Nephrol Dial Transplant (2019) 1–6
doi: 10.1093/ndt/gfz020
Extracellular fluid volume expansion, arterial stiffness
and uncontrolled hypertension in patients with chronic
kidney disease
Branko Braam1,2, Chung Foon Lai1, Joseph Abinader2 and Aminu K. Bello2
1
Department of Medicine, Division of Nephrology, University of Alberta, Edmonton, Alberta, Canada and 2Department of Physiology,
University of Alberta, Edmonton, Alberta, Canada
Correspondence and offprint requests to: Branko Braam; E-mail: branko.braam@ualberta.ca
ABSTRACT
Background. Hypertension is prevalent in patients with
chronic kidney disease (CKD) and is related to extracellular
fluid volume (ECFV) expansion. Arterial stiffening is another
implication of CKD that can be caused by ECFV expansion. In
this study, we hypothesized that CKD patients with uncon-
trolled hypertension are more likely to be fluid volume ex-
panded than normotensive patients, which in turn is associated
with increased arterial stiffness.
Methods. Adult hypertensive patients with mild–severe CKD
(n ¼ 82) were recruited. ECFV was assessed using multifre-
quency bioimpedance and arterial stiffness by applanation
tonometry and oscillometry.
Results. Patients with uncontrolled hypertension had fluid vol-
ume expansion compared with controls (1.0 6 1.5 versus
0.0 6 1.6 L, P < 0.001), and had a higher augmentation index
(AIx) and pulse wave velocity. Fluid volume expansion was
more prevalent in patients with uncontrolled hypertension
(58%) than patients who were at target (27%). Fluid volume ex-
pansion was correlated with age, AIx and systolic blood pres-
sure. In a binary logistic regression analysis, AIx, age and fluid
volume status were independent predictors of uncontrolled hy-
pertension in both univariate and multivariate models.
Discussion. In summary, uncontrolled hypertension among
hypertensive CKD patients is associated with ECFV expansion.
Our data suggest a relationship between ECFV expansion, in-
creased arterial stiffness and uncontrolled hypertension.
Keywords: bioimpendance, chronic renal failure, fluid over-
load, hypertension, vascular stiffness
INTRODUCTION
Extracellular fluid volume (ECFV) expansion is central to the
pathogenesis of hypertension. The kidneys play a vital role in
regulating ECFV. Among patients with chronic kidney disease
(CKD), the prevalence of hypertension is high and increases
C The Author(s) 2019. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.
V 1
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ORIGINAL ARTICLE
with the stage of CKD [1]. Similarly, ECFV expansion is com-
mon in CKD and also increases with declining kidney function
[2]. Not surprisingly, diuretics reduce ECFV and decrease blood
pressure (BP) [1, 3]. However, a significant number of CKD
patients have uncontrolled BP despite treatment [4, 5]. This
raises the question whether CKD patients with uncontrolled BP
are not simply fluid volume expanded. If so, then this would
need careful consideration to mitigate the risk of adverse conse-
quences (morbidity and mortality) across the spectrum of CKD
[6, 7].
Arterial stiffening is another implication of CKD [8, 9],
which can be characterized by an increased augmentation index
(AIx) or pulse wave velocity (PWV) [10]. Arterial stiffening has
been positively associated with the rate of decline of kidney
function in patients with CKD [11, 12]. In addition, ECFV ex-
pansion and hypertension can increase arterial wall stress,
which might lead to structural (arterial wall thickness) and
functional (distensibility) changes of the arterial wall and result
in arterial stiffening [13]. Taken together, our current study fo-
cuses on the effects of ECFV expansion in patients with CKD
on BP control and arterial stiffness.
We hypothesized that CKD patients with uncontrolled BP
are more likely to have fluid volume expansion, which in turn is
then associated with increased arterial stiffness. We therefore
aimed to determine the association between ECFV expansion,
uncontrolled BP and the relationship with arterial stiffness in a
cohort of CKD patients in Canada.
