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Kidney Week

Abstract: FR-PO1121

Dietary Sodium and Potassium Intake and Risk of CKD Progression, ESKD, or Death in the Million Veteran Program

Session Information

Category: CKD (Non-Dialysis)

  • 2301 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Angle, Hannah, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Guide, Andrew, Nashville VA, Nashville, Tennessee, United States
  • Greevy, Robert, Nashville VA, Nashville, Tennessee, United States
  • Wilson, Otis D., Nashville VA, Nashville, Tennessee, United States
  • Triozzi, Jefferson Lorenzo, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Ikizler, Talat Alp, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Terker, Andrew S., Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Akwo, Elvis Abang, Vanderbilt University Medical Center, Nashville, Tennessee, United States
  • Hung, Adriana, Nashville VA, Nashville, Tennessee, United States

Group or Team Name

  • Million Veteran Program; KidPhenGen.
Background

It is established that high sodium (Na) intake and low potassium (K) intake are associated with lower blood pressure and better cardiovascular outcomes. The associations between Na and K intake and chronic kidney disease (CKD) are less clear. This study assessed the relationship between reported Na and K intake and the risk of CKD progression, while accounting for genetic ancestry and other covariates.

Methods

We built a retrospective cohort (n=256,438) from the Million Veteran Program with baseline eGFR >30 ml/min who completed a nutritional survey. The primary outcome was a composite of 40% eGFR decline, ESRD, or death. Stratified Cox proportional hazard models were used to evaluate the individual associations of dietary Na and K intake with the composite outcome, stratified by genetic ancestry. A subgroup analysis by diabetes (DM) was also performed.

Results

In veterans of African (AFR) n=27,896 and European (EUR) ancestry n=219,795, higher Na intake was associated with increased risk for the primary composite (comparing highest to lowest quintile, AFR: aHR 1.06, 95% CI 1.02-1.10, EUR: aHR 1.02, 95% CI 1.00-1.04). Higher K intake was associated with lower risk (AFR: 0.93, 0.90-0.97, EUR: 0.88, 0.87-0.89). Subgroup analyses showed similar effects in patients without DM (AFR: Na aHR 1.09, 1.03-1.15, K aHR 0.89, 0.84-0.94, EUR: Na aHR 1.04, 1.02-1.06, K aHR 0.85, 0.84-0.87). However, in patients with DM the effects were strongly attenuated (AFR: Na aHR 1.01, 0.95-1.08, K aHR 1.00, 0.95-1.07, EUR: Na aHR 0.98, 0.95-1.01, K aHR 0.92, 0.90-0.95).

Conclusion

A diet low in Na and high in K is protective against CKD, though to varying degrees based on ancestry and DM status. Notably, the protective effect of K disappeared in AFR-DM patients. Future nutritional studies accounting for the impact of eGFR, genetics, and DM status are critical.

Fig 1: HR for adjusted Na for any event

Fig 2: HR for adjusted K for any event

Funding

  • Veterans Affairs Support