Hypertension in Dialysis Patients

Hypertension in dialysis patients
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Official reprint from UpToDate

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2010 UpToDate

Authors
William L Henrich, MD, MACP
Lionel U Mailloux, MD, FACP
Section Editors
Steve J Schwab, MD
George L Bakris, MD
Deputy Editor
Theodore W Post, MD
Last literature review version 18.2: May 2010 | This topic last updated: June 14, 2010
INTRODUCTION There are several major issues to consider when approaching hypertension
in dialysis patients [1]:
What is the pathogenesis of the elevation in blood pressure (BP)?
How is hypertension best defined?
What are the target blood pressure goals?
How should the hypertension be treated?
The possibility of bilateral renal artery stenosis should also be considered in patients with
end-stage renal disease of uncertain cause. (See "Chronic kidney disease associated with
atherosclerotic renovascular disease".)
This topic review will present the epidemiology, pathogenesis, and treatment of hypertension in
dialysis patients, with an emphasis on hypertension in patients undergoing hemodialysis. Most
patients undergoing peritoneal dialysis can become normotensive with strict adherence to volume
control, unless there are difficulties attaining effective ultrafiltration. This problem is reviewed
separately. (See "Problems with solute clearance and ultrafiltration in continuous peritoneal
dialysis".)
EPIDEMIOLOGY Hypertension is a common finding in dialysis patients. Based upon multiple
studies, over 50 to 60 percent of hemodialysis patients (up to 85 percent in some reports) and
nearly 30 percent peritoneal dialysis patients are hypertensive [2-5]. These values are lower than
the 80 percent incidence of hypertension at the initiation of dialysis, due largely to better volume
control in most patients [6].
Clinicians should strive for an even better blood pressure control rate [1]. Since poorly controlled
hypertensive hemodialysis patients are more likely to have large interdialytic and excessive
weight gains, persistent hypertension often reflects volume control that remains imperfect despite
the initiation of dialysis [4,7].
Poor blood pressure control has also been reported in children undergoing dialysis. In one study,
approximately one-half of children had uncontrolled hypertension after one year of dialysis
therapy [8].
Cardiovascular risk The relationship between hypertension and cardiovascular mortality in
patients with end-stage renal disease is complicated because of the high prevalence of comorbid
conditions and underlying vascular pathology. Although a positive correlation has been found in
some studies [9-11], a few reports in which patient outcomes were assessed for only one to two
years have found little or no relationship between hypertension and mortality [12].
Enhanced mortality has also been reported among prevalent dialysis patients with the lowest
blood pressures who were followed for short periods [12-16]. This was shown in the following
reports:
In a cohort study of 40,933 hemodialysis patients followed for a 15 month period, the hazard
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ratio for all cause death for a predialysis systolic blood pressure <110 mmHg was 1.60, while the
ratio for a predialysis diastolic blood pressures <50 mmHg was 2.00 [14].
A second cohort study of 16,939 patients found that a low systolic blood pressure (<120
mmHg) was associated with an increased mortality with follow-up of one to two years [15]; by
comparison, an increased mortality after three years was observed in those with systolic blood
pressures greater than 150 mmHg.
The short follow-up period of most of the studies showing a negative correlation may be
inadequate since an elevated blood pressure must be present for a sufficient time period to
contribute to cardiovascular disease and/or mortality and patients with lower pressures may
represent a sicker population [17]. Improved survival and better cardiovascular outcomes due to
adequate blood pressure control have been demonstrated in those studies with the longest
duration of follow-up and with the best design (including adequate control for baseline cardiac
parameters) [16,18-20].
In addition to the period of follow-up, a number of additional factors can affect the general
correlation between elevated blood pressure and lower survival among dialysis patients [21,22].
These include the following:
Enhanced mortality among those with lower blood pressures may be a result of myocardial
dysfunction, extensive comorbid conditions, and/or poor nutrition. This was shown in a
retrospective study of 2770 peritoneal dialysis patients, which found that greater blood pressure
levels were protective against mortality at one year among all patients [16]. By comparison,
there was increased mortality at one year among the nearly 600 patients with increased blood
pressure who were placed on the transplant wait list within six months of initiating dialysis. This
suggests that the general correlation between elevated blood pressure and lower survival can also
be observed among healthier dialysis patients, even with a short period of follow-up.
