Original Article
Postdialysis Hypertension: Associated Factors, Patient
Profiles, and Cardiovascular Mortality
Attilio Losito,1 Lucia Del Vecchio,2 Goffredo Del Rosso,3 and Francesco Locatelli2
BACKGROUND AND OBJECTIVES
A postdialytic increase in blood pressure (BP) is a recognized but often
an overlooked complication. The epidemiology and predisposing
factors are still not well defined. We studied a large sample of Italian
dialysis patients to assess the prevalence of postdialysis hypertension
(PDHYPER), defined as any increase of systolic BP (SBP) >10 mm, Hg
above the predialysis value, the associated factors and its role in cardio-
vascular (CV) mortality.
PATIENTS AND METHODS
In this observational study, we assessed dialysis associated changes in
BP in 4,292 hemodialysis (HD) patients over 1 month (51,504 sessions).
We compared the clinical characteristics of the patients with stable
BP values during the HD session with those with PDHYPER. We also
assessed the impact of PDHYPER on CV mortality.
RESULTS
A total of 994 (23.1%) patients had PDHYPER. Patients with
PDHYPER were more likely to be hypertesive, older, have a shorter
An increase in blood pressure (BP) during hemodialysis (HD),
although recognized for many years, is often overlooked.1
There is also a lack of a unifying criteria for the diagnosis of
postdialytic hypertension (PDHYPER), although an increase
in systolic BP (SBP) >10 mm Hg from pre- to postdialysis has
been proposed and is widely used.2 There is also a scarcity
of systematic studies on its prevalence and consequences.3
Research on the mechanisms causing PDHYPER has been
addressed to both the HD treatment and patient character-
istics. The results obtained are often conflicting. Among the
possible pathogenetic mechanisms, ultrafiltration-induced
hypovolemia may trigger the renin–angiotensin system and
induce vasoconstriction, which is mediated by an increase
in blood viscosity/hemoconcentration favored by higher
hemoglobin (Hb) levels and/or treatment with erythropoiesis
stimulating agents.4 The removal of antihypertensive drugs by
dialysis is another possible cause of intradialytic hypertension.
Finally, electrolyte disequilibrium, sympathetic over activity,
and endothelial cell dysfunction may play a role.5
Unfortunately, the majority of the available studies con-
sidered 1 single hypothetical factor at a time or were per-
formed on a small number of patients from a single center.
Correspondence: Attilio Losito (atlosito@tin.it).
Initially submitted June 27, 2015; date of first revision August 4,
2015; accepted for publication August 30, 2015; online publication
September 21, 2015.
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dialysis vintage, be male, have lower SBP, lower changes in weight
during HD, and receive more antihypertensive medications. These
predictive factors were shown to be associated with an interaction
between weight loss and dialysis, suggesting a volume-related
mechanism in its pathogenesis. PDHYPER was also associated with
CV mortality.
CONCLUSIONS
In our study on a large Italian cohort of dialysis patients, the preva-
lence of PDHYPER was higher than what was previously reported
and is a significant risk factor for CV mortality in dialysis patients.
The pathogenesis is multifactorial but hypertensive state, antihyper-
tensive medications, and extracellular volume expansion appear to
play a major role.
Keywords: blood pressure; hemodialysis; hypertension; postdialysis
hypertension; volume expansion.
doi:10.1093/ajh/hpv162
This represents a potential bias since, in general, a single
center has a homogeneous policy on the dialytic and medi-
cal management of patients. A step forward toward its better
understanding can help reduce the high rate of cardiovascu-
lar (CV) morbidity occurring in HD patients.6
The aim of this large, multicenter, observational study is to
investigate HD- and patient-related factors associated with
PDHYPER and its impact on mortality.
PATIENTS AND METHODS
Study design
The study is a retrospective analysis of data collected for a
previous prospective study.7,8 In brief, patients were assessed
at enrollment and were followed thereafter. CV mortality
was drawn from death certificate and reported by participat-
ing centers. The information requested from participating
units on the cause of death were: death due to cerebrovascu-
lar disease, ischemic or hemorrhagic, death due to any CV
condition, comprising ischemic heart disease, heart failure,
and sudden death.
1Renal Unit, Ospedale Santa Maria Della Misericordia, Perugia, Italy;
2Renal Unit, Ospedale Manzoni, Lecco, Italy; 3Renal Unit, Ospedale
Mazzini, Teramo, Italy.
© American Journal of Hypertension, Ltd 2015. All rights reserved.
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Patients’ characteristics
All adult patients (≥18 years old), in 77 HD centers across
Italy, receiving HD thrice weekly for at least 3 months were
considered for inclusion. Patients with body weights less
than 35 kg, cachexia due to malignancies, severe malnutri-
tion or with known severe heart disease (New York Heart
Association (NYHA) class  III or IV) were excluded. The
diagnosis of heart failure, assigned to consultant cardiolo-
gists of the participating centers, was based mainly on clinical
grounds or on the finding of left ventricular ejection fraction
<50% at transthoracic echocardiography. Along with BP, the