MATERIALS AND METHODS
Recruitment
Adult hypertensive patients with mild–severe CKD [esti-
mated glomerular filtration rate (eGFR): mild, 60–90 mL/min/
1.73 m2; moderate, 30–60 mL/min/1.73 m2; severe, 15–30 mL/
min/1.73 m2] were recruited from the General Nephrology
Clinic of the Northern Alberta Renal Program at the University
of Alberta Hospital between 2014 and 2016. Excluded from the
study were patients with implanted pacemakers and defibrilla-
tors, vascular stents, metallic sutures, artificial joints, pins pre-
sent due to previous orthopedic surgery and pregnant patients,
as these issues could interfere with the accuracy of assessment
of fluid volume status (VS). Hypertension was defined as BP
140/90 mmHg (130/80 mmHg for diabetic patients) or the
use of antihypertensive medications as per standard guideline
recommendation [14]. The study was approved by the
University of Alberta Human Research Ethics Board and writ-
ten consent was obtained from each participant in the study.
Biochemical data collection
Biochemical parameters, such as serum creatinine and albu-
min, were obtained from patient records at the clinic. eGFRs
were calculated using the CKD Epidemiology Collaboration
equation [15].
Measurement of ECFV
To determine fluid VS, we used an approach previously used
in hemodialysis patients by our group [16]. Using the Body
Composition Monitor (BCM; Fresenius Medical Care, Bad
Homburg, Germany), a multifrequency bioimpedance device
that has been validated previously [17], fluid volume expansion
is calculated by comparison of the measured ECFV with the
predicted ECFV using a standard physiological model [18].
This model uses adjustments for subjects with high body mass
index [19]. For each patient in the study, measurements were
performed in triplicate on one occasion. Electrodes were ap-
plied on an ipsilateral arm and foot. The BCM calculates VS,
which is expressed as volume excess or depletion in liters com-
pared with the estimated normal ECFV. Normovolemia was de-
fined as any measurement between 1.1 and 1.1 L relative to
normal ECFV, as 90% of fluid volumes in the healthy popula-
tion are within the range of 1.1 to 1.1 L [20]. Fluid volume
overload was considered >1.1 L above normal ECFV.
Arterial stiffness measurement
Arterial stiffness was defined and assessed using standard
methods [21]. This was evaluated in two ways during the study
period (for technical reasons): the SphygmoCor (AtCor
Medical, Sydney, NSW, Australia) arterial tonometer was used
during the first phase of data collection in 2014 and the
Arteriograph (TensioMed, Budapest, Hungary) was used dur-
ing the second phase in 2016. The SphygmoCor arterial tonom-
eter applies applanation tonometry to measure waveforms at
the radial and carotid arteries three times at each site while the
patient is in a supine position. Through a computerized process,
the aortic pressure waveform was generated [22] and the pulse
wave analysis of the patient obtained [10]. The Arteriograph is
an oscillometric device that applies occlusion on the brachial ar-
tery of the patient to record pulse waves. By calculating the time
difference between the beginning of the first wave and the sec-
ond wave (reflective wave), the AIx and PWV of the patient
were determined [23].
2 B. Braam et al.
Statistical analysis
Comparison groups of patients were determined by BP con-
trol status (controlled versus uncontrolled) and, in the case of
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analyses on arterial stiffness assessment, by year of enrolment.
Differences between groups were tested for continuous varia-
bles by Student’s t-test and for categorical variables by Fisher’s
exact test. All values were expressed as mean 6 standard deviation
and P < 0.05 was taken to be significant. Univariate relationships
between ECFV expansion and related variables were assessed by
Pearson’s correlation analyses. In a binary logistic regression
model, we examined the associations of key predictor variables
(demographic, clinical and laboratory) with uncontrolled BP us-
ing ECFV expansion as the primary predictor variable. Linear re-
gression analyses were also conducted to investigate, if present,
any statistical differences between the results obtained from the
SphygmoCor arterial tonometer (2014 patient cohort) and those
from the Arteriograph (2016 patient cohort).
We also conducted a series of sensitivity analyses. First, we
conducted a series of correlation analyses to examine the effect
of baseline proteinuria and proteinuria changes (baseline to fol-
low-up) on salt retention (fluid VS) and vascular stiffness (AIx).
Second, we investigated the impact of BP control, vascular stiff-
ness and fluid volume expansion on changes in kidney function
from baseline to follow-up (DeGFR) in a multivariate liner re-
gression model adjusting in a stepwise fashion for the key pre-
dictor variables, with DeGFR as the dependent variable.
