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Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, Seoul, Republic of KoreaDivision of Nephrology, Department of Internal Medicine, Yongin Severance Hospital, Yonsei University College of Medicine, Yongin, Republic of Korea
Correspondence: Address to Jung Tak Park, MD, PhD, Department of Internal Medicine, College of Medicine, Institute of Kidney Disease Research, Yonsei University, 50-1 Yonsei-ro, Seodaemun-gu, Seoul 03722, Republic of Korea.
To evaluate the association of sodium-potassium intake balance on kidney function.
Patients and Methods
Data from the Korean Genome and Epidemiology Study were used. The participants were enrolled between June 1, 2001, and January 31, 2003, and were followed-up until December 31, 2016. The 24-hour excretion levels of sodium and potassium were calculated using the Kawasaki formula with spot urinary potassium and sodium measurements. Participants were categorized into tertiles according to the estimated 24-hour urinary sodium-to-potassium (Na/K) ratio. The primary outcome was incident chronic kidney disease (CKD), defined as an estimated glomerular filtration rate of <60 mL/min per 1.73 m2 in two or more consecutive measurements during the follow-up period.
Results
This study included 4088 participants with normal kidney function. The mean age was 52.4±8.9 years, and 1747 (42.7%) were men. The median estimated 24-hour urinary sodium excretion level, potassium excretion level, and Na/K ratio (inter quartile range) were 4.9 (4.1-5.8) g/d, 2.1 (1.8-2.5) g/d, and 2.3 (1.9-2.7) g/d, respectively. During 37,950 person-years of follow-up (median, 11.5 years), 532 participants developed CKD, and the corresponding incidence rate was 14.0 (95% CI, 12.9-15.3) per 1000 person-years. Multivariable Cox hazard analysis revealed that the risk of incident CKD was significantly lower in the lowest tertile than in the highest tertile (HR, 0.78; 95% CI, 0.63-0.97). However, no significant association was found with incident CKD risk when urinary excretion levels of sodium or potassium were evaluated individually.
Conclusion
A low urinary Na/K ratio may relate with lower CKD development risk in adults with preserved kidney function.
Chronic kidney disease (CKD), a predisposition for cardiovascular disease (CVD) and premature death, is a major contributor to the increase in the global socioeconomic burden.
Analysis of the Global Burden of Disease study highlights the global, regional, and national trends of chronic kidney disease epidemiology from 1990 to 2016.
Although treatments for hypertension and diabetes — the most well-known risk factors for CKD — are widespread, the prevalence of CKD is growing steadily.
Once established, CKD is irreversible, and the identification and prevention of modifiable risk factors are important to reduce CKD-related morbidity and mortality.
Because of their close association with hypertension, dietary sodium and potassium intakes have been closely associated with the risk of CKD.
Nonetheless, the investigations evaluating the dietary intakes of sodium and potassium as risk factors for CKD have been inconsistent and inconclusive. The PREVEND (Prevention of Renal and Vascular End-Stage Disease) study has shown that the risk of incident CKD was higher in people with low potassium intake, whereas no connection was identified with sodium intake.
Another study involving 1030 adults revealed that the estimated urinary excretion levels of sodium or potassium were not related to the estimated glomerular filtration rate (eGFR) decline.
On the other hand, a recent investigation that assessed dietary sodium intake using a food frequency questionnaire showed that sodium intake was associated with CKD risk only in a subgroup of people.
Recently, the balance between sodium and potassium intake, rather than the intake of each dietary element itself, has been proposed as a significant factor influencing outcome. In an evaluation of 103,570 people who participated in the PURE (Prospective Urban Rural Epidemiology) study, the combination of very high sodium intake with low potassium intake was associated with the highest cardiovascular event risk.
Additionally, a higher urinary sodium-to-potassium (Na/K) ratio, surrogates of the intake amounts, was found to increase the risk of CKD progression in patients with prevalent CKD.
The ratio of urinary sodium and potassium and chronic kidney disease progression: Results from the KoreaN Cohort Study for Outcomes in Patients with Chronic Kidney Disease (KNOW-CKD).
Nonetheless, the effect of sodium-potassium intake balance on incident CKD development is not well known.
Therefore, in this study, the association between sodium-potassium intake balance and CKD development in people with normal kidney function was evaluated. This was assessed using the urinary Na/K ratio as a representative of intake balance.