The relationship between hypertension and vascular disease may be dissociated since,
because of swings in volume status and the effects of hemodialysis, a wide range of blood
pressures are observed in individuals as well as the dialysis population.
Elevated blood pressure alone fails to account for the possible deleterious effect of an
increased pulse pressure, which is defined as the systolic minus diastolic pressure [23,24]. A
retrospective study of over 44,000 dialysis patients found that an increased pulse pressure
directly increased the risk of mortality at one year follow-up, even after adjustment for the
systolic blood pressure alone [23]. (See "Increased pulse pressure".)
A higher mortality may be due to the presence of left ventricular hypertrophy (on ECG or
echocardiography), which is associated with increases in the incidence of heart failure, ventricular
arrhythmias, death following myocardial infarction, sudden cardiac death, aortic root dilation, and
a cerebrovascular event. Some evidence suggests that partial regression of hypertrophy due to
adequate hypertensive therapy lowers the risk of mortality among dialysis patients [11]. (See
"Clinical implications and treatment of left ventricular hypertrophy in hypertension".)
There are conflicting data concerning a possible loss of the usual diurnal variation in BP in
end-stage renal disease [25,26]. To the degree that some patients may have a diminution of the
expected decline in BP during the night (or even nocturnal hypertension) [25], it may be
erroneous to conclude that a "borderline" daytime blood pressure is actually lower the rest of the
day. This loss of dipping, termed nocturnal hypertension, is associated with an increased risk of
adverse cardiovascular outcomes [27].
PATHOGENESIS The etiology of hypertension in end-stage renal disease is multifactorial, as
one or more of the following factors play a role in individual patients [6,28,29]:
Sodium and volume excess due to diminished sodium excretory capacity. Accumulating
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evidence, for example, suggests that patients on chronic ambulatory peritoneal dialysis may
become hypertensive after many years, possibly because of the loss in part of ultrafiltrating
capacity by the peritoneal membrane [30-35]. A decrease in dialysate sodium may also be
associated with a decrease in blood pressure [36].
Activation of the renin-angiotensin-aldosterone system due to primary vascular disease or to
regional ischemia induced by scarring.
Increased activity of the sympathetic nervous system.
An increase in endothelium-derived vasoconstrictors (such as endothelin) or a reduction in
endothelium-derived vasodilators (such as nitric oxide).
The administration of erythropoietin.
An increase in intracellular calcium induced by parathyroid hormone excess [37]. The
observation that correction of hyperparathyroidism via either vitamin D administration or
parathyroidectomy lowers the blood pressure is compatible with this hypothesis [37,38]. In one
report, the mean systolic pressure fell over a period of months by a mean of 9 mmHg after
parathyroidectomy [38].
Calcification of the arterial tree.
Preexistent essential hypertension.
Volume overload Volume expansion is perhaps the major factor in the development of
hypertension in dialyzed patients [39]. It leads to an elevation in BP via the combination of a rise
in cardiac output and an inappropriately high systemic vascular resistance [6,28]. The latter
finding may result from activation of the renin-angiotensin system or from the secretion of
ouabain-like inhibitors of Na-K-ATPase, leading to elevations in intracellular sodium and calcium.
The rise in cell calcium in vascular smooth muscle cells can then induce vasoconstriction. (See
"Natriuretic hormones: Atrial peptides and ouabain-like hormone", for a discussion of this
phenomenon).
Regardless of the mechanism, removal of the excess sodium and attainment of "dry weight" (see
below) can result in the normalization of BP in more than 60 percent of hemodialysis-dependent
patients and nearly all patients undergoing peritoneal dialysis [6,40-45]. The degree of
extracellular volume expansion may be insufficient to induce edema; thus, the absence of edema
does not exclude hypervolemia.
Increased sympathetic activity Sympathetic overactivity is a common finding in end-stage
renal disease, correlating with the increase in both vascular resistance and systemic BP [46]. The
mechanism by which this occurs is unclear, but the afferent signal may arise within the kidney,
since sympathetic activation is not seen in anephric patients [46]. It has therefore been proposed
that activation of chemoreceptors within the kidney by uremic metabolites may play an important
role. Activation of these chemoreceptors leads to a neural reflex that traverses afferent pathways
to the central nervous system, resulting in increased efferent sympathetic tone.
