Abstract
The objective of this study was to evaluate the association between sodium intake and blood pressure (BP) control in hypertensive patients taking antihypertensive medications by using 24‐hour urine collection and 24‐hour ambulatory BP. This is a cross‐sectional community‐based study and conducted in 2011 and 2012. A total of 1128 participants were recruited from five cities in Korea. Among them, 740 participants who had complete 24‐hour urine collection and valid 24‐hour ambulatory BP data were included in this study. Participants were divided into four groups: normotensives (NT, n = 441), untreated hypertensive patients (UTHT, n = 174), controlled hypertensive patients (CHT, n = 62), and uncontrolled hypertensive patients (UCHT, n = 63). UCHT and CHT groups showed higher mean age than NT and UTHT groups. UCHT and UTHT groups showed higher 24‐hour systolic BP (SBP) and diastolic BP (DBP) than NT and CHT groups. UCHT group had the highest level of 24‐hour urine sodium. Multivariate analysis adjusted with age, gender, body mass index, estimated glomerular filtration rate, and use of diuretics showed higher level of 24‐hour urine sodium in UCHT group than that in CHT group. Multivariate logistic regression analysis revealed independent association of the amount of 24‐hour urine sodium with uncontrolled BP in hypertensive patients on antihypertensive drug treatment. Higher level of 24‐hour urine sodium excretion in uncontrolled hypertensive patients suggests that excessive sodium intake could be associated with blunted BP lowering efficacy of antihypertensive medications.
Keywords: antihypertensive drugs, hypertension, sodium
1. INTRODUCTION
Hypertension is a well‐known risk factor of cardiovascular disease, and poor blood pressure (BP) control is associated with increased risk of cardiovascular events.1
Among risk factors of hypertension, salt intake is an important lifestyle factor. Excessive sodium intake is associated with elevated blood pressure (BP).2 It can attribute to poor BP control despite the use of antihypertensive medications. However, only a few short‐term controlled trials with small sample size3, 4, 5, 6, 7 and cross‐sectional studies8, 9 have evaluated the association between high sodium intake and poor BP control. These cross‐sectional studies measured sodium intake by dietary survey method and spot urine method known to have limitations.10, 11 Moreover, they measured casual BP, not ambulatory BP known to have stronger association with future cardiovascular events than casual BP.12
Therefore, the objective of this study was to evaluate the association between sodium intake and BP control in hypertensive patients taking antihypertensive medications by using 24‐hour urine collection and 24‐hour ambulatory BP.
2. METHODS
2.1. Study population
The study design of participant recruitment and measurement protocol has been described elsewhere.13, 14 Briefly, adults were recruited by using list‐assisted random digit dialing (LARDD) from five cities (Goyang, Paju, Seoul, Chuncheon, and Gyeongju) in Korea. This study was conducted in Goyang in 2011 and in other cities (Paju, Seoul, Chuncheon, and Gyeongju) in 2012 using the same study protocol. From five cities, 1128 individuals (971 participants who were invited by LARDD and 157 participants who were relatives or friends of the invited participants) participated in this study. Among them, data from 740 participants who had both complete 24‐hour urine collection and satisfactory 24‐hour ambulatory BP monitoring were analyzed.
2.2. Study protocol
Participants, who visited the study's clinical trial centers in the morning, were provided detailed instructions for the study procedure and written informed consent. They were given urine collection kit and detailed instruction for method of 24‐hour urine collection. The collected urine sample was transferred to the Biochemistry Laboratory of Dongguk University Ilsan Hospital (Goyang, Korea) in 2011 and Green Cross LabCell (Yongin, Korea) in 2012 to measure sodium and potassium concentrations by an ion‐selective electrode method (Modular DPE chemistry; Roche Diagnostics) and creatinine levels by Jaffe reaction (Kinetic colorimetric assay; Roche Diagnostics) in both facilities. Fasting blood glucose, total cholesterol, triglyceride, high‐density lipoprotein cholesterol, low‐density lipoprotein cholesterol, serum sodium, and potassium levels were measured after overnight fasting for at least 8 hours.
