scholarly journals Impaired Daytime Urinary Sodium Excretion Impacts Nighttime Blood Pressure and Nocturnal Dipping at Older Ages in the General Population

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2013
Author(s):  
Rosaria Del Giorno ◽  
Chiara Troiani ◽  
Sofia Gabutti ◽  
Kevyn Stefanelli ◽  
Sandro Puggelli ◽  
...  

The circadian rhythm of urinary sodium excretion is related to the diurnal blood pressure regulation (BP) and the nocturnal dipping pattern. The renal sodium excretion expressed as daytime/nighttime ratio impacts BP, but a limited number of studies have investigated this topic to date. In this cross-sectional study, we aimed to investigate the impact of different daily patterns of sodium excretion (comparing low with high ratios) on BP and nocturnal dipping and to explore the relationship with age. Twenty-four-hour ambulatory BP monitoring and daytime and nighttime urinary sodium collections were used to assess 1062 subjects in Switzerland. Analyses were performed according to the day/night urinary sodium excretion ratio quartiles (Q1–Q4) and by age group (≤50 and ≥50 years). Subjects in Q1 can be considered low excretors of sodium during the daytime since the rate of sodium excretion during the daytime was 40% lower than that of subjects in Q4. Quartiles of the day/night urinary sodium excretion ratio showed that subjects in Q1 were 7 years older and had respectively 6 and 5 mmHg higher nighttime systolic and diastolic BP and a higher nocturnal dipping compared with subjects in Q4 (p-value ≤0.001). Associations found were significant only for subjects older than 50 years (all p < 0.05). The present results suggest that a decreased capacity to excrete sodium during daytime is more prevalent as age increases and that it impacts nighttime blood pressure and nocturnal dipping in older subjects.

Hypertension ◽  
2008 ◽  
Vol 51 (4) ◽  
pp. 891-898 ◽  
Author(s):  
Lise Bankir ◽  
Murielle Bochud ◽  
Marc Maillard ◽  
Pascal Bovet ◽  
Anne Gabriel ◽  
...  

2019 ◽  
Vol 105 (3) ◽  
pp. e484-e493
Author(s):  
Christian Adolf ◽  
Daniel A Heinrich ◽  
Finn Holler ◽  
Benjamin Lechner ◽  
Nina Nirschl ◽  
...  

Abstract Context High dietary salt intake is known to aggravate arterial hypertension. This effect could be of particular relevance in the setting of primary aldosteronism (PA), which is associated with cardiovascular damage independent of blood pressure levels. The aim of this study was to determine the impact of therapy on salt intake in PA patients. Patients and Methods A total of 148 consecutive PA patients (66 with unilateral and 82 with bilateral PA) from the database of the German Conn’s Registry were included. Salt intake was quantified by 24-hour urinary sodium excretion before and after initiation of PA treatment. Study design Observational longitudinal cohort study. Setting Tertiary care hospital. Results At baseline, unilateral PA patients had a significantly higher urinary sodium excretion than patients with bilateral disease (205 vs 178 mmol/d, P = 0.047). Higher urinary sodium excretion correlated with an increased cardiovascular risk profile including proteinuria, impaired lipid, and glucose metabolism and was associated with higher daily doses of antihypertensive drugs to achieve blood pressure control. In unilateral disease, urinary sodium excretion dropped spontaneously to 176 mmol/d (P = 0.012) 1 year after unilateral adrenalectomy and remained low at 3 years of follow-up (174 mmol/d). In contrast, treatment with mineralocorticoid receptor antagonists (MRA) in bilateral PA patients was not associated with a significant change in urinary sodium excretion at follow-up (179 mmol/d vs 183 mmol/d). Conclusion PA patients consuming a high-salt diet, estimated based on urinary sodium excretion, respond to adrenalectomy with a significant reduction of salt intake, in contrast to MRA treatment.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaofu Du ◽  
Le Fang ◽  
Jianwei Xu ◽  
Xiangyu Chen ◽  
Yamin Bai ◽  
...  