Patients and Methods
Study Population
This study was performed in accordance with the Declaration of Helsinki and was approved by the Institutional Review Board of the Yonsei University Health System Clinical Trial Center (9-2021-0021).
Data were retrieved from the KoGES (Korean Genome and Epidemiology Study), a prospective community-based study. The KoGES consists of middle-aged (40-69 years of age) participants residing in Ansan (an urban area) or Ansung (a rural area), Korea. Detailed cohort profiles and methods for the development of the KoGES have been published previously.
Participants who underwent urinary sodium and potassium measurements were screened. Patients with known kidney disease, proteinuria, or an eGFR <60 mL/min per 1.73 m2 at baseline were excluded. Participants who did not attend the follow-up visits were also excluded. The final analysis comprised 4088 people (Supplemental Figure 1, available online at http://www.mayoclinicproceedings.org).
Data collection
Detailed data collection methods are described in the Supplemental Methods (available online at http://www.mayoclinicproceedings.org). Demographic data including age, sex, household income, marital status, education level, daily physical activity level, and medical history were recorded at baseline. Anthropometric data were collected by trained nurses using standardized protocols and calibrated devices. Blood samples were obtained after 8 hours or more of fasting and analyzed at a central laboratory. Serum creatinine levels were determined using the Jaffe assay. The eGFR was calculated using the CKD Epidemiology Collaboration (CKD-EPI) equation.
For substitution in the CKD-EPI equation, the creatinine levels were reduced by a 5% calibration factor for standardization with the value obtained by isotope dilution mass spectrometry reference method.
Expressing the Modification of Diet in Renal Disease Study equation for estimating glomerular filtration rate with standardized serum creatinine values.
Proteinuria was classified based on a color scale that quantified proteinuria as absent, trace, 1+, 2+, or 3+. This scale correlates approximately with urine protein levels of less than 10, 10 to 20, greater than 30, greater than 100, and greater than 500 mg/dL, respectively.
The presence of proteinuria was considered as a urinalysis result higher than trace level.
Exposure and Outcome
The primary exposure was the urinary Na/K ratio. Urine samples were collected in the morning after the first voiding at baseline. Urinary sodium, potassium, and creatinine levels were measured using a Cobas Integra 800 Analyzer (Roche Diagnostics) at a central laboratory. Twenty-four–hour urinary excretion levels of sodium and potassium were estimated from a fasting morning urine sample using the Kawasaki formula.
The primary endpoint was incident CKD, which was defined as an eGFR less than 60 mL/min per 1.73 m2 at two or more consecutive measurements during the follow-up period. Participants were followed-up from the baseline visit to occurrence of the primary outcome, loss to follow-up, or up to 14 years from the baseline visit.
Statistical Analysis
Detailed statistical analysis methods are described in the Supplemental Methods. Statistical analyses were conducted using STATA version 16.1. (Stata Corp). The natural log-transformed urinary Na/K ratio was used as a continuous variable because of the skewed distribution. Cox proportional hazards regression analysis was used to evaluate the relationship between urinary Na/K ratio and CKD development. To test the nonlinear relationship between urinary Na/K ratio and incident CKD risk, restricted cubic spline analyses were conducted with the urinary Na/K ratio as a continuous variable. The missing values were accounted for less than 7% of all covariates (Supplemental Table 1, available online at http://www.mayoclinicproceedings.org), and multiple imputation by the chained equations method was used to impute 10 independent copies of the data for multivariable Cox proportional hazards models. In the time-updated model, the CVD history and systolic blood pressure (BP) was considered as time-updated covariates. A P value of less than .05 was considered statistically significant.
Results
Baseline Characteristics
The baseline characteristics of the participants according to urinary Na/K ratios are shown in Table 1. The mean age was 52.4±8.9 years, and 1747 (42.7%) participants were male. The median estimated 24-hour urinary sodium excretion level, potassium excretion level, Na/K ratio (inter quartile range) were 4.9 (4.1-5.8) g/d, 2.1 (1.8-2.5) g/d, and 2.3 (1.9-2.7), respectively. Participants with a higher urinary Na/K ratio were younger, physically inactive, and had higher fasting glucose levels. The proportion of participants with either high sodium or potassium excretion amounts are shown in Supplemental Table 2 (available online at http://www.mayoclinicproceedings.org). Differences in the proportions of patients with hypertension, diabetes, or CVD were nonsignificant across the urinary Na/K ratio tertiles.