The 24‐hour urine collection was validated by both self‐reported urine diary and 24‐hour urine creatinine‐based determination. If self‐reported loss of a urine sample was more than 100 mL at a time or more than once, or if the creatinine index [24‐hour urine creatinine, mg/dL / (21 × body weight)] was <0.7, the collected urine sample was considered to be incomplete for a 24‐hour period collection.13, 15
The 24‐hour ambulatory BP was measured simultaneously with 24‐hour urine collection (Mobil‐O‐Graph; IEM GmbH).16 More than 70% of the attempted measurement, at least 14 measurements during the daytime (9 am‐9 pm) and at least seven measurements at night time (00:00‐06:00), were regarded as satisfactory measurement.17
Hypertension was defined based on average of 24‐hour systolic BP (SBP) ≥130 mm Hg and/or diastolic BP (DBP) ≥80 mm Hg or current use of antihypertensive medication.18 The Institutional Review Board of each participating hospital approved the study protocol.
2.3. Statistical analysis
All data are presented as percentages or mean ± standard deviation. Study population were divided into four groups according to the BP control status and whether they are on the antihypertensive medications or not: normotensives group (24‐hour averaged ambulatory BP <130/80 mm Hg and not on antihypertensive drug treatment, NT, n = 441), untreated hypertensive group (24‐hour averaged ambulatory BP ≥130/80 mm Hg and not on antihypertensive drug treatment, UTHT, n = 174), treated and controlled hypertension group (24‐hour averaged ambulatory BP <130/80 mm Hg and on antihypertensive drug treatment, CHT, n = 62), and treated but uncontrolled hypertension group (24‐hour averaged ambulatory BP ≥130/80 mm Hg and on antihypertensive drug treatment, UCHT, n = 63). Comparisons of baseline data between groups were performed using chi‐square test (categorical variables), Student's t test (continuous variables), or analysis of variance. Difference of urine sodium, potassium, and sodium‐to‐potassium ratio was further analyzed by analysis of covariance adjusted with age, gender, body mass index (BMI), estimated glomerular filtration rate (eGFR), and use of diuretics. In multivariate logistic regression analysis for the determinant of uncontrolled BP, 24‐hour urine sodium, age, gender, BMI, use of diuretics, fasting blood glucose, and high‐density lipoprotein (HDL) cholesterol were included. Statistical analyses were performed using MedCalc version 18.11 (MedCalc Software bvba). A P value <0.05 was considered statistically significant.
3. RESULTS
Baseline demographics and clinical characteristic of subjects are presented in Table 1. Mean age of CHT and UCHT groups was higher than those of NT and UTHT groups. The BMI of UCTH group was the highest among all groups. The 24‐hour SBP and DBP of UTHT and UCHT groups were significantly higher than those of NT and CHT groups (P < 0.05). There was no significant difference in 24‐hour SBP and DBP between UTHT and UCHT groups. The number of antihypertensive drugs was 1.67 in UCHT group and 1.51 in CHT group, showing no difference between the two groups. There was no significant difference in classes of antihypertensive drugs between CHT and UCHT groups either.
Table 1.
Demographic and clinical characteristics of study population
| NT | UTHT | CHT | UCHT | P * | |