AbstractThe direction and magnitude of the association between sodium and potassium excretion and blood pressure (BP) may differ depending on the characteristics of the study participant or the intake assessment method. Our objective was to assess the relationship between BP, hypertension and 24-h urinary sodium and potassium excretion among Chinese adults. A total of 1424 provincially representative Chinese residents aged 18 to 69 years participated in a cross-sectional survey in 2017 that included demographic data, physical measurements and 24-h urine collection. In this study, the average 24-h urinary sodium and potassium excretion and sodium-to-potassium ratio were 3811.4 mg/day, 1449.3 mg/day, and 4.9, respectively. After multivariable adjustment, each 1000 mg difference in 24-h urinary sodium excretion was significantly associated with systolic BP (0.64 mm Hg; 95% confidence interval [CI] 0.05–1.24) and diastolic BP (0.45 mm Hg; 95% CI 0.08–0.81), and each 1000 mg difference in 24-h urinary potassium excretion was inversely associated with systolic BP (− 3.07 mm Hg; 95% CI − 4.57 to − 1.57) and diastolic BP (− 0.94 mm Hg; 95% CI − 1.87 to − 0.02). The sodium-to-potassium ratio was significantly associated with systolic BP (0.78 mm Hg; 95% CI 0.42–1.13) and diastolic BP (0.31 mm Hg; 95% CI 0.10–0.53) per 1-unit increase. These associations were mainly driven by the hypertensive group. Those with a sodium intake above about 4900 mg/24 h or with a potassium intake below about 1000 mg/24 h had a higher risk of hypertension. At higher but not lower levels of 24-h urinary sodium excretion, potassium can better blunt the sodium-BP relationship. The adjusted odds ratios (ORs) of hypertension in the highest quartile compared with the lowest quartile of excretion were 0.54 (95% CI 0.35–0.84) for potassium and 1.71 (95% CI 1.16–2.51) for the sodium-to-potassium ratio, while the corresponding OR for sodium was not significant (OR, 1.28; 95% CI 0.83–1.98). Our results showed that the sodium intake was significantly associated with BP among hypertensive patients and the inverse association between potassium intake and BP was stronger and involved a larger fraction of the population, especially those with a potassium intake below 1000 mg/24 h should probably increase their potassium intake.


2021 ◽  
pp. 1-42
Author(s):  
Yi-Jie Wang ◽  
Kuo-Lioug Chien ◽  
Hsiu-Ching Hsu ◽  
Hung-Ju Lin ◽  
Ta-Chen Su ◽  
...  

Abstract Urinary sodium excretion is a potential risk factor for cardiovascular diseases (CVD). However, the underlying biological mechanisms and effects of salt sensitivity are unclear. The purpose of this study was to characterize the relative contribution of biological factors to the sodium-CVD association. A total of 2112 participants were enrolled in this study. Structured questionnaires and blood and urine samples were obtained. Twenty-four-hour sodium excretion was estimated using a single overnight urine sample. Hypertension, metabolic syndrome, and overweight status were considered to indicate salt sensitivity. Cox proportional hazard models were used to investigate the effects of salt sensitivity on urinary sodium excretion and CVD risk. The traditional mediation approach was used to calculate the proportion of mediation. The mean age (standard deviation) of the 2112 participants was 54.5 (12.2) years, and they were followed up for a mean of 14.1 [8.1] years. Compared with those in the lowest quartile, the highest baseline urinary sodium excretion (>4.2g/24 hours) was associated with a 43% higher CVD risk (hazard ratio, 1.43; 95% confidence interval, 1.02-1.99). Participants with high urinary sodium excretion, hypertension, or metabolic syndrome had a significantly high risk of CVD. The carotid intima-media thickness had the largest mediating effect (accounting for 35% of the sodium-CVD association), followed by systolic blood pressure (33%), left ventricular mass (28%), and diastolic blood pressure (14%). Higher urinary sodium excretion increased the risk of CVD, which was explained largely by carotid media-thickness and systolic blood pressure.


PLoS ONE ◽  
2019 ◽  
Vol 14 (12) ◽  
pp. e0227035 ◽  
Author(s):  
Esther Cuadrado-Soto ◽  
África Peral-Suarez ◽  
Elena Rodríguez-Rodríguez ◽  
Aránzazu Aparicio ◽  
Pedro Andrés ◽  
...  

