| |

Received: 30 January 2019    Revised: 15 April 2019    Accepted: 29 April 2019

DOI: 10.1111/jch.13610

ORIG INAL PAPER

Difference in 24‐hour urine sodium excretion between controlled

and uncontrolled patients on antihypertensive drug treatment

Moo‐Yong Rhee MD, PhD1 | Sang‐Ho Jo MD, PhD2  | Ji‐Hyun Kim MD, PhD1 |

Kwang‐Il Kim MD, PhD3 | Deuk‐Young Nah MD, PhD4 | Sun‐Woong Kim PhD5 |
Namyi Gu MD, PhD6 | Ki‐Chul Sung MD, PhD7 | Kyung‐Soon Hong MD, PhD8 |
Eun‐Joo Cho MD, PhD9 | Sim‐Yeol Lee PhD10
1
Cardiovascular Center, Dongguk University Ilsan Hospital, Goyang‐si, Korea
2
Division of Cardiology, Hallym University Sacred Heart Hospital/Hallym University College of Medicine, Anyang‐si, Korea
3
Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam‐si, Korea
4
Division of Cardiology, Department of Internal Medicine, Dongguk University Gyeongju Hospital, Gyeongju‐si, Korea
5
Department of Statistics, Survey and Health Policy Research Center, Dongguk University, Seoul, Korea
6
Department of Clinical Pharmacology and Therapeutics, Dongguk University Ilsan Hospital, Goyang‐si, Korea
7
Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea
8
Hallym University College of Medicine, Chuncheon, Korea
9
Division of Cardiology, Department of Internal Medicine, St Paul's Hospital, Catholic University, Seoul, Korea
10
Department of Home Economics Education, Dongguk University, Seoul, Korea

Correspondence
Sang‐Ho Jo, MD, PhD, Division of
Cardiology, Department of Internal
Medicine, Hallym University Sacred Heart
Hospital, 896 Pyeongchon‐dong, Dongan‐
gu, Anyang‐si, Gyeonggi‐do, 14103, Korea.
Email: sophi5neo@gmail.com
and
Moo‐Yong Rhee, MD, PhD, Cardiovascular
Center, Dongguk University Ilsan Hospital,
27 Dongguk‐ro, Ilsandong‐gu, Goyang‐si,
Gyeonggi‐do, 10326, Korea.
Email: mooyong_rhee@dumc.or.kr
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).
Abstract
The objective of this study was to evaluate the association between sodium intake and
blood pressure (BP) control in hypertensive patients taking antihypertensive medica‐
tions 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 pa‐
tients (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 hyperten‐
sive 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.

J Clin Hypertens. 2019;21:1057–1062. ©2019 Wiley Periodicals, Inc. |  1057

wileyonlinelibrary.com/journal/jch  
 |
1058       RHEE et al.
1 |  I NTRO D U C TI O N
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 import‐
ant lifestyle factor. Excessive sodium intake is associated with
elevated blood pressure (BP). 2 It can attribute to poor BP con‐
trol despite the use of antihypertensive medications. However,
3-7
only a few short‐term controlled trials with small sample size
8,9
and cross‐sectional studies have evaluated the association be‐
tween high sodium intake and poor BP control. These cross‐sec‐
tional 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 ca‐
sual BP.12
Therefore, the objective of this study was to evaluate the asso‐
ciation between sodium intake and BP control in hypertensive pa‐
tients taking antihypertensive medications by using 24‐hour urine
collection and 24‐hour ambulatory BP.
2 |  M E TH O DS
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 rela‐
tives 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 morn‐
ing, 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 col‐
lected 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 measure‐
ments during the daytime (9  am‐9  pm) and at least seven measure‐
ments at night time (00:00‐06:00), were regarded as satisfactory
measurement.17
Hypertension was defined based on average of 24‐hour sys‐
tolic 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 devia‐
tion. Study population were divided into four groups according to
the BP control status and whether they are on the antihyperten‐
sive 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 antihyperten‐
sive drug treatment, UTHT, n = 174), treated and controlled hyper‐
tension 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 ambula‐
tory 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 regres‐
sion 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 statisti‐
cally significant.
3 | R E S U LT S
Baseline demographics and clinical characteristic of subjects are
presented in Table 1. Mean age of CHT and UCHT groups was higher
RHEE et al. |
      1059