|---|---|---|---|---|---|
| n | 441 | 174 | 62 | 63 | |
| Age (y) | 45.9 ± 10.3a | 49.8 ± 8.9b | 57.3 ± 8.0c | 53.9 ± 8.0c | <0.001 |
| Men, n (%) | 121 (27.4) | 118 (67.8) | 26 (41.9)c | 39 (61.9) | <0.001 |
| BMI, kg/m2 | 22.9 ± 2.8a | 24.6 ± 3.0b | 25.0 ± 3.3b | 26.3 ± 3.2c | <0.001 |
| Diabetes, n (%) | 14 (3.2) | 21 (12.1) | 12 (19.4) | 9 (14.3) | <0.001 |
| No. of antihypertensive medications | |||||
| Average, n | 1.51 | 1.67 | |||
| 1, n | 31 | 27 | 0.515 | ||
| 2, n | 27 | 28 | |||
| 3, n | 2 | 6 | |||
| 4, n | 1 | 1 | |||
| Antihypertensive medications | |||||
| Calcium channel blocker, n | 32 | 32 | |||
| Angiotensin receptor blockers, n | 36 | 38 | |||
| Angiotensin‐converting enzyme inhibitors, n | 2 | 3 | |||
| Beta blockers, n | 6 | 10 | |||
| Diuretics, n | 18 | 21 | |||
| Alpha blockers, n | 1 | 0 | |||
| 24‐h SBP, mm Hg | 110.6 ± 7.5a | 126.7 ± 9.0b | 114.4 ± 7.1c | 125.9 ± 7.1b | <0.001 |
| 24‐h DBP, mm Hg | 70.3 ± 6.3a | 87.1 ± 6.0b | 72.0 ± 5.2a | 86.7 ± 5.2b | <0.001 |
| Serum Na (mmol/dL) | 141.2 ± 2.4 | 141.1 ± 2.3 | 141.7 ± 2.3 | 141.3 ± 2.5 | 0.345 |
| Serum K (mmol/dL) | 4.3 ± 0.4 | 4.3 ± 0.3 | 4.3 ± 0.4 | 4.2 ± 0.4 | 0.278 |
| Serum creatinine (mg/dL) | 0.74 ± 0.14 | 0.82 ± 0.16 | 0.82 ± 0.22 | 0.86 ± 0.18 | <0.001 |
| 24‐h urine creatine (mg/24h) | 1191.3 ± 434.8a | 1376.1 ± 372.8b | 1189.6 ± 337.2a | 1426.6 ± 321.2b | <0.001 |
| 24‐h urine volume (mL) | 1489.6 ± 592.1 | 1565.2 ± 572.3 | 1535.8 ± 572.7 | 1691.5 ± 659.1 | 0.062 |
| eGFR (mL/min/1.73 m2) | 95.8 ± 16.7a | 93.6 ± 15.6a | 86.4 ± 16.1b | 86.6 ± 14.7b | <0.001 |
| Total cholesterol, mg/dL | 193.7 ± 34.5a,b | 203.7 ± 36.7a | 192.9 ± 37.3a,b | 186.9 ± 35.3b | 0.002 |
| LDL cholesterol, mg/dL | 119.3 ± 31.7a,b | 127.2 ± 32.8a | 117.3 ± 35.7a,b | 112.9 ± 31.0 | 0.007 |
| HDL cholesterol, mg/dL | 59.2 ± 14.9a | 52.1 ± 14.3b | 54.8 ± 14.1a,b | 49.8 ± 13.9b | <0.001 |
| Triglyceride, mg/dL | 108.1 ± 69.6a | 165.4 ± 109.0b,c | 147.8 ± 87.9b | 184.8 ± 196.0c | <0.001 |
| Fasting glucose, mg/dL | 93.7 ± 15.0a | 103.4 ± 27.5b | 103.5 ± 18.8b | 108.4 ± 28.8b | <0.001 |
Different alphabets represent significant difference between groups at alpha level of 0.05 by post hoc Tukey HSD analysis.
Abbreviations: BMI, body mass index; CHT, controlled hypertension group; DBP, diastolic blood pressure; eGFR, estimated glomerular filtration rate by Modification of Diet in Renal Disease (MDRD) formula; HDL, high‐density lipoprotein; K, potassium; LDL, low‐density lipoprotein; Na, sodium; NT, normotensives group; SBP, systolic blood pressure; UCHT, uncontrolled hypertension group; UTHT, untreated hypertension group.
P values obtained by analysis of variance or chi‐square test for difference between four groups.
The UCHT group had the highest level of 24‐hour urine sodium among all groups in unadjusted and adjusted analyses (Table 2, P < 0.001 and P = 0.023, respectively). The level of 24‐hour urine sodium in the UCHT group was higher than in the CHT group in adjusted analysis (P = 0.048). There was no significant difference in 24‐hour urine potassium and sodium‐to‐potassium ratio between groups. Multivariate logistic regression analysis revealed the independent association of the amount of 24‐hour urine sodium and age with uncontrolled BP in hypertensive patients on antihypertensive drug treatment (Table 3).
Table 2.