following data were recorded: age, sex, smoking and alco-
hol intake history, serum cholesterol, body mass index, and
a history of diabetes serum albumin, Hb, parathyroid hor-
mone. Recorded parameters concerning dialysis treatment
were: length of session and dialysis modality, Kt/V as meas-
ured with 2-point Daugirdas formula, Δ body weight during
HD (as a proxy of ultrafiltration). Due to the frequent modi-
fications in antihypertensive treatment in dialysis patients,
we asked the participating centers to maintain the therapy
stable during the 12 dialysis period and to provide informa-
tion about antihypertensive medication (yes/no). The type
and dose of erythropoiesis stimulating agent were also col-
lected. HD modality was divided into 2 categories according
to the use of convective techniques.
Blood pressure measurement
In every dialysis unit, BP was measured by trained nurses
according to National Kidney Foundation Outcomes Quality
Initiative (KDOQI) guidelines.9 The nursing staff was spe-
cifically instructed accordingly. Predialysis BP was measured
after the patient had been sitting for at least 5 minutes before
the needles for dialysis access were placed. Postdialysis BP
was measured at least 5 minutes after the end of the proce-
dure for 12 consecutive sessions. Likewise, predialysis and
postdialysis pulse pressures were calculated from the meas-
ured BP; heart rate (HR) was also recorded.
For the analysis, we used the mean of BP changes in 12
consecutive HD sessions. A change (Δ) in SBP was defined as
postdialysis minus predialysis SBP. On the basis of published
evidence, showing an increase was associated with a number
of complications and with mortality, we defined PDHYPER
as being an increase in SBP during HD greater than 10 mm
Hg above the predialysis BP measurement.2 According to
current guidelines, postdialysis hypotension (PDHYPO) is
defined as a decrease of SBP greater than 20 mm Hg below
the predialysis value.10
For the analysis, we divided the patients into 3 groups
according to SBP changes during HD: group 1: Δ SBP
between −20 and + 10 mm Hg, group 2: Δ SBP > +10 mm
Hg, group 3: Δ SBP > −20 mm Hg. Patients with heart failure
were examined separately.
Statistical analysis
Continuous variables are presented as means and
SDs unless otherwise specified. Categorical variables are
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Postdialytic Hypertension and Cardiovascular Mortality
presented as proportions and compared by Pearson’s χ2.
Means were compared by the analysis of variance with
Dunnett’s post hoc test. To detect the predictors of postdi-
alysis changes in SBP, we performed a multiple regression
analysis with Δ SBP as the continuous dependent variable.
Logistic regression analysis was used to detect factors associ-
ated with PDHYPER as a dichotomous dependent variable.
The analysis was also carried out using different thresholds
for PDHYPER: 5 and 15 mm Hg. An unadjusted model
was built only with the variables that were significant to the
model. The adjusted model also included nonsignificant
variables. Both models were evaluated for goodness of fit
by the Hosmer and Lemeshow test and by the area under
the receiver-operating characteristic curve. On the basis of
the results of the logistic regression analysis, we investigated
biological interaction, as defined by Rothman, among pre-
dialysis SBP, Δ weight during HD and the use of antihyper-
tensive medications.11 We calculated the relative excess risk
because of interaction (RERI) by using the methods outlined
by Andersson et al.12 In the absence of a biological interac-
tion, the RERI is 0.  Logistic regression was repeated after
stratification by tertiles of weight loss due to dialysis.
Survival analysis
The association between Δ SBP and mortality was assessed
by the Cox proportional hazard model. Models were built
with the following covariates: age, sex, dialysis vintage, pres-
ence of diabetes, CHOL, body mass index, albumin, Hb, par-
athyroid hormone, Kt/V, Δ weight, and predialysis SBP. The
proportional hazards assumption of the models was assessed
using the Shoenfeld residuals. In the analysis, the etiology of
kidney disease was tested for its association with PHYPER
and mortality.
All tests were performed by Stata 11 statistical package
(Stata, College Station, TX).
RESULTS
At the baseline, we obtained data from 4,292 dialysis
patients (>99% Caucasian) for a total of 51,504 dialysis ses-
sions; 2,353 patients were assessed for the presence of heart
failure that was detected in 557 subjects (23.6%). The main
characteristics of the whole cohort and those of patients
grouped according to SBP changes with dialysis are pre-
sented in Table 1. A mean postdialysis SBP increase >10 mm
Hg (PDHYPER) was detected in 994 (23.1%) patients,
among them 73.5% had a diagnosis of hypertension. In
patients with a predialysis SBP <140 mm Hg, the prevalence
was 28.7%, in those with a predialysis SBP >140 mm Hg the
prevalence was 15.4% (P < 0.001, relative risk 0.537).
Multivariable regression analysis with dialytic Δ SBP as a
continuous dependent variable produced a significant model
(adjusted R2 = 0.212, F = 74.1, Prob > F = 0.0001) (Table 2).
Postdialysis hypertension
Compared to patients with no changes in BP (group
1), those with PDHYPER (group 2)  were more likely to
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 Losito et al.