Table 1Baseline Characteristics According to Urinary Na/K Ratio
During 37,950 person-years of follow-up (median, 11.5 years), 532 participants developed CKD, and the corresponding CKD incidence rate was 14.0 (95% CI, 12.9 to 15.3) per 1000 person-years (Table 2). Cox proportional hazards analysis revealed that after adjustment for age, sex, and baseline eGFR, the HRs (95% CIs) were 0.77 (0.62 to 0.95) and 1.09 (0.88 to 1.34) for urinary Na/K tertiles 1 and 2 (comparison: tertile 3 [highest tertile]), respectively (model 1, Table 3). The results were similar after adjusting for socioeconomic and medical history–related factors (model 2). Additionally, the fully adjusted model including body mass index (BMI), systolic BP, C-reactive protein levels, high-density lipoprotein cholesterol levels, fasting glucose levels, physical activity levels, and daily dietary caloric intake showed that the lowest urinary Na/K ratio tertile had a 22% lower risk of CKD development than the highest tertile (HR, 0.78; 95% CI 0.63 to 0.97; model 3). The C-statistics of model 3 for predicting CKD development was 0.82 (95% CI: 0.78 to 0.86) (Supplemental Table 3, available online at http://www.mayoclinicproceedings.org). Similar results were observed when the log-transformed urinary Na/K ratio was treated as a continuous variable; for a log increase in the urinary Na/K ratio, the risk of CKD development was increased by 55% (HR, 1.55; 95% CI, 1.14 to 2.09) (Table 3). However, the association between incident CKD risk and individual urinary excretion of sodium or potassium was nonsignificant (Supplemental Figure 2, available online at http://www.mayoclinicproceedings.org). Similarly, comparable results were noted when the time-updated models with CVD and systolic BP as time-varying covariates were evaluated (for a log increase in the urinary Na/K ratio: HR, 1.57; 95% CI, 1.16-2.13; model 3) (Supplemental Table 4, available online at http://www.mayoclinicproceedings.org). Spline regression analysis revealed that the HR for CKD development increased steeply up to 1 in analysis using log-transformed urine Na/K values, but there was no significant increase thereafter (Figure 1A). However, when the relationship between incident CKD risk and individual urinary excretion of sodium or potassium was assessed, no significant association was observed (Figures 1B and 1C).
Table 2Incidence Rates of CKD Development According to Urinary Na/K Excretion Ratio
Model 3: Model 2 + BMI, systolic blood pressure, C-reactive protein level, HDL-C level, fasting glucose level, dietary energy intake, and physical activity level.
Urine Na/K ratio and C-reactive protein, HDL-C, and fasting glucose levels were natural log-transformed because of skewed distribution.
1.56 (1.16-2.10)
.004
1.49 (1.10-2.02)
.01
1.55 (1.14-2.09)
.01
Urine Na/K excretion ratio tertile
1
0.77 (0.62-0.95)
.02
0.79 (0.64-0.98)
.03
0.78 (0.63-0.97)
.03
2
1.09 (0.88-1.34)
.35
1.10 (0.89-1.35)
.38
1.09 (0.88-1.34)
.42
3
Reference
a BMI, body mass index; eGFR, estimated glomerular filtration rate; HDL-C, high-density lipoprotein cholesterol; Na/K, sodium-to-potassium.
b Model 1: Adjusted for age, sex, and eGFR.
c Model 2: Model 1 + education level, household income, diabetes, and cardiovascular disease.
d Model 3: Model 2 + BMI, systolic blood pressure, C-reactive protein level, HDL-C level, fasting glucose level, dietary energy intake, and physical activity level.
e Urine Na/K ratio and C-reactive protein, HDL-C, and fasting glucose levels were natural log-transformed because of skewed distribution.