TA B L E 1   Demographic and clinical characteristics of study population

  NT UTHT CHT UCHT P*

n 441 174 62 63  
a b c c
Age (y) 45.9 ± 10.3 49.8 ± 8.9 57.3 ± 8.0 53.9 ± 8.0 <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 ± 3.0 b 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     2 3  
inhibitors, n
Beta blockers, n     6 10  
Diuretics, n     18 21  
Alpha blockers, n     1 0  
a b c b
24‐h SBP, mm Hg 110.6 ± 7.5 126.7 ± 9.0 114.4 ± 7.1 125.9 ± 7.1 <0.001
24‐h DBP, mm Hg 70.3 ± 6.3a 87.1 ± 6.0 b 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 ± 109.0 b,c 147.8 ± 87.9b 184.8 ± 196.0 c <0.001
a b b b
Fasting glucose, mg/dL 93.7 ± 15.0 103.4 ± 27.5 103.5 ± 18.8 108.4 ± 28.8 <0.001

Note: 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.

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 antihy‐
pertensive drugs was 1.67 in UCHT group and 1.51 in CHT group,
showing no difference between the two groups. There was no signif‐
icant difference in classes of antihypertensive drugs between CHT
and UCHT groups either.
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 po‐
tassium 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 hy‐
pertensive patients on antihypertensive drug treatment (Table 3).
 |
1060       RHEE et al.

TA B L E 2   Level of urinary salt excretion

  NT UTHT CHT UCHT P* P** P***

a a a b
24‐h urine Na 157.9 ± 63.9 170.6 ± 65.3 160.2 ± 62.8 200.3 ± 78.8 <0.001 0.023 0.048
a a,b b,c c
24‐h urine K 56.1 ± 20.0 57.8 ± 21.9 64.4 ± 27.5 65.9 ± 21.5 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.

4 |  D I S CU S S I O N TA B L E 3   Risk for uncontrolled blood pressure in treated

patients
In the present study, the level of 24‐hour urine sodium was the Model Odds ratio (95% CI) P value
highest in uncontrolled hypertension patients and high sodium in‐
Age 0.949 (0.902‐0.999) 0.046
take was independently associated with uncontrolled BP. These re‐
Gender 0.813 (0.344‐1.921) 0.637
sults suggest that a high sodium intake is an important barrier for
Body mass index 0.996 (0.867‐1.144) 0.953
optimal BP control in hypertensive patient taking antihypertensive
Use of diuretics 1.052 (0.448‐2.473) 0.907
medications.
High sodium intake can elevate BP and has been considered an Fasting blood glucose 1.006 (0.990‐1.024) 0.450