Table 1.  Characteristics of the cohort 

Variable Whole cohort Controls PDHYPO PDHYPER

Number 4,292 2,580 718 994

Age (years, mean ± SD) 65.1 ± 18.9 64.1 ± 19.6 65.3 ± 17.2 70.2 ± 13.3*
Male sex (%) 62.0 62.6 55.8* 64.2
Dry weight (kg, mean ± SD) 65.9 ± 16.4 66.0 ± 17.8 67.6 ± 14.1 64.0 ± 12.9
Delta weight with dialysis (kg, mean ± SD) 2.55 ± 0.88 2.56 ± 0.86 2.88 ± 0.84* 2.29 ± 0.93*
Body mass index (kg/m2) 24.2 ± 4.3 24.2 ± 4.3 25.2 ± 4.8* 23.4 ± 3.9*
Dialytic vintage (months, mean ± SD) 67.5 ± 74.9 61.2 ± 81.8 64.6 ± 68.4 57.2 ± 63.2*
Dialysis session time (min, mean ± SD) 231.7 ± 20.0 230.9 ± 20.5 234.7 ± 18.5* 231.1 ± 19.0
Single pool Kt/V 1.31 ± 0.26 1.31 ± 0.26 1.33 ± 0.26* 1.31 ± 0.23
Hemoglobin (g/dl, mean ± SD) 11.4 ± 1.2 11.4 ± 1.2 11.6 ± 1.3 11.3 ± 1.27
Albumin (g/dl, mean ± SD) 3.82 ± 0.48 3.82 ± 0.48 3.84 ± 0.46 3.79 ± 0.49
Cholesterol (mg/dl, mean ± SD) 164.2 ± 41.2 164.1 ± 41.1 167.9 ± 41.1 164.2 ± 42.3
PTH (pg/ml, mean ± SD) 291.2 ± 285.9 292.6 ± 287.6 337.6 ± 334.8* 255.7 ± 288.2*
Convective HD (%) 24.9 25.4 26.7 22.9
Predialysis SBP (mm Hg, mean ± SD) 136.3 ± 20.6 134.2 ± 20.2 149.7 ± 19.1* 130.7 ± 18.4*
Predialysis PP (mm Hg, mean ± SD) 63.9 ± 18.2 61.2 ± 15.8 75.9 ± 24.6* 61.8 ± 15.6
Predialysis heart rate (b/min, mean ± SD) 73.1 ± 10.2 73.5 ± 9.8 74.6 ± 10.1 71.2 ± 10.5*
Postdialysis heart rate (b/min, mean ± SD) 74.3 ± 11.3 74.5 ± 11.0 76.1 ± 11.6 72.3 ± 11.6*
Diabetes (%) 19.4 18.2 25.5* 17.7
ESA (%) 90.4 90.2 89.8 91.8
Antihypertensive medications (%) 56.5 54.9 59.0 65.7*
Heart failure (%) 23.6 24.6 29.1* 22.1