Figure 1Association of estimated 24-hour urinary electrolyte excretion with the risk of chronic kidney disease. A, Estimated urinary sodium-to-potassium (Na/K) ratio and the risk of chronic kidney disease. B, Estimated urinary sodium excretion and the risk of chronic kidney disease. C, Estimated urinary potassium excretion and the risk of chronic kidney disease Incident chronic kidney disease (CKD) was defined as two consecutive estimated glomerular filtration rate (eGFR) measurements of <60 mL/min per 1.73 m2 during follow-up. Models are adjusted for age, sex, eGFR, education level, household income, diabetes, cardiovascular disease, body mass index, systolic blood pressure, C-reactive protein level, high-density lipoprotein cholesterol level, fasting glucose level, and physical activity level. Urinary Na/K ratio and C-reactive protein, high-density lipoprotein cholesterol, and fasting glucose levels were natural log-transformed because of skewed distribution.
Subgroup analyses were performed in groups stratified by age (<60 or ≥60 years), sex (male or female), BMI (≤25 or >25 kg/m2), diabetes (with or without), and hypertension (with or without) to assess the effect modification of subgroups had on the relationship between urinary Na/K ratio and CKD development (Figure 2). There were no significant interactions in any of the subgroups, suggesting that the relationship between urinary Na/K ratio and CKD risk was maintained across the subgroups.
Figure 2Forest plot. Models are adjusted for age, sex, estimated glomerular filtration rate, education level, household income, diabetes, cardiovascular disease, body mass index (BMI), systolic blood pressure, C-reactive protein level, high-density lipoprotein cholesterol level, fasting glucose level, and physical activity level. Urinary sodium-to-potassium ratio and C-reactive protein, high-density lipoprotein cholesterol, and fasting glucose levels were natural log-transformed because of skewed distribution. BMI, body mass index; CKD, chronic kidney disease; DM, diabetes mellitus; HTN, hypertension.
When sensitivity analysis was performed excluding participants with less than 2 years of follow-up (n=221) or who developed the primary outcome within 2 years of enrollment (n=52), incident CKD risk was positively associated with increases in the urinary Na/K ratio (HR, 1.44; 95% CI, 1.05 to 1.97; model 3) (Supplemental Table 5, available online at http://www.mayoclinicproceedings.org). Similar associations were found in the analysis excluding participants with a baseline eGFR of less than or equal to 66 mL/min per 1.73 m2 to ensure a more definite decline in kidney function to define the primary outcome (HR, 1.49; 95% CI, 1.06 to 2.02; model 3) (Supplemental Table 6, available online at http://www.mayoclinicproceedings.org). Moreover, this positive relationship between the urinary Na/K ratio and CKD risk was maintained when CKD was defined as a single episode of eGFR less than 60 mL/min per 1.73 m2 during the follow-up period (HR, 1.36; 95% CI, 1.08 to 1.70) (Supplemental Table 7, available online at http://www.mayoclinicproceedings.org). The comparable associations resulted in a repeated base in the Tanaka equation (Supplemental Table 8, available online at http://www.mayoclinicproceedings.org).
Discussion
In this study, the association between the urinary Na/K ratio and CKD development was assessed in a community-based prospective cohort of adults with preserved kidney function. The risk of CKD development was significantly lower in the tertile with the lowest urinary Na/K ratio than in the tertile with the highest urinary Na/K ratio. Additionally, when the urinary Na/K ratio was considered a continuous variable, the risk of incident CKD increased in proportion with the increase in the urinary Na/K ratio. These associations were independent of confounding variables. Cubic spline analysis revealed that this steady increase in risk was valid for log-transformed urinary Na/K ratios lower than 1 and remained steady thereafter. However, no significant association was observed with incident CKD risk when the urinary excretion levels of sodium or potassium were evaluated individually.
A higher urinary Na/K ratio was significantly associated with an increased risk of CKD in this study. However, a previous study of 7063 participants from Japan evaluating the association between repeated measurements of spot urine Na/K ratios and eGFR decline suggested that the possibility of the urinary Na/K ratio having a physiological relationship with eGFR decline would be low.
This was because of the probable effect of regression to the mean. Although the urinary Na/K ratio was related to rapid eGFR decline, it was also positively correlated with the baseline eGFR. Compared with the values in that study, the baseline eGFR did not differ among the urinary Na/K ratio groups in this study. Additionally, only participants with preserved kidney function at baseline were included in the analysis, unlike former investigations that included those with prevalent CKD. Urinary excretion of sodium and potassium may not accurately represent their intake in patients with underlying kidney diseases.