2018 ◽  
Vol 148 (12) ◽  
pp. 1946-1953 ◽  
Author(s):  
Magali Rios-Leyvraz ◽  
Pascal Bovet ◽  
René Tabin ◽  
Bernard Genin ◽  
Michel Russo ◽  
...  

ABSTRACT Background The gold standard to assess salt intake is 24-h urine collections. Use of a urine spot sample can be a simpler alternative, especially when the goal is to assess sodium intake at the population level. Several equations to estimate 24-h urinary sodium excretion from urine spot samples have been tested in adults, but not in children. Objective The objective of this study was to assess the ability of several equations and urine spot samples to estimate 24-h urinary sodium excretion in children. Methods A cross-sectional study of children between 6 and 16 y of age was conducted. Each child collected one 24-h urine sample and 3 timed urine spot samples, i.e., evening (last void before going to bed), overnight (first void in the morning), and morning (second void in the morning). Eight equations (i.e., Kawasaki, Tanaka, Remer, Mage, Brown with and without potassium, Toft, and Meng) were used to estimate 24-h urinary sodium excretion. The estimates from the different spot samples and equations were compared with the measured excretion through the use of several statistics. Results Among the 101 children recruited, 86 had a complete 24-h urine collection and were included in the analysis (mean age: 10.5 y). The mean measured 24-h urinary sodium excretion was 2.5 g (range: 0.8–6.4 g). The different spot samples and equations provided highly heterogeneous estimates of the 24-h urinary sodium excretion. The overnight spot samples with the Tanaka and Brown equations provided the most accurate estimates (mean bias: −0.20 to −0.12 g; correlation: 0.48–0.53; precision: 69.7–76.5%; sensitivity: 76.9–81.6%; specificity: 66.7%; and misclassification: 23.0–27.7%). The other equations, irrespective of the timing of the spot, provided less accurate estimates. Conclusions Urine spot samples, with selected equations, might provide accurate estimates of the 24-h sodium excretion in children at a population level. At an individual level, they could be used to identify children with high sodium excretion. This study was registered at clinicaltrials.gov as NCT02900261.


2007 ◽  
Vol 293 (2) ◽  
pp. F586-F593 ◽  
Author(s):  
Xiao C. Li ◽  
L. Gabriel Navar ◽  
Yuan Shao ◽  
Jia L. Zhuo

We and others have previously shown that high levels of ANG II are accumulated in the rat kidney via a type 1 (AT1) receptor-mediated mechanism, but it is not known which AT1 receptor is involved in this process in rodents. We tested the hypothesis that AT1a receptor-deficient mice (Agtr1a−/−) are unable to accumulate ANG II intracellularly in the kidney because of the absence of AT1a receptor-mediated endocytosis. Adult male wild-type (Agtr1a+/+), heterozygous (Agtr1a+/−), and Agtr1a−/− were treated with vehicle, ANG II (40 ng/min ip via osmotic minipump), or ANG II plus the AT1 antagonist losartan (10 mg·kg−1·day−1 po) for 2 wk. In wild-type mice, ANG II induced hypertension (168 ± 4 vs. 113 ± 3 mmHg, P < 0.001), increased kidney-to-body weight ratio ( P < 0.01), caused pressure natriuresis ( P < 0.05), and elevated plasma and whole kidney ANG II levels ( P < 0.001). Concurrent administration of ANG II with losartan attenuated these responses to ANG II. In contrast, Agtr1a−/− mice had lower basal systolic pressures ( P < 0.001), smaller kidneys with much fewer AT1b receptors ( P < 0.001), higher basal 24-h urinary sodium excretion ( P < 0.01), as well as basal plasma and whole kidney ANG II levels ( P < 0.01). However, intracellular ANG II levels in the kidney were lower in Agtr1a−/− mice. In Agtr1a−/− mice, ANG II slightly increased systolic pressure ( P < 0.05) but had no effect on the kidney weight, urinary sodium excretion, and whole kidney ANG II levels. Losartan restored systolic pressure to basal levels and decreased whole kidney ANG II levels by ∼20% ( P < 0.05). These results demonstrate a predominant role of AT1a receptors in blood pressure regulation and in the renal responses to long-term ANG II administration, that AT1b receptors may play a limited role in blood pressure control and mediating intrarenal ANG II accumulation in the absence of AT1a receptors.


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