Student’s t-test and correlations were performed using
GraphPad Prism 7 (GraphPad Software, La Jolla, CA, USA). All
regression analyses were performed using Statistical Package
for the Social Sciences, version 25.0 (IBM, Armonk, NY, USA).
RESULTS
Patient characteristics
Of the total 82 patients (52 male and 30 female) enrolled in
the study, 72 patients (88%) were on BP-lowering medications
and 40 patients (49%) were receiving diuretic treatment; 38
patients (46%) displayed uncontrolled BP. Overall, patients had
mild–severe CKD, with a mean eGFR value of 46 6 26 mL/
min/1.73 m2. In total, 28 patients (34%) were diabetic and 35
patients (43%) had signs of edema (Table 1). Regarding fluid
VS, 34 patients (41%) were found to be fluid volume overloaded
(1.1 L above normal ECFV). The patients displayed substan-
tial variation of fluid VS, ranging from 3.5 to 4.5 L below and
above the estimated normal ECFV (Figure 1A).
Differences between patients with controlled versus
uncontrolled BP
The 82 hypertensive CKD patients were categorized into two
groups based on whether they had controlled BP or not (uncon-
trolled: systolic BP 140 mmHg or diastolic BP 90 mmHg for
nondiabetic patients and 130 mmHg or 80 mmHg for dia-
betic patients). The two groups did not differ in BMI, diastolic
BP, serum creatinine level, eGFR, presence of diabetes and use
of antihypertensive medication. However, patients with uncon-
trolled BP had a higher average fluid volume than patients with
controlled BP (P ¼ 0.0052) (Table 1). Furthermore, 58% of
Table 1. Patient characteristics

Characteristics All Controlled BP Uncontrolled BP P-values

M/F, n/n (%) 82 (52/30) 44 (31/13) (53.7%) 38 (21/17) (46.3%)

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Fluid VS (L) 0.5 6 1.62 0.0 6 1.57 1.0 6 1.52 0.0052
Age (years) 63 6 14.4 57.9 6 15.0 68.8 6 11.3 0.0005
BMI (kg/m2) 29.2 6 7.00 29.0 6 6.62 29.6 6 7.50 NS
Systolic BP (mmHg) 135 6 20.5 121 6 12.4 152 6 13.8 <0.0001
Diastolic BP (mmHg) 74.6 6 12.8 71.7 6 11.7 78.0 6 13.4 NS
PP (mmHg) 60.8 6 18.0 49.5 6 11.2 74.5 6 15.9 <0.0001
MAP (mmHg) 94.9 6 13.2 88.1 6 10.9 103 6 11.3 <0.0001
Serum creatinine (lmol/L) 157 6 76.4 143 6 59.1 177 6 85.8 NS
Baseline eGFR (mL/min/1.73 m2) 46 6 26 53 6 27 39 6 23 NS
Diabetic (yes), n (%) 28 (34.1) 11 (25.0) 17 (44.7) NS
Signs of edema (yes), n (%) 35 (42.7) 14 (31.8) 21 (55.3) 0.0443
Use of antihypertensive medications (yes), n (%) 72 (87.8) 39 (88.6) 33 (86.8) NS
Use of diuretics (yes), n (%) 40 (48.8) 14 (31.8) 26 (68.4) 0.0017
Values are expressed as mean 6 SD unless stated otherwise. P-values: unpaired Student’s t-test between patients with fluid volume overload and normal fluid VS. PP, pulse pressure;
MAP, mean arterial pressure; NS, not significant; M, male; F, female.

Binary logistic regression between uncontrolled BP and

FIGURE 1: (A) Fluid VS distribution among 82 hypertensive
patients with mild–severe CKD. (B) ECFV expansion is associated
with uncontrolled BP.
patients with uncontrolled BP (n ¼ 22) were fluid volume over-
loaded, whereas only 27% of patients with controlled BP
(n ¼ 12) were fluid overloaded (P ¼ 0.007; Figure 1B). The aver-
age pulse pressure and mean arterial pressure were significantly
higher in patients with uncontrolled BP. Edema was more prev-
alent in patients with uncontrolled BP and there were more
patients in that group receiving diuretics (P ¼ 0.0323) (Table 1).