Level of urinary salt excretion
| NT | UTHT | CHT | UCHT | P * | P ** | P *** | |
|---|---|---|---|---|---|---|---|
| 24‐h urine Na | 157.9 ± 63.9a | 170.6 ± 65.3a | 160.2 ± 62.8a | 200.3 ± 78.8b | <0.001 | 0.023 | 0.048 |
| 24‐h urine K | 56.1 ± 20.0a | 57.8 ± 21.9a,b | 64.4 ± 27.5b,c | 65.9 ± 21.5c | 0.001 | 0.143 | 0.812 |
| 24‐h urine Na/K | 3.01 ± 1.19a,b | 3.15 ± 1.15b | 2.70 ± 1.02a | 3.30 ± 1.58b | 0.023 | 0.194 | 0.162 |
Abbreviations: CHT, controlled hypertension group; K, potassium; Na, sodium; Na/K, sodium‐to‐potassium ratio; NT, normotensives group; UCHT, uncontrolled hypertension group; UTHT, untreated hypertension group.
P value by analysis of variance, and different alphabets represent significant difference at alpha level of 0.05 by post hoc Tukey HSD analysis.
P value by analysis of covariance between four groups and adjusted for age, gender, body mass index, estimated glomerular filtration rate, and use of diuretics.
P value by analysis of covariance between uncontrolled hypertension group vs controlled hypertension group, adjusted for age, gender, body mass index, estimated glomerular filtration rate, and use of diuretics.
Table 3.
Risk for uncontrolled blood pressure in treated patients
| Model | Odds ratio (95% CI) | P value |
|---|---|---|
| Age | 0.949 (0.902‐0.999) | 0.046 |
| Gender | 0.813 (0.344‐1.921) | 0.637 |
| Body mass index | 0.996 (0.867‐1.144) | 0.953 |
| Use of diuretics | 1.052 (0.448‐2.473) | 0.907 |
| Fasting blood glucose | 1.006 (0.990‐1.024) | 0.450 |
| HDL cholesterol | 0.983 (0.954‐1.014) | 0.272 |
| 24‐h urine sodium | 1.008 (1.001‐1.015) | 0.027 |
Multivariate logistic regression analysis. Age, gender, body mass index, use of diuretics, fasting blood glucose, HDL cholesterol, and 24‐h urine sodium were included in the model.
Abbreviation: HDL, high‐density lipoprotein.
4. DISCUSSION
In the present study, the level of 24‐hour urine sodium was the highest in uncontrolled hypertension patients and high sodium intake was independently associated with uncontrolled BP. These results suggest that a high sodium intake is an important barrier for optimal BP control in hypertensive patient taking antihypertensive medications.
High sodium intake can elevate BP and has been considered an attributing factor to poor BP control in patients who are taking antihypertensive medications. However, majority of intervention studies have evaluated the effect of high sodium intake on BP elevation, but not on BP control, because they evaluated the effect of sodium intake on BP in patients not taking antihypertensive drugs.
Only a few studies have evaluated the effect of high sodium intake on BP control.3, 4, 5, 6, 7, 8, 9 Intervention trials for the effect of sodium intake in patients taking antihypertensive medication have been performed in short‐term studies, and most of them were performed with small sample sizes. In patients with treatment‐resistant hypertension, lowering of sodium intake from 250 mmol/d for 7 days to 50 mg/d for 7 days has reduced SBP by 22.7 mm Hg and DBP by 9.1 mm Hg.19 Education for salt intake reduction in 150 treated hypertensive patients reduced SBP by 5.3 mm Hg and DBP by 2.9 mm Hg after 2 months. The reduction was significantly larger than that in the control group.4
Sodium intake reduction can potentiate effects of antihypertensive drugs. Such effects are more obvious for renin‐angiotensin‐aldosterone system‐related drugs.3, 5, 6, 7 Regarding mechanisms by which low sodium intake can potentiate BP lowering effects of antihypertensive drugs, Weir et al5 have suggested that lower sodium intake may reverse to angiotensin II–dependent form of hypertension, that is, more susceptible to angiotensin‐converting enzyme inhibitor. High sodium intake can reduce the bioavailability of antihypertensive drugs20, 21 by modulating intestinal transporters. Reduced bioavailability of antihypertensive drugs by high sodium intake may attenuate the BP lowering efficacy of ingested drugs.