attributing factor to poor BP control in patients who are taking an‐
tihypertensive medications. However, majority of intervention stud‐
ies 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 in‐
take on BP control.3-9 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 hy‐
pertension, 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 evaluated the association of sodium intake on BP control. Chinese
Sodium intake reduction can potentiate effects of antihyper‐
tensive drugs. Such effects are more obvious for renin‐angioten‐
sin‐aldosterone system‐related drugs. 3,5-7
Regarding mechanisms
by which low sodium intake can potentiate BP lowering effects of
5
antihypertensive drugs, Weir et al have suggested that lower so‐
dium intake may reverse to angiotensin II–dependent form of hyper‐
tension, that is, more susceptible to angiotensin‐converting enzyme
inhibitor. High sodium intake can reduce the bioavailability of antihy‐
pertensive 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
HDL cholesterol 0.983 (0.954‐1.014) 0.272
24‐h urine sodium 1.008 (1.001‐1.015) 0.027
Note: 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.
relatively small population. A real world may be different from the
environment of controlled trial although RCTs provide the best evi‐
dence. 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 antihyper‐
tensive drugs treatment. 23 Only a few cross‐sectional studies have
hypertensive patients consuming more than 6  g/d salt which was
estimated by using food frequency questionnaire had lower BP con‐
trol 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 er‐
rors of dietary survey method10,24 and spot urine method.11,25 The
24‐hour urine collection method is widely regarded as the gold stan‐
dard method in the assessment of salt intake. In the measurement
RHEE et al.
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 ambula‐
tory 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, life‐
style 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 accu‐
rately, three or more days of 24‐hour urine collection has been sug‐
gested 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 pres‐
sure 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 recom‐
mended to hypertensive patients, although they are on antihyper‐
tensive drug treatment.
C O N FL I C T O F I N T E R E S T
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 re‐
search 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.
AU T H O R ' S C O N T R I B U T I O N S
MYR conceptualized and designed the study, acquired funding, ana‐
lyzed 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
|
      1061
prepared methodology of the study. All authors read and approved
the manuscript.
ORCID
Sang‐Ho Jo  https://orcid.org/0000-0002-2063-1542
REFERENCES
1. Thomopoulos C, Parati G, Zanchetti A. Effects of blood pressure
lowering on outcome incidence in hypertension: 7. Effects of more
vs. less intensive blood pressure lowering and different achieved
blood pressure levels ‐ updated overview and meta‐analyses of ran‐
domized trials. J Hypertens. 2016;34(4):613‐622.
2. Intersalt: an international study of electrolyte excretion and
blood pressure. Results for 24 hour urinary sodium and potas‐
sium excretion. Intersalt Cooperative Research Group. BMJ.
1988;297(6644):319‐328.
3. Singer DR, Markandu ND, Cappuccio FP, Miller MA, Sagnella GA,
MacGregor GA. Reduction of salt intake during converting en‐
zyme inhibitor treatment compared with addition of a thiazide.
Hypertension. 1995;25(5):1042‐1044.
4. Pinjuh Markota N, Rumboldt M, Rumboldt Z. Emphasized warn‐
ing reduces salt intake: a randomized controlled trial. J Am Soc
Hypertens. 2015;9(3):214‐220.
5. Weir MR, Chrysant SG, McCarron DA, et al. Influence of race
and dietary salt on the antihypertensive efficacy of an an‐
giotensin‐converting enzyme inhibitor or a calcium chan‐
nel antagonist in salt‐sensitive hypertensives. Hypertension.
1998;31(5):1088‐1096.
6. Weir MR, Yadao AM, Purkayastha D, Charney AN. Effects of high‐
and low‐sodium diets on ambulatory blood pressure in patients
with hypertension receiving aliskiren. J Cardiovasc Pharmacol Ther.