Systolic BP, age and AIx were positively correlated with fluid
volume overload. However, all the key variables tested demon-
strated weak coefficients of correlation ranging from r2 ¼ 0.105
to 0.153 (Figure 2).
predictor variables
Being controlled or uncontrolled with respect to BP was
used as a categorical variable and was analyzed as the outcome
variable, with patients being at controlled (target) BP as the ref-
erence group. In univariate analyses, relationships between the
outcome variable and individual independent variables were
studied separately (Table 2). Age, pulse pressure, fluid VS,
eGFR, signs of edema and diuretic treatment showed statisti-
cally significant associations with the outcome variable. Except
for eGFR, the statistically significant odds ratios (ORs) were
>1, indicating positive relationships with uncontrolled BP.
Multivariate analysis was also conducted to study the associ-
ations between the outcome variable and predictor variables
chosen based on clinical plausibility (Table 2). Among the pre-
dictor variables examined, only age and fluid VS showed strong
associations with the outcome variable in the multivariate
model {OR 1.060 [95% confidence interval (CI) 1.005–1.117]
and 1.531 [1.041–2.252], respectively} (Table 2).
To further investigate the contribution of predictors to uncon-
trolled BP, we built separate binary logistic regression models for
systolic BP and diastolic BP (uncontrolled for non-diabetic
patients: systolic BP 140 mmHg, diastolic BP 90 mmHg;
uncontrolled for diabetic patients: systolic BP 130 mmHg, dia-
stolic BP 80 mmHg) (Supplementary data, Tables S1 and S2).
The results from the secondary analysis on systolic BP as the out-
come variable (Supplementary data, Table S1) were similar to
those from the primary analysis (Table 1), where age and fluid
VS exhibited strong associations with the outcome variable in
both univariate and multivariate models [OR 1.062 (95% CI
1.006–1.121) and 1.579 (1.068–2.333), respectively]. In contrast,
the secondary analysis on diastolic BP as the outcome variable
(Supplementary data, Table S2), the only predictor variable that
displayed a statistically significant association, was fluid VS in the
multivariate model [OR 1.681 (95% CI 1.045–2.706)].
Analyses on arterial stiffness assessment
To determine if there were differences between the results
obtained from the two methods of arterial stiffness assessment,

ECFV overload and uncontrolled hypertension 3

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FIGURE 2: Correlations between fluid VS and (A) systolic BP, (B) age and (C) AIx. r2, coefficient of determination.

not shown). Furthermore, we did not find any significant asso-

Table 2. Predictors of uncontrolled BP
ciations between baseline eGFR, change in renal function from
Predictor variables Odd ratios (95% CI) P-value baseline to follow-up (DeGFR) and BP control. However, fluid
Univariate VS showed a strong association with the outcome
Age (years) 1.080 (1.036–1.125) <0.001 variable (DeGFR) among diabetic patients (Supplementary
PP (mmHg) 1.112 (1.061–1.166) <0.001 data, Table S5).
Fluid VS (L) 1.851 (0.304–2.626) 0.001
eGFR (mL/min/1.73 m2) 0.977 (0.958–0.996) 0.017
Edema 3.39 (1.343–8.579) 0.010
Use of diuretics 2.731 (1.115–6.687) 0.028 DISCUSSION
Diabetes 2.570 (0.978–6.753) 0.055
In this study we demonstrated that fluid volume overload
Use of BP-lowering medications 0.756 (0.219–2.613) 0.659
Multivariate among patients with hypertension and CKD was common,
Age (years) 1.060 (1.005–1.117) 0.031 with a wide and uneven distribution across patients. Fluid vol-
Fluid VS (L) 1.531 (1.041–2.252) 0.030 ume overload was more prevalent in patients with uncontrolled
eGFR (mL/min/1.73 m2) 1.001 (0.978–1.024) 0.942 BP. In a binary logistic regression analysis, fluid VS, age and
Diuretics 1.973 (0.651–5.983) 0.230
AIx as indicators of arterial stiffness were identified as predic-
PP, pulse pressure. tors for uncontrolled BP. Moreover, in diabetic patients, fluid
overload was associated with a more pronounced decline in kid-
a master table with the 2014 and 2016 cohorts was first con- ney function over time. Although the study design does not al-
structed. Since the mean values of augmentation are signifi- low one to draw conclusions about causality, fluid overload is
cantly different between the cohorts (P ¼ 0.003), linear suggested to be a relevant factor in control of BP and vascular
regression analyses were also used to study the relationship be- stiffness, as well as decline in renal function over time.
