Estimation of Sodium and Potassium Intake: Current Limitations and Future Perspectives.

Globally, average dietary sodium intake is double the recommended amount, whereas potassium is often consumed in suboptimal amounts. High sodium diets are associated with increased cardiovascular and renal disease risk, while potassium may have protective properties. Consequently, patients at risk of cardiovascular and renal disease are urged to follow these recommendations, but dietary adherence is often low due to high sodium and low potassium content in processed foods. Adequate monitoring of intake is essential to guide dietary advice in clinical practice and can be used to investigate the relationship between intake and health outcomes. Daily sodium and potassium intake is often estimated with 24-h sodium and potassium excretion, but long-term balance studies demonstrate that this method lacks accuracy on an individual level. Dietary assessment tools and spot urine collections also exhibit poor performance when estimating individual sodium and potassium intake. Collection of multiple consecutive 24-h urines increases accuracy, but also patient burden. In this narrative review, we discuss current approaches to estimating dietary sodium and potassium intake. Additionally, we explore alternative methods that may improve test accuracy without increasing burden.

The association between salt intake and arterial stiffness is influenced by a sex-specific mediating effect through blood pressure in normotensive adults: The ELSA-Brasil study.

High salt intake is known to increase blood pressure (BP) and also to be associated with carotid-femoral pulse wave velocity (cf-PWV). However, recent data showed a sex-specific pattern in the salt-induced rise of BP. Thus, we aimed to investigate whether the association between salt intake and arterial stiffness also has a sex-specific pattern. A total of 7755 normotensive participants with a validated 12-h overnight urine collection in which daily salt intake was estimated were included. cf-PWV, as well as clinical and anthropometric parameters, was measured. Salt intake positively correlated with cf-PWV, in which the linear regression was steeper in women than in men (0.0199 ± 0.0045 vs 0.0326 ± 0.0052 m/s per gram of salt, P < .05). cf-PWV increases over the salt quartiles in men and women. However, after adjustment for confounders, the association remained significant only for men. In the path analysis, the direct path (men: 0.048 P < .001, women: 0.029 P = .028) was higher in men while that mediated by SBP (men: 0.020 P < .001, women: 0.034 P < .001) was higher in women. We clearly demonstrated that high salt intake has a direct and independent effect increasing arterial stiffness regardless of sex. Also, the association between salt intake and arterial stiffness is more dependent on BP in normotensive women than it is in normotensive men. These results highlight the need for a sex-specific approach in the evaluation of cardiovascular risk associated with dietary habits.

Impact of fractional excretion of sodium on a single morning void urine collection as an estimate of 24-hour urine sodium.

The standard for assessing dietary sodium intake is to measure 24-hour urine sodium. On average, 93% of daily sodium intake is excreted over 24-hours. Expense and difficulties in obtaining complete 24-hour collections have led to the measurement of sodium concentration in spot and single-void urine samples, using predictive equations to estimate 24-hour urine sodium. Although multiple predictive equations have been developed, in addition to having an average bias, all the equations overestimate 24-hour sodium at lower levels of 24-hour sodium and underestimate 24-hour urine sodium at higher levels of 24-hour sodium. One of the least biased estimating equations is the INTERSALT equation, which incorporates a spot urine creatinine concentration. The authors hypothesized that differential fractional excretion of sodium (FeNa)(derived from a morning void collection) relative to creatinine would impact on the accuracy of the INTERSALT equation in estimating 24-hour urine sodium. In a prospective study of 139 adults aged 65 years and over, three sequential morning void and 24-hour urine samples were examined. There was a significant correlation between increasing FENa and the difference between estimated and measured 24-hours urine sodium (r = 0.358, P < .01). In the lowest quartile of FENa, the INTERSALT equation overestimated 24-hour urine sodium, but underestimated 24-hour urine sodium with greater magnitude in each of the subsequent quartiles of FENa. Differential excretion of sodium relative to creatinine, potentially impacted by renal blood flow and hydration, among other factors, affected the accuracy of the INTERSALT equation. Additional research may refine the INTERSALT and other predictive equations to increase their accuracy.

Comparison of 24-hour urine and 24-hour diet recall for estimating dietary sodium intake in populations: A systematic review and meta-analysis.

This systematic literature review and meta-analysis examined whether 24-hour diet recall is a valid way to measure mean population sodium intake compared with the gold standard 24-hour urinary assessment. The authors searched electronic databases MEDLINE, Embase, and Scopus using pre-defined terms. Studies were eligible for inclusion if they assessed adult humans in free-living settings, and if they included group means for 24-hour diet recall and 24-hour urinary collection of sodium intake in the same participants. Studies that included populations with an active disease state that might interfere with normal sodium metabolism were excluded. Results of 28 studies are included in the meta-analysis. Overall, 24-hour diet recall underestimated population mean sodium intake by an average of 607 mg per day compared to the 24-hour urine collection. The difference between measures from 24-hour urine and 24-hour diet recall was smaller in studies conducted in high-income countries, in studies where multiple-pass methods of 24-hour diet recall were reported and where urine was validated for completeness. Higher quality studies also reported smaller differences between measures than lower quality studies. Monitoring of population sodium intake with 24-hour urinary excretion remains the most accurate method of assessment. Twenty-four-hour diet recall tends to underestimate intake, although high-quality 24-hour diet recall improves accuracy, and may be used if 24-hour urine is not feasible.

The urine output definition of acute kidney injury is too liberal.

INTRODUCTION: The urine output criterion of 0.5 ml/kg/hour for 6 hours for acute kidney injury (AKI) has not been prospectively validated. Urine output criteria for AKI (AKIUO) as predictors of in-hospital mortality or dialysis need were compared. METHODS: All admissions to a general ICU were prospectively screened for 12 months and hourly urine output analysed in collection intervals between 1 and 12 hours. Prediction of the composite of mortality or dialysis by urine output was analysed in increments of 0.1 ml/kg/hour from 0.1 to 1 ml/kg/hour and the optimal threshold for each collection interval determined. AKICr was defined as an increase in plasma creatinine≥26.5 µmol/l within 48 hours or ≥50% from baseline. RESULTS: Of 725 admissions, 72% had either AKICr or AKIUO or both. AKIUO (33.7%) alone was more frequent than AKICr (11.0%) alone (P<0.0001). A 6-hour urine output collection threshold of 0.3 ml/kg/hour was associated with a stepped increase in in-hospital mortality or dialysis (from 10% above to 30% less than 0.3 ml/kg/hour). Hazard ratios for in-hospital mortality and 1-year mortality were 2.25 (1.40 to 3.61) and 2.15 (1.47 to 3.15) respectively after adjustment for age, body weight, severity of illness, fluid balance, and vasopressor use. In contrast, after adjustment AKIUO was not associated with in-hospital mortality or 1-year mortality. The optimal urine output threshold was linearly related to duration of urine collection (r2=0.93). CONCLUSIONS: A 6-hour urine output threshold of 0.3 ml/kg/hour best associated with mortality and dialysis, and was independently predictive of both hospital mortality and 1-year mortality. This suggests that the current AKI urine output definition is too liberally defined. Shorter urine collection intervals may be used to define AKI using lower urine output thresholds.