Concordance of dietary sodium intake and concomitant phosphate load: Implications for sodium interventions

Jun 9, 2016Nutrition, metabolism, and cardiovascular diseases : NMCD

How Eating Salt and Phosphate Together Affects Salt Reduction Efforts

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Abstract

Sodium excretion correlated with phosphate excretion across various populations, with a correlation coefficient of 0.519 in renal transplant recipients.

Sodium and phosphate loads are both linked to increased cardiovascular risk in chronic kidney disease and possibly in other populations.
A significant positive correlation between sodium and phosphate excretion was observed in healthy controls, patients with type 2 diabetes, and renal transplant recipients.
In nondiabetic and diabetic chronic kidney disease cohorts, moderate sodium restriction led to a significant reduction in phosphate excretion.
The findings suggest that dietary sodium and phosphate exposure are interconnected, irrespective of renal function impairment.
Adjustments for age, gender, BMI, and kidney function did not change the correlation between sodium and phosphate excretion.

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BACKGROUND AND AIMS: Both a high dietary sodium and high phosphate load are associated with an increased cardiovascular risk in patients with chronic kidney disease (CKD), and possibly also in non-CKD populations. Sodium and phosphate are abundantly present in processed food. We hypothesized that (modulation of) dietary sodium is accompanied by changes in phosphate load across populations with normal and impaired renal function.

METHODS AND RESULTS: We first investigated the association between sodium and phosphate load in 24-h urine samples from healthy controls (n = 252), patients with type 2 diabetes mellitus (DM, n = 255) and renal transplant recipients (RTR, n = 705). Secondly, we assessed the effect of sodium restriction on phosphate excretion in a nondiabetic CKD cohort (ND-CKD: n = 43) and a diabetic CKD cohort (D-CKD: n = 39). Sodium excretion correlated with phosphate excretion in healthy controls (R = 0.386, P < 0.001), DM (R = 0.490, P < 0.001), and RTR (R = 0.519, P < 0.001). This correlation was also present during regular sodium intake in the intervention studies (ND-CKD: R = 0.491, P < 0.001; D-CKD: R = 0.729, P < 0.001). In multivariable regression analysis, sodium excretion remained significantly correlated with phosphate excretion after adjustment for age, gender, BMI, and eGFR in all observational cohorts. In ND-CKD and D-CKD moderate sodium restriction reduced phosphate excretion (31 ± 10 to 28 ± 10 mmol/d; P = 0.04 and 26 ± 11 to 23 ± 9 mmol/d; P = 0.02 respectively).

CONCLUSIONS: Dietary exposure to sodium and phosphate are correlated across the spectrum of renal function impairment. The concomitant reduction in phosphate intake accompanying sodium restriction underlines the off-target effects on other nutritional components, which may contribute to the beneficial cardiovascular effects of sodium restriction. (f) Registration numbers: Dutch Trial Register NTR675, NTR2366.

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Concordance of dietary sodium intake and concomitant phosphate load: Implications for sodium interventions

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