Although randomized controlled trials (RCTs) showed beneficial effect of sodium intake reduction in treatment of hypertension with antihypertensive drugs, most studies were short‐term trials with relatively small population. A real world may be different from the environment of controlled trial although RCTs provide the best evidence. Long‐term compliance to low sodium diet in the real world is quite different from that in RCTs.22 Cohort study or cross‐sectional epidemiologic study may be close to real world. A relatively long‐term study of lifestyle education including salt intake reduction has failed to reduce sodium intake and BP in patients with antihypertensive drugs treatment.23 Only a few cross‐sectional studies have evaluated the association of sodium intake on BP control. Chinese hypertensive patients consuming more than 6 g/d salt which was estimated by using food frequency questionnaire had lower BP control rate compared with patients consuming less than 6 g/d salt.8 In the analysis of Korean National Health and Nutritional Survey, among patients with cardiovascular disease, hypertension group (≥140/90 mm Hg) had higher 24‐hour urinary sodium excretion which was estimated from spot urine sodium, compared with the normal BP group.9
The distinguishing feature of our study from previous studies is the measurement method of salt intake and BP. We used 24‐hour urine collection method in the estimation of salt intake to avoid errors of dietary survey method10, 24 and spot urine method.11, 25 The 24‐hour urine collection method is widely regarded as the gold standard method in the assessment of salt intake. In the measurement of BP, we measured 24‐hour ambulatory BP. Although casual BP is significantly related to future cardiovascular events, ambulatory BP is better than casual BP in the prediction of cardiovascular events.12 No previous study has evaluated the association between BP control and salt intake by measuring 24‐hour urine electrolyte and ambulatory BP in the general population. With these distinguished features, we found a significant association between high sodium intake and poor BP control, providing an indirect evidence that high sodium intake might be an important barrier in the optimal treatment of hypertension.
The present study has some limitations. First, the present study was a cross‐sectional one. Therefore, the effect of long‐term sodium intake reduction on BP control could not be evaluated. Second, lifestyle modification such as try to reduce sodium intake or increase potassium, exercise, or moderation of alcohol consumption was not explored in our study. The third limitation was the measurement method of urine electrolyte. Single collection of 24‐hour urine may not be precise to measure daily mean salt intake. To estimate accurately, three or more days of 24‐hour urine collection has been suggested to be sufficient.26, 27 However, multiple collection of 24‐hour urine is difficult and impractical in large population‐based study like ours. Fourth, the result of the present study may be biased by small sample size of each group and poor adherence to antihypertensive medications. We did not check adherence to medication. Poor or non‐adherence to medication may contribute to poor blood pressure control.
In conclusion, higher level of 24‐hour urine sodium excretion in uncontrolled hypertensive patients suggests that excessive sodium intake could attenuate BP lowering efficacy of antihypertensive drug treatment. Sodium intake reduction should be strongly recommended to hypertensive patients, although they are on antihypertensive drug treatment.
CONFLICT OF INTEREST
MYR has received lecture honoraria from Pfizer Inc, LG Life Sciences Ltd, Boehringer Ingelheim Pharma GmbH & Co. KG., Hanmi Pharm. Co. Ltd., Yuhan Co. Ltd., Boryung Pharmaceutical Co. Ltd., and research grant from Boryung Pharmaceutical Co. Ltd. and Dong‐A Pharmaceutical Co., Ltd. The authors have no conflicts of interest in study design, study conduction, data interpretation, and the writing of the manuscript based on the data. The funding body had no role in data interpretation and the writing of the manuscript based on the data.
AUTHOR'S CONTRIBUTIONS
MYR conceptualized and designed the study, acquired funding, analyzed the data, supervised the study, and revised the manuscript. SHJ analyzed the data, and drafted and revised the manuscript. JHK, KIK, DYN, KCS, KSH, and EJC participated in patient enrollment and data collection. SWK participated in statistical analysis. NG and SYL prepared methodology of the study. All authors read and approved the manuscript.
Rhee M‐Y, Jo S‐H, Kim J‐H, et al. Difference in 24‐hour urine sodium excretion between controlled and uncontrolled patients on antihypertensive drug treatment. J Clin Hypertens. 2019;21:1057–1062. 10.1111/jch.13610
Funding information
This study was supported by the Research Program funded by the Ministry of Food and Drug Safety in 2011 (11162KFDA162) and 2012 (12162MFDS103).
Contributor Information
Moo‐Yong Rhee, Email: mooyong_rhee@dumc.or.kr.
Sang‐Ho Jo, Email: sophi5neo@gmail.com.
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