Altered endothelial cell function An intriguing concept regarding the pathogenesis of
hypertension in end-stage renal disease is abnormal endothelial release of hemodynamically
active compounds. As an example, elevated plasma levels of the potent vasoconstrictor
endothelin-1 have been found in uremic subjects [47,48]. The concentration of other endothelin
isoforms also may be increased, but only endothelin-1 has been linked to high BP [49].
It should be appreciated, however, that these observations do not prove a cause and effect
relationship. The development of a method to inhibit the activity of endothelin (such as a receptor
blocker) will be necessary to determine the physiologic importance of endothelin in these
patients.
The endothelium also produces vasodilators, such as prostacyclin and nitric oxide (NO or
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endothelium-derived relaxing factor). NO is a synthetic product of L-arginine in endothelial cells

and is a potent vasodilator. There is evidence that uremic plasma contains a higher level of an
endogenous compound asymmetrical dimethylarginine that is an inhibitor of NO synthesis
[50]. This observations raises the possibility that NO deficiency may contribute to the
development of hypertension in end-stage renal disease.
Erythropoietin An increase in BP of 10 mmHg or more may occur in patients with renal failure
who are treated with erythropoietin. The risk is greatest in those with rapid correction of severe
anemia and with preexistent hypertension. (See "Hypertension following erythropoietin in chronic
kidney disease".)
METHOD OF BLOOD PRESSURE MEASUREMENT A reliance upon immediate predialysis
and/or postdialysis BP measurements alone to detect hypertension in patients undergoing
hemodialysis may be misleading. The predialysis systolic BP may overestimate the mean
interdialytic SBP by 10 mmHg, while the postdialysis systolic BP may underestimate the mean
systolic BP by 7 mmHg [51]. Some studies, however, have suggested that the postdialysis BP
may be more reflective of interdialytic BP [52,53].
Continuous monitoring is therefore warranted in patients suspected of poor control (such as those
with large interdialytic weight gain) [25,54-57]. The results with ambulatory blood pressure
monitoring appear to be relatively reproducible [56,58].
Ambulatory BP monitoring may also be useful in determining the "systolic load," which is the
amount of time the systolic pressure exceeds 140 mmHg during the day [25,59-61]. This load
may be an important factor in the development of left ventricular hypertrophy. The ambulatory
BP is also associated with significant prognostic value [59]. Interdialytic hypertension does not
appear to be a problem with the Tassin and nocturnal hemodialysis regimens of long, slow dialysis
[62].
Home blood pressure monitoring may also improve hypertension detection and prognostic value
[60,63]:
In one study, the finding of an average systolic BP greater than 150 mmHg at home was more
accurate than conventional blood pressure monitoring in helping diagnose hypertension (as
determined by ambulatory BP) [63].
The best prognosis was observed with a home measurement of a systolic blood pressure of
125 to 145 mmHg [60].
Uremic patients have an additional problem in that they lose the usual diurnal variation in blood
pressure, possibly leading to nocturnal hypertension [25]. Thus, even patients thought to be well
controlled with daytime BP measurements may still be at risk for hypertension-induced
cardiovascular morbidity [64]. This problem should be suspected if, for example, left ventricular
mass increases (on echocardiography) despite seemingly adequate control of hypertension and
anemia. (See "Myocardial dysfunction in end-stage renal disease".)
OPTIMAL BLOOD PRESSURE Current blood pressure target ranges for dialysis patients have
been extrapolated from those suggested for the non-dialysis patient population. There have been
no randomized prospective studies evaluating the target blood pressure in dialysis patients. In
general, the targeting of exact blood pressure goals (whether to a specific level or below a certain
value) should ideally be set individually based upon the patient's cardiac and neurologic status,
comorbid conditions, age, and other clinical factors [1].