tween AIx and potential predictors. By combining the cohorts, A previous study investigated the relationship between
eGFR and signs of edema exhibited a statistically significant as- ECFV expansion and cardiovascular risk factors in CKD
sociation with AIx in both univariate and multivariate linear re- patients [24]. VS was measured by bioimpedance spectroscopy
gression models (Supplementary data, Table S3). In the 2014 and fluid volume overload was defined as fluid VS 7% of esti-
cohort, signs of edema showed a statistically significant associa- mated ideal ECFV, which is quite similar to our definition of
tion with the outcome variable in the univariate linear regres- fluid volume 1.1 L relative to normal ECFV. In that study,
sion model (Supplementary data, Table S4). In the 2016 cohort, 52% of patients were identified as fluid volume overloaded. The
diastolic BP and eGFR displayed a statistically significant asso- slight percentage difference with our results (41% fluid volume
ciation with the outcome variable in the univariate and multi- overloaded) could be explained by less severe kidney dysfunc-
variate linear regression models, respectively (Supplementary tion in our study compared with theirs (mean eGFR 46 versus
data, Table S4). 29 mL/min/1.73 m2, respectively). Moreover, in that study, sys-
tolic BP correlated positively and eGFR negatively with fluid
volume overload. Similarly, our correlation study showed weak
Sensitivity analyses but significant relationships between these same parameters. In
To test the robustness of our findings, we conducted a series another study, fluid volume overload was observed in 50% of
of sensitivity analyses that included a series of correlation analy- patients with Stages 4 and 5 CKD and was determined to be as-
ses. We did not find any significant relationships between base- sociated with cardiovascular morbidity and all-cause mortality
line proteinuria and proteinuria changes (baseline to follow-up) [25]. Taken together, we confirm that fluid volume overload is
on salt retention (fluid VS) and vascular stiffness (AIx) (data prevalent among hypertensive CKD patients.

4 B. Braam et al.
 Several predictors for uncontrolled BP were identified in bi-
nary logistic regression analysis. First, fluid VS was strongly as-
sociated with the outcome variable in both univariate and
multivariate models, indicating a higher chance for patients to
have uncontrolled BP if they have increased ECFVs. This was
not investigated in previous clinical studies in the CKD popula-
tion. Another identified predictor was age, which showed
strong associations in both univariate and multivariate models,
indicating that older CKD patients are less likely to be uncon-
trolled. With its negative correlation with fluid VS, aging plays
a critical role in contributing to ECFV expansion and hyperten-
sion, as aging is a significant modifier of hypertension in CKD
patients [4, 26]. Interestingly, arterial stiffness, measured by AIx
and PWV, was associated with uncontrolled hypertension. In
binary logistic regression analyses in both the 2014 and 2016
cohorts, AIx and PWV showed strong positive associations in
the univariate model, indicating that CKD patients with en-
hanced arterial stiffness are less likely to be controlled.
Interestingly, being diabetic was not a predictor for fluid over-
load as observed previously by others [27].
A major implication of this study is on understanding the
pathophysiology as well as management approach to resistant
hypertension [28]. A previous study demonstrated that patients
with resistant hypertension on a low-salt diet showed a reduc-
tion of mean office systolic and diastolic BP compared with
patients on a regular, high-salt diet [29]. In a double-blind
study, arterial stiffness (baseline PWV) was determined as a sig-
nificant independent predictor of achieving a reduction in sys-
tolic BP after 12 months of treatment [30]. Although patients
enrolled in our study had CKD and were not categorized on the
basis of resistant hypertension, similar predictors—fluid vol-
ume and arterial stiffness—were identified in our binary logistic
regression analyses. Therefore ECFV expansion could well be a
factor in resistant hypertension without CKD as well.
Fluid volume overload was significantly and positively corre-
lated with systolic BP, age and AIx. Therefore a relationship be-
tween ECFV expansion and arterial stiffness is suggested.
Although the PWV data collected in our study were not ade-
quate for correlation analysis, PWV has been associated with
fluid volume overload among peritoneal dialysis patients in a
small study (n ¼ 122) [31]. Also, correction of ECFV expansion
was shown to improve AIx in hemodialysis patients [32].
