, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
  • Ishida, Hiroaki, Department of Transplant Surgery, Tokai University School of Medicine, Isehara, Japan
  • Hamano, Naoto, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
  • Sawada, Kaichiro, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
  • Fajol, Abul, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
  • Wada, Takehiko, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
  • Nakamura, Michio, Department of Transplant Surgery, Tokai University School of Medicine, Isehara, Japan
  • Fukagawa, Masafumi, Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Isehara, Japan
Background

Animal studies and epidemiological studies suggest that high phosphate diet accelerates the progression of chronic kidney disease. However, little is known whether high dietary phosphate intake affects the severity of acute kidney injury (AKI).

Methods

Six-week-old male rats were subjected to 35-min bilateral ischemia reperfusion injury (IRI) or sham surgery. For 1 week preceding the surgery, the rats were fed either standard diet (0.9% calcium and 0.8% phosphate) or high phosphate diet (0.9% calcium and 1.2% phosphate). After surgery, all rats were placed on standard diet. We evaluated the time course of changes in renal function and mineral metabolism for 3 days following IRI.

Results

Compared to rats on standard diet, rats fed high phosphate diet for 1 week showed normal renal function, normophosphatemia, non-significant increases in FGF23 and PTH, and markedly increased urinary phosphate excretion. In rats kept on standard diet, IRI led to a 10-fold increase in blood urea nitrogen on day 1, which were accompanied by a 1.7-fold increase in serum phosphorus, a 2.4-fold increase in PTH, an 8-fold increase in FGF23, and a 2-fold decrease in 1,25-dihydroxyvitamin D. Rats fed high phosphate diet for 1 week prior to IRI showed more severe kidney injury and alterations in mineral metabolism. The renal and metabolic changes following IRI stared to regress by day 3 in rats kept on standard diet, but persisted for 3 days in rats fed high phosphate diet prior to surgery.

Conclusion

We show that high phosphate diet exacerbates AKI in rats even if they are switched to standard diet at onset. Our results suggest the need for routine dietary phosphate restriction in individuals who are at high risk for AKI.

Funding

  • Commercial Support –