A recent investigation of 1030 adults from the CARDIA (Coronary Artery Risk Development In Young Adults) study showed that the Na/K ratio measured using 24-hour urine samples was significantly associated with CKD development in some of the examined multivariate models.
However, the significance was lost in the fully adjusted model. Compared with that in the current study, sodium excretion was relatively low in that study, while potassium excretion was comparable. Therefore, the actual range of analyzed urinary Na/K ratios in that investigation may have differed from the range in this study. Additionally, patients with hypertension accounted for 6.6% of the population in the CARDIA study, compared with 33.7% of the population in this study. Patients with hypertension are more sensitive to sodium than those without hypertension. This difference in cohort characteristics may have led to the difference in results. This possibility was supported by a recent study that showed a close association of sodium intake with CKD risk only in women with hypertension.
The risk of CKD linearly decreased with lower urinary Na/K ratios, despite the relatively high intake of sodium in the participants. The WHO guidelines recommend a diet resulting in a urinary sodium excretion level of less than 2.0 g/d to minimize the risk of CVD.
Noticeably, none of the participants in this study met the WHO recommendations. Restricting dietary intake with respect to recommendations is difficult. A survey from the United States, Mexico, France, and the United Kingdom reported that only 0.1% to 0.5% of the population complied with the WHO dietary intake goal.
Therefore, generously increasing the potassium intake rather than restricting the sodium intake could be a more achievable dietary goal to reduce the risk of CKD. This approach was supported by a recent study that showed that the risk of CVD was the lowest in those with a high potassium intake despite a moderate sodium intake.
However, further investigations including wide ranges of sodium and potassium intakes are required to confirm this possibility.
The relationship between the urinary Na/K ratio and CKD development can be attributed to several mechanisms. Previous investigations have shown the dietary intakes of sodium and potassium to be closely related to BP. Positive dose-response associations between urinary sodium excretion and BP have been reported,
Association between urinary sodium and potassium excretion and blood pressure among adults in the United States: National Health and Nutrition Examination Survey, 2014.
Association between urinary sodium and potassium excretion and blood pressure among adults in the United States: National Health and Nutrition Examination Survey, 2014.
A recent cluster randomized trial for sodium substitution with potassium-enriched salt showed that decreasing sodium intake and increasing potassium intake decreased BP, cardiovascular events, and mortality.
Considering that hypertension is one of the most well-known risk factors for CKD, the possibility of BP-related mediation in the association between the urinary Na/K ratio and incident CKD risk is high. However, the prevalence of hypertension did not differ among the urinary Na/K ratio groups at baseline. Additionally, the association between the urinary Na/K ratio and CKD development remained significant even after adjustment for hypertension. The presence of other mediators should also be considered. Recently, the urinary Na/K ratio has been reported to be linked to adverse metabolic outcomes, which could be another mediator leading to kidney function decline. An analysis of 3722 adults showed that the urinary Na/K ratio was correlated with insulin resistance.
Additionally, a recent prospective observational study reported that the urinary Na/K ratio was significantly associated with the development of obesity, suggesting that an increase in the urinary Na/K ratio may induce metabolic derangements which may consequently affect kidney function.
Dietary characteristics differ among ethnicities and cultural backgrounds, and this would have had influence on the amount of sodium and potassium intake in this study. Koreans are known to consume more sodium and less potassium compared with the Western population.
Intersalt Cooperative Research Group Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion.
In addition, main food sources that contribute to the sodium intake in Koreans are reported to be noodles, kimchi, and soups which are rarely consumed among Americans.
Therefore, the findings of this study may be limited to the specific ethnic group of Asians included in the evaluation. Further assessments including other ethnic populations are needed to generalize the results to other nations.
Obtaining 24-hour urine collections and ensuring their integrity and completeness are obstacles especially for epidemiological studies.
Association between urinary sodium and potassium excretion and blood pressure among adults in the United States: National Health and Nutrition Examination Survey, 2014.
Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies.
The Kawasaki formula had been shown to be more accurate in estimating 24-hour urinary sodium excretion amounts from spot urine measurements than the Tanaka formula.
Validation and comparison of three formulae to estimate sodium and potassium excretion from a single morning fasting urine compared to 24-h measures in 11 countries.
