Abstract
BackgroundMany studies showed an association between dietary salt intake, blood pressure and increased CVD risk. The potential reason may be related to vascular structural and functional changes, through alterations in endothelial function. The central retinal arteriolar equivalent and urinary albumin reflected vascular endothelial dysfunction in different part of the body. The urinary sodium-creatinine ratio of causal urine specimens could represent the 24-h urinary sodium intake to estimate sodium intake.MethodsThe 24-h sodium excretion was estimated by urinary sodium-creatinine ratio. Urinary albumin-creatinine ratio (UACR), reflecting renal arterial damage, was also determined. The central retinal arteriolar equivalent (CRAE) was detected by fundus photography and was further analyzed by semi-quantitative software.ResultsParticipants included 951 hypertensive patients with the average sodium excretion of 11.62 ± 3.01 g. The sodium excretion was significantly higher (P < 0.01) in the hypertensive as compared to that of the non-hypertensive participants. Prevalence of hypertension was increased with increasing sodium excretion. The sodium excretion was positively correlated with systolic blood pressure (SBP) and diastolic blood pressure (DBP), respectively (r = 0.20 and 0.14; P < 0.01). Furthermore, UACR and CRAE were significantly (P < 0.01) different within the sodium excretion quartiles (Q1-Q4). After adjusting the confounding variables, such as age and sex, the binary logistic regression analysis showed that sodium excretion was an independent factor of UACR and CRAE (P < 0.01).ConclusionOur results suggest that sodium excretion in the hypertensive participants were higher. The high sodium excretion was related with the renal arterial damage as well as retinal arteriolar changes.
Highlights
Many studies showed an association between dietary salt intake, blood pressure and increased Risk factor for cardiovascular disease (CVD) risk
The chi-square test for trend showed that the prevalence of hypertension increased with the increasing 24-h sodium excretion within the quartiles, in those with sodium excretion higher than 12.6 g, 55.62 % suffered from hypertension
The results showed that the probability of the Urinary albumin-creatinine ratio (UACR)/central retinal arteriolar equivalent (CRAE) abnormality was significantly (P < 0.01) increased as the sodium excretion group changed from Q1, Q2, Q3, to Q4 (Table 4)
Summary
Many studies showed an association between dietary salt intake, blood pressure and increased CVD risk. The potential reason may be related to vascular structural and functional changes, through alterations in endothelial function. There is much evidence from epidemiological studies and animal experiments have shown that dietary sodium plays an important role in the regulation of blood pressure [1]. A positive relationship between sodium intake and blood pressure has been documented both in hypertensive and normotensive individuals [2, 3]. The INTERSALT study was an observational study showed an association between dietary salt intake and blood pressure. The potential BP-independent increased CVD risk under a high salt diet may be related to
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