Key result
Urinary sodium and albuminuria are synergistically linked to higher central pulse pressure.
Why the study?
Excess sodium intake and albuminuria predict cardiovascular disease, but their cross-sectional relationships with central pulse pressure in a general population cohort were not established.
Does albuminuria modify the association between dietary sodium intake and central pulse pressure in healthy adults?
Cross-Sectional (n=933)
Does albuminuria modify the association between dietary sodium intake and central pulse pressure in healthy adults?
p-value: p=<0.001
Microalbuminuria synergistically strengthens the positive association between urinary sodium excretion and central pulse pressure, suggesting excess sodium intake may magnify cardiovascular risk particularly in patients with chronic kidney disease.
Albuminuria may modify sodium excretion's link to central pulse pressure; hypothesis-generating and requires prospective validation before clinical application.
BACKGROUND: Central pulse pressure (cPP) is responsible for the hemodynamics of vital organs, and monitoring this parameter is important for cardiovascular disease (CVD) prevention. Excess sodium intake and (micro)albuminuria (a manifestation of renal microvascular damage) are known to be strong predictors of CVD. We sought to investigate the cross-sectional relationships among dietary sodium intake, albuminuria, and cPP in a general population cohort. METHODS: The subjects were 933 apparently healthy adults (mean age, 56 ± 10 years). Radial pressure waveforms were recorded with applanation tonometry to estimate mean arterial pressure (MAP), cPP, forward and backward pressure amplitudes, and augmentation index. The urinary sodium/creatinine and albumin/creatinine ratios were measured in spot urine samples. RESULTS: Both the urinary sodium/creatinine and albumin/creatinine ratios were positively correlated with cPP, even after adjusting for MAP (P < 0.001). Moreover, both ratios had a synergistic influence on increasing the cPP independent of age, sex, estimated glomerular filtration rate, hyperlipidemia, and diabetes (interaction P = 0.04). A similar synergistic influence was found on the forward pressure amplitude, but not on the backward pressure amplitude or augmentation index. The overall results were not altered when the urinary albumin/creatinine ratio was replaced with the existence of chronic kidney disease (CKD). CONCLUSIONS: (Micro)albuminuria strengthens the positive association between urinary sodium excretion and cPP and systolic forward pressure. Excess sodium intake may magnify the cardiovascular risk by widening the aortic pulsatile pressure, particularly in the presence of concomitant CKD.
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Tagawa et al. (2021) conducted a cross-sectional in apparently healthy adults (n=933). Urinary sodium excretion and albuminuria was evaluated on Central pulse pressure (cPP) (p=<0.001). Urinary sodium excretion and albuminuria had a synergistic positive association with central pulse pressure independent of age, sex, and comorbidities (interaction P = 0.04).
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