Control, group 1: Δ SBP between −20 and + 10 mm Hg, group 2: Δ SBP > −20 mm Hg, group 3: Δ SBP > +10 mm Hg.
Abbreviations: SBP, systolic blood pressure; HD, hemodialysis; PP, pulse pressure; PTH, parathyroid hormone; ESA, erythropoiesis stimulat-
ing agent; PDHYPO, postdialysis hypotension; PDHYPER, postdialysis hypertension.
*P < 0.05 in the comparison with group 1.

Table 2.  Multivariable regression model results for Δ SBP (mm Hg) in dialysis patients

Δ SBP (mm Hg)

Variable Coefficient SE P Overall adjusted R2

Δ Weight (kg) −3.798 0.378 <0.0001 0.2067

Predialysis SBP (mm Hg) −0.336 0.019 <0.001
Predialysis PP (mm Hg) 0.098 0.025 <0.001
Predialysis HR (b/min) −0.096 0.044 0.002
Postdialysis HR (b/min) −0.121 0.040 0.002
Hb (g/dl) −0.813 0.243 0.001
BMI (kg/m2) −0.310 0.071 <0.001
Dialytic vintage (months) −0.010 0.004 0.011

Abbreviations: SBP, systolic blood pressure; PP, pulse pressure; HR, heart rate; Hb, hemoglobin; BMI, body mass index.

be older, have a shorter dialysis vintage, lower body mass
index, lower Δ weight during HD, lower Hb, lower para-
thyroid hormone, lower predialysis SBP, and heart rate.
Furthermore, the proportion of patients on antihyperten-
sive medications was higher, as well as the percentage of
patients with an ejection fraction <50%. Logistic regression
analysis, using PDHYPER as a dichotomous depend-
ent variable, produced 2 significant models (1 adjusted
and 1 unadjusted) (Table  3). For the unadjusted model,
the area under the receiver-operating characteristic curve
was  =  0.729, correctly classified as 85.34%. The Hosmer
and Lemeshow χ2 was 4.91 with probabilities > χ2 =0.767.

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 Postdialytic Hypertension and Cardiovascular Mortality

Table 3.  Unadjusted and adjusted odds ratios for postdialysis hypertension

Unadjusted Adjusted

Predictor OR 95% CI P OR 95% CI P

Age 1.02 1.01–1.03 <0.001 1.02 1.01–1.03 0.030

Male sex 1.36 1.04–1.78 0.024 1.33 0.99–1.78 0.058
Dialysis session time 1.01 1.00–1.02 <0.001 1.01 0.99–1.02 0.065
Δ Weight with dialysis 0.57 0.49–0.68 <0.001 0.59 0.49–0.70 <0.001
Predialysis SBP 0.96 0.95–0.97 <0.001 0.96 0.95–0.97 <0.001
Predialysis PP 1.02 1.01–1.03 0.003 1.02 1.01–1.03 0.002
Predialysis HR 0.98 0.96–0.99 0.030 0.98 0.96–0.99 0.002
ESA 0.58 0.37–0.91 0.019 0.55 0.35–0.87 0.010
Antihypertensive medications 2.35 1.76–3.14 <0.001 1.57 1.01–2.43 0.044
Body mass index 0.98 0.94–1.01 0.233
Diabetes 0.90 0.63–1.28 0.573
Single pool Kt/V 1.09 0.65–1.81 0.741
Hemoglobin 0.94 0.87–1.02 0.133
Albumin 0.99 0.99–1.01 0.934
Cholesterol 1.00 0.99–1.00 0.843
PTH 0.99 0.99–1.00 0.338
Convective HD 1.97 0.70–1.34 0.858

Abbreviations: CI, confidence interval; ESA, erythropoiesis stimulating agent; SBP, systolic blood pressure; PP, pulse pressure; HR, heart
rate; HD, hemodialysis; PTH, parathyroid hormone.