Therefore we propose that ECFV expansion is associated with
arterial stiffness in our cohort of CKD patients.
To enhance the robustness of our findings, we have con-
ducted a series of sensitivity analyses in order to determine if
there are any interesting associations between salt retention
(fluid VS) and vascular stiffness (AIx) with proteinuria in the
subjects with and without diabetes, and there were no signifi-
cant findings in both study groups. Furthermore, we also exam-
ined the impact of BP control (using different measures of BP
measurements), ECFV expansion and vascular stiffness on re-
nal function decline, and this also showed no significant rela-
tionship between baseline eGFR, change in renal function
(DeGFR) and BP control and our key outcomes. However, in-
triguingly, fluid VS showed a strong association with the out-
come variable among diabetic patients in the regression models
ECFV overload and uncontrolled hypertension
using different baseline BP measures, which indicated the im-
pact of ECFV expansion on GFR decline. We were also in-
trigued that a third of the patients with uncontrolled BP were
not receiving diuretics, and this could be partly explained by the
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inability of practitioners to detect volume overload using clini-
cal examination only. This might reflect practice variations
across settings and within practitioners. This is an important
practice implication of our findings. This is an additional impe-
tus for the use of bio-impedance (even considering its limita-
tions) for volume assessments, as demonstrated in our previous
work [16].
Our study has several limitations. First, this was a snapshot
study, as all data were collected only once for this study; longi-
tudinal assessments and interventions were not applied.
Second, the sample size was small and could possibly not repre-
sent the general CKD population across the full spectrum.
However, the finding of a high prevalence of fluid volume over-
load is in keeping with existing literature in the field studies [16,
17, 20]. Third, the assessment of ECFV using multifrequency
bioimpedance spectroscopy comes with some error. Yet the
method seems comparable in performance to radioisotope
methods [33]. Lastly, the two cohorts of patients in this study
had their arterial stiffness assessed by different methods due to
technical issues with the equipment initially used in measure-
ments. The results obtained by both methods were comparable
and did not impact on our conclusions and implications of this
study, but they still share slight discrepancies that make merg-
ing the data not justifiable [34]. In our study, AIx was signifi-
cantly different between the patients in 2014 and 2016, which
was likely due to the differences in age and renal function.
Recognizing these limitations, our conclusions still hold with
respect to ECFV expansion being a determinant of uncontrolled
BP and a likely determinant of arterial stiffness. Other limita-
tions with potential implications for further work in this area
included a lack of data in this analysis on other comorbid con-
ditions and hospitalization rates, as well as laboratory markers
such as serum B-type natriuretic peptide and C-reactive
protein.
An increase in total body sodium is the basis for ECFV ex-
pansion. Several studies have indicated that high-sodium states
could lead to increased vascular stiffness [35–37]. In salt-resis-
tant healthy humans, a high-sodium diet was associated with
decreased endothelium-dependent vasodilation [35]. There is
accumulating evidence that the mechanism for impaired vascu-
lar function is related to the composition and function of the
endothelial glycocalyx [36, 37]. While plasma sodium levels
were not significantly different between controlled and uncon-
trolled subjects and the study was not designed to investigate
endothelial function and the glycocalyx, it is possible that the
differences in vascular stiffness and in outcome in diabetic
patients were related to endothelial glycocalyx alterations.
In summary, our study demonstrated associations of ECFV
expansion with uncontrolled BP among hypertensive CKD
patients. Also, causes of uncontrolled BP are multifactorial, in-
volving patient age, fluid volume overload and likely arterial
stiffening. Therefore we suggest that better fluid volume control
would help improve BP control and preserve arterial function,
5
which prevent patients from progression to adverse renal and
cardiovascular outcomes. A prospective randomized controlled
trial targeting fluid volume overload is needed to better define
the relationship between fluid overload and vascular stiffness
and would lead to insight into whether prevention of fluid over-
load will also prevent adverse cardiovascular outcomes.
SUPPLEMENTARY DATA
Supplementary data are available at ndt online.
FUNDING
B.B. was supported by the Kidney Health Translational
Research Chair by the Faculty of Medicine and Dentistry,
Department of Medicine and Division of Nephrology.
CONFLICT OF INTEREST STATEMENT
Fresenius Canada made the BCM available for the present
study.
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Received: 26.8.2018; Editorial decision: 14.1.2019