VERIFY AND EVALUATE FOUR SPOT URINARY METHODS FOR ESTIMATING 24-HOUR URINARY SODIUM EXCRETION RATE IN TIBETAN POPULATION

To investigate the role of renal synthesis of atrial natriuretic peptide (ANP) as a contributor to the water-sodium homeostasis, we studied the effects of electrolyte-water imbalance on renal ANP mRNA levels, plasma ANP concentrations, and urinary ANP excretion rates by using reverse transcription-polymerase chain reaction (PCR) and radioimmunoassay. Male Wistar rates divided into the following three groups: 1) the control group, 2) deoxycorticosterone acetate (DOCA)-salt-treated group, and 3) low-salt-treated group. The urinary sodium excretion rate and urine volume in the DOCA-salt rats were significantly elevated at 2 days and for the 10-day study. The urinary ANP excretion rate in DOCA-salt rats was significantly increased at 2 days after treatment and was well correlated to the urinary sodium excretion rate (r = 0.76, P < 0.01). Plasma ANP levels in the DOCA-salt rats were elevated on the day of death. In contrast, plasma renin activities were markedly suppressed in DOCA-salt rats and increased in low-salt rats. By immunohistochemical study, immunoreactive ANP materials were mainly localized in the proximal and distal cortical tubules of the kidney. With the PCR cloning and sequencing technique, ANP cDNA was cloned from the rat kidney, and the sequences were identical to that of ANP identified in the atria. By semiquantitative PCR technique, the expression of ANP mRNA in the ventricle and renal cortex tissues was significantly enhanced in the DOCA-salt rats. Our results confirm that the rat kidney is a site of ANP synthesis and indicate that renal ANP synthesis is enhanced in a volume-expansion state. We propose that renal synthesized natriuretic peptide participates in the intrarenal regulation of water-electrolyte homeostasis and may contribute to renal adaptation during the mineralocorticoid escape phenomenon.

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Faculty Opinions recommendation of Urinary sodium excretion, blood pressure, cardiovascular disease, and mortality: a community-level prospective epidemiological cohort study.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.733790826.793552587 ◽

2018 ◽

Author(s):

Carmine Zoccali ◽

Davide Bolignano

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Cohort Study ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Community Level ◽

Epidemiological Cohort

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Multiple, random spot urine sampling for estimating urinary sodium excretion

European Journal of Pediatrics ◽

10.1007/s00431-021-04170-4 ◽

2021 ◽

Author(s):

Gianluigi Ardissino ◽

Antonio Vergori ◽

Cesare Vergori ◽

Laura Martelli ◽

Valeria Daccò ◽

...

Keyword(s):

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Spot Urine ◽

Urine Sampling

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Association between 24-h urinary sodium and potassium excretion and blood pressure among Chinese adults aged 18–69 years

Scientific Reports ◽

10.1038/s41598-021-83049-8 ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Xiaofu Du ◽

Le Fang ◽

Jianwei Xu ◽

Xiangyu Chen ◽

Yamin Bai ◽

...

Keyword(s):

Blood Pressure ◽

Sodium Excretion ◽

Sodium Intake ◽

Urinary Sodium Excretion ◽

Urinary Sodium ◽

Inverse Association ◽

Potassium Excretion ◽

Chinese Adults ◽

Potassium Intake ◽

Sodium And Potassium

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.

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Association of a Tobacco-specific Nitrosamine Carcinogen with Urinary Cotinine, Urinary Sodium Excretion, and Total Energy Intake in Adolescents and Children

Current Medical Science ◽

10.1007/s11596-021-2343-0 ◽

2021 ◽

Vol 41 (2) ◽

pp. 270-278

Author(s):

Jong Weon Choi ◽

Tatsuyoshi Fujii ◽

Noriyoshi Fujii

Keyword(s):

Total Energy ◽

Energy Intake ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Total Energy Intake ◽

Urinary Sodium ◽

Urinary Cotinine

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Urinary sodium excretion and the risk of cardiovascular disease: A community-based cohort study in Taiwan

British Journal Of Nutrition ◽

10.1017/s0007114521001768 ◽

2021 ◽

pp. 1-42

Author(s):

Yi-Jie Wang ◽

Kuo-Lioug Chien ◽

Hsiu-Ching Hsu ◽

Hung-Ju Lin ◽

Ta-Chen Su ◽

...

Keyword(s):

Blood Pressure ◽

Metabolic Syndrome ◽

Systolic Blood Pressure ◽

Sodium Excretion ◽

Urinary Sodium Excretion ◽

Salt Sensitivity ◽

Urinary Sodium ◽

Mediating Effect ◽

Cvd Risk ◽

Media Thickness

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.

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