For the adjusted model, the area under receiver-operating
characteristic curve was = 0.732, correctly classified 85.53%.
The Hosmer and Lemeshow χ2 was 5.50, with probabilities
>χ2 = 0.702. The tests indicated a good discrimination for
both models. The use of antihypertensive medications, male
sex, increased predialysis pulse pressures, increased age, and
longer length of the HD session were significant predictors
of PDHYPER. Conversely, Δ weight during HD, erythro-
poiesis stimulating agent use, predialysis SBP, and predialy-
sis HR were predictors, inversely associated, of postdialysis
hypertension. Diabetes and heart failure were found not to
be predictors. The analysis, repeated after stratification by
tertiles of weight loss by dialysis, showed that the follow-
ing variables were significantly predictive: use of antihyper-
tensive medications, predialysis SBP, and predialysis pulse
pressures. Logistic regression was also carried out with 2
different thresholds for PDHYPER (5 and 15 mm Hg). With
the 5 mm Hg threshold, found in 28.7% of the patients, the
results were concordant with those obtained with the 10 mm
Hg threshold. Raising the threshold to 15 mm Hg, 10.5% of
the patients presented PDHYPER. In the analysis, only age,
Δ weight, and heart rate were significant predictors.
Interaction between factors
We found a significant interaction between predialysis
SBP and Δ weight during HD (RERI −2.830, confidence
interval (CI) −3.088 to 2.573), between Δ weight during HD
and the use of antihypertensive medications (RERI −1.881,
CI −2.631 to 1.131) and between predialysis SBP and use of
antihypertensive medications (RERI −1.793, CI −2.572 to
1.015). These values indicate interaction on an additive scale,
meaning that the combined effect is less than the sum of the
factors examined singly. 
Patients with heart failure
The logistic regression performed in patients with heart
failure showed the following predictors of PDHYPER: pre-
dialysis SBP (OR 1.25, CI 1.17–1.34; P < 0.001), female sex
(0.17, CI = 0.05–0.63; P = 0.008). 
Survival and changes in BP with dialysis
Patients were followed up for a mean of 26.8 ± 11.1 months;
348 patients who were lost to follow-up were either trans-
planted or transferred to different units. On the basis of the
results of the above logistic regression, we excluded from
the analysis subjects with heart failure. We had data for CV
mortality in the remaining 3,196 patients, among whom
420 deaths were recorded. Of those, 318 were ascribed to
a heart disease and 102 to a cerebrovascular event. The
Cox analysis produced a significant model with the fol-
lowing predictors of CV mortality: age (HR 1.05, CI 1.03–
1.07; P  <  0.001), dialysis vintage (HR 1.01, CI 1.00–1.02;
P = 0.038), PDHYPER (HR 1.69, CI 1.12–2.57; P = 0.012)
(Figure 1). Predialysis SBP (> or <140 mm Hg) was not a
predictor of mortality. Apart from hypertension, no other
association was found between the etiology of kidney dis-
ease and PHYPER or mortality.

