Abstract: FR-PO269

Effect of Dietary Sodium and Phosphorus Intake on Fibroblast Growth Factor-23 in Patients with Diabetic Nephropathy

Session Information

Category: Mineral Disease

  • 1202 Mineral Disease: Vitamin D, PTH, FGF-23

Authors

  • Bhattarai, Manoj, University of Texas Health Science Center at San Anotonio, San Antonio, Texas, United States
  • Gandhi, Jeet, University of Texas Health Science Center at San Anotonio, San Antonio, Texas, United States
  • Velagapudi, Chakradhar, University of Texas Health Science Center at San Anotonio, San Antonio, Texas, United States
  • Lee, Shuko, South Texas Veterans Health Care System, San Antonio, Texas, United States
  • Cunningham, Sue ED, University of Texas Health Science Center at San Anotonio, San Antonio, Texas, United States
  • Debnath, Subrata, University of Texas Health Science Center at San Anotonio, San Antonio, Texas, United States
  • Hu, Shirley L, UTHealth Houston, McALlen, Texas, United States
  • Bansal, Shweta, University of Texas Health Science Center at San Anotonio, San Antonio, Texas, United States
Background

High FGF23 levels independently associate with cardiovascular and all-cause mortality in CKD patients. Higher dietary phosphorus intake increases FGF23 levels in healthy individuals. However, this association in CKD patients in unclear. FGF23 levels have been positively associated with markers of volume status in renal transplant patients suggesting possible role of dietary sodium intake. The relationship between dietary sodium and phosphorus and plasma FGF-23 levels is not well-studied in advance diabetic nephropathy patients.We hypothesize that high dietary sodium and phosphorus associate with high plasma FGF23 levels in patients with diabetic nephropathy.

Methods

We conducted a sub-analysis of a randomized-controlled trial where subjects with type 2 DM with albumin-creatinine ratio of >150 mg/g and eGFR 15-60 ml/min were recruited to test the anti-proteinuric effect of Silybin and N-acetylcysteine. Dietary phosphorus intake was assessed from 3-day diet record. Daily sodium intake was estimated by measuring 12-hour urinary sodium excretion. Plasma FGF23 was measured using a second generation C-terminal ELISA kit.

Results

The study population was 62.9±7.5 years old, 89% male, 65% Hispanic, and 27% non-Hispanic white, had BMI of 35±8.54 kg/m2, and eGFR of 36.4±13.3 ml/min. Mean dietary phosphorus intake and urinary sodium was 1418±438 mg/d and 3882±2486 mg/d, respectively with median plasma FGF23 78 [44, 127] RU/ml at baseline. On univariate analysis, plasma FGF23 correlated negatively with eGFR (r=-0.6, p<0.001) and positively with serum phosphorus (r=0.5, p<0.001) and NGAL (r=0.7, p<0.001). There was no correlation between plasma FGF23 and daily phosphorus or sodium intake. In multivariable regression model including age, eGFR, daily sodium and phosphorus intake, serum phosphorus and NGAL, only eGFR predicted the plasma FGF23 significantly (β=-0.47, p=0.02).

Conclusion

Daily sodium and phosphorus intake do not correlate with plasma FGF23 in patients with advance diabetic nephropathy. This observation is in contrast with healthy individuals where high phosphorus intake increases plasma FGF23 levels.

Funding

  • Other NIH Support