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Kidney Week

Abstract: FR-PO112

Sodium and Phosphate Dietary Additives Exacerbate Progression of CKD and Lead to Early Mortality

Session Information

Category: CKD (Non-Dialysis)

  • 1903 CKD (Non-Dialysis): Mechanisms

Authors

  • Gerber, Claire, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Neuburg, Samantha, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Dussold, Corey, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Qi, Lixin, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Courbon, Guillaume, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Capella, Maralee, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Francis, Connor, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Wang, Xueyan, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • Wolf, Myles, Duke University, Durham, North Carolina, United States
  • Martin, Aline, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
  • David, Valentin, Northwestern University - Feinberg School of Medicine, Chicago, Illinois, United States
Background

Fibroblast growth factor 23 (FGF23) increases in response to high phosphate diets and states of impaired phosphate excretion, such as chronic kidney disease (CKD). Excess FGF23 hasemerged as a novel and powerful risk factor for cardiovascular disease (CVD) and death in patients with CKD and in the general population. Multiple studies have shown that excess FGF23 is often due to high consumption of processed foods, enriched in phosphate and sodium additives, that stimulate FGF23 production and increase risks of death. We hypothesized that consumption of excess phosphate stimulates FGF23 production, and that presence of CKD and simultaneous consumption of excess sodium exacerbates FGF23 negative outcomes.

Methods

To investigate the effects of dietary intake of phosphate and sodium on cardiovascular and CKD disease progression, 5 week old wild-type (WT) and Col4a3KO (CKD) mice were fed a control (Ctr), high sodium (HN), high phosphate (HP), or a high sodium-high phosphate (HPN) diet for 18 weeks. We assessed survival, renal function and serum FGF23 in 23 week old mice.

Results

Phosphate and/or sodium did not impact renal function or overall survival in WT mice. In contrast, HP, HN and HPN diets further impaired renal function in CKD animals compared to CKD-CTR mice. HP and HN diets decreased survival in CKD mice, CKD-HN and CKD-HP mice showing an average survival of 26 and 22 weeks, repectively, compared to CKD-CTR mice that live in average 34 weeks (p<0.05). Interestingly, phosphate and sodium in HPN diet did not show additive effects on the overall survival of CKD mice (27 weeks). Consumption of phosphate in HP and HPN diets increased (p<0.05) FGF23 in WT mice, by 20 fold in WT-HP and by 3 fold in WT-HPN compared to WT-CTR mice, whereas HN did not affect FGF23 levels in WT mice. CKD-CTR mice showed increased FGF23 (3 fold) compared to WT-CTR mice. HP, HN and HPN diets all increased FGF23 in CKD groups, with the highest increase found in CKD-HP mice (20-fold) while CKD-HN and CKD-HPN animals showed only 3 and 5 fold increase respectively, in FGF23 (p<0.05 vs CKD-CTR).

Conclusion

Overall, our data suggest that consumption of high phosphate rather than high sodium raises FGF23 in CKD, exacerbates decline in kidney function, and leads to early mortality.

Funding

  • NIDDK Support