2010;15(4):356‐363.
7. Houlihan CA, Allen TJ, Baxter AL, et al. A low‐sodium diet poten‐
tiates the effects of losartan in type 2 diabetes. Diabetes Care.
2002;25(4):663‐671.
8. Qin YU, Li T, Lou P, et al. Salt intake, knowledge of salt intake, and
blood pressure control in Chinese hypertensive patients. J Am Soc
Hypertens. 2014;8(12):909‐914.
9. Lee J, Lee H, Kim K, Park JH, Kim S, Oh J. A higher salt intake leads
to a lower rate of adequate blood pressure control. J Korean Med Sci.
2014;29(Suppl 2):S103‐S108.
10. McLean RM. Measuring population sodium intake: a review of
methods. Nutrients. 2014;6(11):4651‐4662.
11. Rhee M‐Y, Kim J‐H, Shin S‐J, et al. Estimating 24‐Hour urine so‐
dium from multiple spot urine samples. J Clin Hypertens (Greenwich).
2017;19(4):431‐438.
12. ABC‐H Investigators, Roush GC, Fagard RH, et al. Prognostic im‐
pact from clinic, daytime, and night‐time systolic blood pressure
in nine cohorts of 13,844 patients with hypertension. J Hypertens.
2014;32(12):2332‐2340.
13. Rhee MY, Shin SJ, Park SH, Kim SW. Sodium intake of a city popu‐
lation in Korea estimated by 24‐h urine collection method. Eur J Clin
Nutr. 2013;67(8):875‐880.
14. Kyung Kim MI, Kwon M, Rhee M‐Y, et al. Dose‐response associ‐
ation of 24‐hour urine sodium and sodium to potassium ratio
with nighttime blood pressure at older ages. Eur J Prev Cardiol.
2019;26(9):952‐960.
15. Knuiman JT, Hautvast JG, van der Heyden L, et al. A multi‐centre
study on completeness of urine collection in 11 European centres. I.
Some problems with the use of creatinine and 4‐aminobenzoic acid
 |
1062       RHEE et al.
as markers of the completeness of collection. Hum Nutr Clin Nutr.
1986;40(3):229‐237.
16. Wei W, Tolle M, Zidek W, van der Giet M. Validation of the mobil‐O‐
Graph: 24 h‐blood pressure measurement device. Blood Press Monit.
2010;15(4):225‐228.
17. O'Brien E, Asmar R, Beilin L, et al. European Society of Hypertension
recommendations for conventional, ambulatory and home blood
pressure measurement. J Hypertens. 2003;21(5):821‐848.
18. Mancia G, De Backer G, Dominiczak A, et al. 2007 guidelines for
the management of arterial hypertension: the task force for the
management of arterial hypertension of the European Society of
Hypertension (ESH) and of the European Society of Cardiology
(ESC). J Hypertens. 2007;25(6):1105‐1187.
19. Pimenta E, Gaddam KK, Oparil S, et al. Effects of dietary sodium re‐
duction on blood pressure in subjects with resistant hypertension:
results from a randomized trial. Hypertension. 2009;54(3):475‐481.
20. Azizi M, Blanchard A, Charbit B, et al. Effect of contrasted sodium
diets on the pharmacokinetics and pharmacodynamic effects of renin‐
angiotensin system blockers. Hypertension. 2013;61(6):1239‐1245.
21. Darbar D, Fromm MF, Dell’Orto S, et al. Modulation by di‐
etary salt of verapamil disposition in humans. Circulation.
1998;98(24):2702‐2708.
22. Luft FC, Morris CD, Weinberger MH. Compliance to a low‐salt diet.
Am J Clin Nutr. 1997;65(2 Suppl):698S‐703S.
23. Kastarinen MJ, Puska PM, Korhonen MH, et al. Non‐pharmacologi‐
cal treatment of hypertension in primary health care: a 2‐year open
randomized controlled trial of lifestyle intervention against hyper‐
tension in eastern Finland. J Hypertens. 2002;20(12):2505‐2512.
24. Yoshita K, Miura K, Okayama A, et al. A validation study on
food composition tables for the international coopera‐
tive INTERMAP study in Japan. Environ Health Prev Med.
2005;10(3):150‐156.
25. Polonia J, Lobo MF, Martins L, Pinto F, Nazare J. Estimation of pop‐
ulational 24‐h urinary sodium and potassium excretion from spot
urine samples: evaluation of four formulas in a large national repre‐
sentative population. J Hypertens. 2017;35(3):477‐486.
26. Luft FC, Fineberg NS, Sloan RS. Estimating dietary sodium intake
in individuals receiving a randomly fluctuating intake. Hypertension.
1982;4(6):805‐808.
27. Sun Q, Bertrand KA, Franke AA, Rosner B, Curhan GC, Willett WC.
Reproducibility of urinary biomarkers in multiple 24‐h urine sam‐
ples. Am J Clin Nutr. 2017;105(1):159‐168.
How to cite this article: 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. https​://doi.
org/10.1111/jch.13610​