The Relationship Between Daily Urinary Sodium Excretion and Metabolic Syndrome in Patients with Kidney Transplantation

2014 ◽  
Vol 19 ◽  
pp. 397-402 ◽  
Author(s):  
Oktay Oymak
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.


Author(s):  
Abu Mohd Naser ◽  
Feng J. He ◽  
Mahbubur Rahman ◽  
Norm R.C. Campbell

We evaluated the relationship between estimated 24-hour urinary sodium excretion from the Kawasaki, Tanaka, and INTERSALT (International Study of Sodium, Potassium, and Blood Pressure) formulas and blood pressure (BP). We pooled 10 034 person-visit data from 3 cohort studies in Bangladesh that had measured 24-hour urine sodium (m-24hUNa), potassium, creatinine excretion, and BP. We used m-24hUNa, potassium, and creatinine where necessary, rather than spot urine values in the formulas. Bland-Altman plots were used to determine the bias associated with formula-estimated sodium relative to m-24hUNa. We compared the sodium excretion and BP relationships from m-24hUNa versus formula-estimated sodium excretions, using restricted cubic spline plots for adjusted multilevel linear models. All formulas overestimated 24-hour sodium at lower levels but underestimated 24-hour sodium at higher levels. There was a linear relationship between m-24hUNa excretion and systolic BP, while estimated sodium excretion from all 3 formulas had a J-shaped relationship with systolic BP. The relationships between urine sodium excretion and diastolic BP were more complex but were also altered by using formulas. All formulas had associations with BP when a sex-specific constant sodium concentration was inserted in place of measured sodium. Since we used the m-24hUNa, potassium, and creatinine concentrations in formulas, the J-shaped relationships are due to intrinsic problems in the formulas, not due to spot urine sampling. Formula-estimated 24-hour urine sodium excretion should not be used to examine the relationship between sodium excretion and BP since they alter the real associations.


2000 ◽  
Vol 98 (4) ◽  
pp. 495 ◽  
Author(s):  
Leonardo CENTONZA ◽  
Giovanna CASTOLDI ◽  
Roberto CHIANCA ◽  
Giuseppe BUSCA ◽  
Raffaello GOLIN ◽  
...  

2020 ◽  
Vol 26 (Supplement 1) ◽  
pp. S43
Author(s):  
Kaname Tagawa ◽  
Yusuke Tsuru ◽  
Katsumi Yokoi ◽  
Takanori Aonuma ◽  
Junichiro Hashimoto

Medicine ◽  
2016 ◽  
Vol 95 (15) ◽  
pp. e3153 ◽  
Author(s):  
Jong Chul Won ◽  
Jae Won Hong ◽  
Jung Hyun Noh ◽  
Dong-Jun Kim

2013 ◽  
Vol 126 (2) ◽  
pp. 147-154 ◽  
Author(s):  
Renata Libianto ◽  
George Jerums ◽  
Que Lam ◽  
Angela Chen ◽  
Sara Baqar ◽  
...  

Although low dietary salt intake has beneficial effects on BP (blood pressure), low 24hUNa (24 h urinary sodium excretion), the most accurate estimate of dietary salt intake, is associated with increased mortality in people with diabetes. In the non-diabetic population, low salt intake is associated with increased RAAS (renin–angiotensin–aldosterone system) activity. In this cross-sectional study, we examined the relationship between 24hUNa, PRA (plasma renin activity), serum aldosterone and BNP (brain natriuretic peptide) in patients with diabetes. Clinical characteristics, 24hUNa, PRA, serum aldosterone and BNP were recorded in 222 consecutive patients (77% with Type 2 diabetes) attending a diabetes clinic at a tertiary hospital. The relationship between 24hUNa, serum aldosterone, PRA, BNP, urinary potassium excretion, serum potassium, serum sodium, eGFR (estimated glomerular filtration rate), urinary albumin excretion and HbA1c (glycated haemoglobin) was examined by a multivariable regression model. Levels of 24hUNa significantly predicted serum aldosterone in a linear fashion (R2=0.20, P=0.002). In the subgroup of patients (n=46) not taking RAAS-modifying agents, this relationship was also observed (R2=0.10, P=0.03), and the effect of 24hUNa on serum aldosterone was found to be more pronounced than in the whole cohort (coefficient=−0.0014, compared with −0.0008). There was no demonstrable relationship between 24hUNa and PRA or BNP. Low 24hUNa is associated with increased serum aldosterone in people with diabetes, in the presence and absence of RAAS-modifying agents. This raises the possibility that stimulation of the RAAS may be a mechanism that contributes to adverse outcomes observed in patients with low 24hUNa.


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