In addition, the Kawasaki formula had been used in several large worldwide observational analyses evaluating the relation between urinary and potassium and adverse outcomes.
Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies.
Therefore, the Kawasaki formula was used for estimating urinary sodium and potassium excretion amounts in this study. The mean sodium excretion amount of 4.9 g/d estimated through the Kawasaki formula was comparable to the 4.7 g/d mean 24-hour excretion amount in Koreans assessed in the INTERSALT (International Study of Sodium, Potassium, and Blood Pressure) study, suggesting that the probability of the spot urine estimation would not largely differ from the actual 24-hour excretion amount.
Intersalt Cooperative Research Group Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion.
Nonetheless, evaluations measuring sodium and potassium excretion amounts through actual 24-hour urine collections are needed to confirm the findings of this study.
Study Limitations
First, urine specimens for urine electrolyte measurements were collected only at baseline. As individuals’ dietary habits may change over time, sodium and potassium intake at baseline may not precisely reflect the dietary pattern of an individual during the observation period. Evaluations considering urinary excretion levels of electrolytes as time-varying variables are needed. Second, the primary outcome of the current study follows the Kidney Disease: Improving Global Outcomes definition of CKD which has been used in several epidemiologic studies.
However, the possibility of acute kidney injury being the reason for eGFR decline cannot be fully ruled out. Nonetheless, eGFR recovered to greater than or equal to 60 mL/min per 1.73m2 after primary outcome in only 6 (1.6%) people, suggesting that the probability of acute kidney injury being included as an outcome would not be high. Third, the detailed type of medications including antihypertensive medication had not been collected in the current study. However, the prevalence of diabetes, which would be one of the main indications for renin-angiotensin aldosterone system blockade use, was comparable among the Na/K tertile groups. In addition, the prevalence of antihypertensive medication use was, in fact, highest in the group with the lowest urine Na/K values. Therefore, the possibility of proteinuria being masked through renin-angiotensin aldosterone system blockade usage would not be high. Regarding diuretics, only five people were reported to be prescribed with diuretics, and the proportion of diuretic users was similar across the urine Na/K ratio tertile groups. Therefore, the use of diuretics may have had minimal effect on the results. Nevertheless, the likelihood of antihypertensive medication type being a bias of outcome cannot be completely eliminated, and other medications such as vasopressin may have influenced the urine sodium or potassium concentration. Fourth, because of the observational nature of the study, a clear causal relationship between the urinary Na/K ratio and CKD development cannot be concluded.
Conclusion
A low urinary Na/K ratio was associated with a decreased risk of CKD among adults with preserved kidney function. The balance between dietary sodium and potassium intakes may have a greater effect on kidney function than the dietary intake of sodium or potassium alone. However, further evaluations are required to confirm these findings.
Potential Competing Interests
The authors report no potential competing interests.
Acknowledgments
The authors thank the staff and participants of the Korean Genome and Epidemiology Study (KoGES) for important contributions.
The epidemiologic data used in this study were obtained from the Korean Genome and Epidemiology Study (KoGES; 4851–302) of the National Research Institute of Health, Centers for Disease Control and Prevention, Ministry for Health and Welfare, Republic of Korea.
Funding sources for KoGES had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or the decision to submit the manuscript for publication.
Analysis of the Global Burden of Disease study highlights the global, regional, and national trends of chronic kidney disease epidemiology from 1990 to 2016.
The ratio of urinary sodium and potassium and chronic kidney disease progression: Results from the KoreaN Cohort Study for Outcomes in Patients with Chronic Kidney Disease (KNOW-CKD).
Expressing the Modification of Diet in Renal Disease Study equation for estimating glomerular filtration rate with standardized serum creatinine values.
Association between urinary sodium and potassium excretion and blood pressure among adults in the United States: National Health and Nutrition Examination Survey, 2014.
Associations of urinary sodium excretion with cardiovascular events in individuals with and without hypertension: a pooled analysis of data from four studies.
Validation and comparison of three formulae to estimate sodium and potassium excretion from a single morning fasting urine compared to 24-h measures in 11 countries.
This month’s feature highlights three articles that appear in the current issue of Mayo Clinic Proceedings. These articles are also featured on the Mayo Clinic Proceedings’ YouTube Channel ( https://youtu.be/86yRRW6LlwY ).
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