ASSOCIATION OF DIETARY SODIUM INTAKE AND 24H URINE SODIUM EXCRETION WITH ENDOTHELIAL DYSFUNCTION AND URINARY ALBUMIN EXCRETION IN EARLY-STAGE HYPERTENSIVE INDIVIDUALS

Abstract

Objective: Monitoring of dietary sodium intake is essential in hypertension and efforts have been made to find the least troublesome method to accurately estimate sodium consumption. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide, which is implicated in abnormal pressure-natriuresis. Increased urinary albumin excretion (UAE) has been associated with sodium intake, possibly through alteration of intrarenal hemodynamics. We investigated which method of measuring sodium intake, including dietary and urinary assessment, correlates better with endothelial dysfunction and UAE and may be a better indicator of vascular damage in newly-diagnosed, never-treated hypertensive patients. Design and method: Untreated individuals free from cardiovascular comorbidities were eligible to participate, whose 24 h systolic/diastolic blood pressure exceeded 130 and/or 80 mmHg based on their ambulatory blood pressure recording (MobilOGraph). Asymmetric dimethylarginine (ADMA) was measured in serum samples using commercially available competitive enzyme-linked immunosorbent assay (ELISA) kit. UAE was measured in 24 h urine samples. Dietary sodium intake was estimated with a) a 24hour diet recall that corresponded to the same day as the 24hour urine collection, b) a salt score questionnaire based on a 0–10 scale, with higher values indicating higher salt intake, and c) urinary sodium excretion in 24hour urine sample. Results: A total of 50 hypertensive patients, 28 males and 22 females, with a mean age of 47.0 ± 10.9 years and mean 24hour ambulatory systolic/diastolic blood pressure 135.2 ± 10.0/88.5.0 ± 9.1 mmHg, were included. Urinary albumin excretion was 6.1 (4.3–10.5) mg/24 h and ADMA levels were 0.99 ± 0.42 μmol/l. Urinary sodium excretion was 83.3 (48.4–146.5) mmol/24 h, estimated dietary sodium intake was 79.2 (36.7–130.4) mmol/24 h, and salt score was scaled at 4.9 ± 1.5. Urinary sodium excretion was the only sodium indicator that positively and strongly correlated with both urinary albumin excretion (r = 0.347, p = 0.043) and ADMA levels (r = 0.389, p = 0.025). Conclusions: In a population of untreated, relatively young, early-stage hypertensive individuals, urinary sodium excretion, yet not other dietary measures of sodium, may reflect microvascular damage. These results support the widely perceived premise that 24hour urine collection is more accurate, although more cumbersome to perform, than other dietary sodium assessments, in terms of pathophysiology and clinical significance.