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 Losito et al.
Figure 1.  Cox analysis in patients without heart failure. CV mortality plot. Controls are patients with a postdialysis SBP Δ comprised between −20 and
+ 10 mm Hg, PDHYPER: Δ SBP > +10 mm Hg, PDHYPO: Δ SBP > −20 mm Hg. Only PDHYPER shows a significant difference from controls. Abbreviations:
PDHYPO, postdialysis hypotension; PDHYPER, postdialysis hypertension.
DISCUSSION
PDHYPER is generally perceived as an uncommon com-
plication of dialytic treatment.13,14 In different surveys, adopt-
ing the same criteria as the present study, the occurrence of
an increase in BP from pre- to postdialysis was found in less
than 15% of maintenance HD patients.4 In our large sample
of Italian dialysis patients, we showed that PDHYPER is a
relatively common phenomenon, occurring in nearly 1 of 4
patients. We also found that the main factors influencing SBP
changes during HD were a hypertensive state, predialysis SBP
and pulse pressures, pre- and postdialysis HR, Δ weight during
HD, Hb, dialytic vintage, and body mass index.
We have also found that, in patients without heart failure,
PDHYPER is a significant predictor of CV mortality. The
mechanism leading to PDHYPER is not so straightforward.
The interaction between the use of antihypertensive medi-
cations and Δ weight during HD may suggest an increased
need for medications in patients with inadequate intradia-
lytic weight loss compared to their dry weight. Medications
explain lower predialysis SBP and their removal with dialy-
sis is a reasonable cause of PDHYPER. Furthermore, these
patients are more likely to have a shorter dialysis vintage
and thus residual diuresis and/or adherence to a low sodium
diet. This setting may lead to a reduced sodium pool, as testi-
fied by lower predialysis SBP. A lower Δ weight during HD
may lead to reduced convective loss of sodium when using
a standard dialysate with a sodium concentration of 139
mEq/l. This may allow a diffusive flux of sodium toward the
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body compartment, especially in patients with a low pre-
dialysis plasma sodium concentration (as is often the case
in patients with low sodium intake). The consequence of a
positive sodium balance at the end of the dialytic session is
an increase in extracellular fluid volume that may be over-
looked.15 The end of the process is a positive sodium balance
with consequent hypertension requiring ever more antihy-
pertensive medications. A longer duration of the dialysis ses-
sion, which is associated with postdialysis hypertension, may
increase drug removal and give more time for the diffusive
transport of sodium from the dialysate to the plasma and,
thus, a more positive sodium balance. Unfortunately, we did
not collect information regarding sodium concentrations in
plasma and in dialysate to better support this hypothesis.
Nevertheless, this interpretation is in line with data from
small cohorts of dialysis patients16 and experimental studies
aimed at investigate specific mechanisms of PDHYPER.17 In
a post hoc analysis of the Dry-weight reduction in hyperten-
sive hemodialysis patients (DRIP) trial, the authors meas-
ured the slopes of intradialytic BP during dialysis and tested
the effect of dry-weight reduction on these slopes and found
that intradialytic BP changes were associated with changes in
dry body weight.18 These results suggested that PDHYPER is
a marker of volume excess. Recently, Nongnuch et al. sub-
mitted 531 dialysis patients to multiple-frequency bioelectri-
cal impedance and found that the ratio of extracellular water
to total body water was significantly higher in the patients
with PDHYPER.19

The prevalence of heart failure in dialysis patients is high
and the prognosis is ominous, especially in the presence of
hypertension.20In patients with heart failure in our study, the
factors associated with PDHYPER were not the same as the
ones we found in the others. Interestingly, Δ weight was not a
predictor, indicating a more complex mechanism operating
in this subset of patients. Predialysis SBP was a more sig-
nificant predictor. These findings show that factors associ-
ated with changes in BP during dialysis vary according to the
individual characteristics of patients.
Our study has a number of limitations. We did not per-
form a direct examination of extracellular volume.21 Thus,
we can give only indirect evidence about the causative effect
of volume expansion on PDHYPER and we cannot rule out
other contributing factors, such as dialysate sodium concen-
tration, renin–angiotensin–aldosterone system, and sympa-
thetic activation. We did not collect information on the class
and number of antihypertensive medications. Thus, we can
just speculate around medication removal by dialysis. On
the other hand, the large number of enrolled patients and
collected variables, together with the homogeneity of the
population, strengthen the validity of the results obtained.
In conclusion, our multicenter study shows that the preva-
lence of PDHYPER is higher than that previously reported
and that it is associated with high CV mortality.
ACKNOWLEDGMENTS
The study was brought about on behalf of the of hyperten-
sion study group of The Italian Society of Nephrology.
DISCLOSURE
The authors declared no conflict of interest.
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