For some dialysis patients, we suggest that goal BP levels be a predialysis value of below 140/90
mmHg and a postdialysis value of below 130/80 mmHg [19,41,65-68]. If clinical characteristics
permit and ambulatory pressures are measured, a "normal" BP, defined as a mean ambulatory BP
less than 135/85 mmHg during the day and less than120/80 mmHg by night, is a reasonable
target goal.
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However, controversy exists over the blood pressure target; some investigators have postulated
that excessively low systemic pressures lead to enhanced mortality (a so-called J- or U-shaped
curve) [13,69-72]:
A report of nearly 4500 hemodialysis patients found a significantly increased adjusted
mortality risk among patients with a low predialysis systolic pressure (<110 mmHg); risk was
also increased in patients with high postdialysis diastolic (>110 mmHg) and systolic pressures
(>180 mmHg) [13].
In an observational study of 56,338 and 69,590 incident and prevalent hemodialysis patients,
respectively, a markedly increased risk of death was noted among those with systolic blood
pressures less than 120 mmHg versus those with systolic blood pressures between 160 and 180
mmHg (hazard ratio of 2.63 to 3.68 based upon different statistical adjustments) [71].
A retrospective analysis of 13,792 incident hemodialysis patients evaluated the correlation
between survival and achieving K/DOQI clinical practice guidelines for multiple parameters [72].
An increased mortality was associated with achieving the goal predialysis blood pressure of less
than 140/90 mmHg (1.90, 95% CI 1.73-2.10).
Whether these results are due to a direct effect of a relatively low blood pressure or to an
associated comorbid condition is unclear.
In summary, the target goals should generally be realized based upon individual patient
characteristics [1]. In some younger patients, the target BP may even be set as low as 120/80
mmHg.
TREATMENT
Control of volume status Control of volume status can either normalize the BP or make the
hypertension easier to control in the great majority of dialysis patients. Nearly all peritoneal
dialysis patients, for example, can become normotensive with strict adherence to volume control
[43,73].
Avoidance of large weight gains in the interdialytic period is clearly desirable. To achieve this
goal, patients should adhere to a restricted salt diet (750 to 1000 mg of sodium/day), which also
helps decrease thirst [19,74,75]. However, patient compliance is often suboptimal. (See "Patient
information: Low sodium diet".)
As a result, heavy reliance is placed on the dialysis procedure to gradually remove fluid over a
period of days to weeks until a stable "dry weight" is achieved [6,19,40,41,66,68,76-78]. The
exact definition of dry weight remains uncertain, but multiple definitions have been advanced. As
examples, dry weight has been defined clinically as that weight at which:
Either the BP has normalized or symptoms of hypovolemia appear, not merely the absence of
edema.
The seated BP is optimized, and symptomatic orthostatic hypotension and clinical fluid
overload are not present postdialysis [79].
At the end of dialysis, the patient remains normotensive until the next dialysis without
antihypertensive medication [80].
Numerous attempts have been made to utilize alternative methods to more accurately assess dry
weight. These include bioimpedance plethysmography, and measurement of the inferior cava
diameter, plasma natriuretic peptide (particularly atrial and brain) concentrations, blood volume,
and other parameters. However, these methods are frequently impractical, are not necessarily
accurate, and a large prospective study has not yet been performed that compares these methods
to clinical assessment alone [81-84]. The clinician must therefore define the dry weight and goal
blood pressure for each dialysis patient based upon his or her best judgment.
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Unfortunately, one problem with a reliance upon a clinical assessment of volume status is that
volume expansion may persist even among those thought to have attained dry weight. This
possibility was illustrated in a report in which the blood volume, inferior vena cava diameter, and
posthemodialysis dry weight were evaluated in 35 stable hemodialysis patients (17 with and 18
without hypertension, respectively) [85]. Despite the attainment of dry weight as determined by
traditional clinical standards, the blood volume of hypertensive patients was significantly higher
than in normotensive patients both before (3.53 versus 2.82 L/m2) and after (2.88 and 2.49
L/m2) dialysis. In this study, the timing of the postdialysis inferior vena cava measurement was
critical, since many hours are required to reconstitute the plasma volume and intravascular
compartment. By comparison, other studies are flawed by too early a determination [86].
The view that volume expansion underlies the inability to control blood pressure in many
hemodialysis patients is also supported by studies that rely upon plasma atrial natriuretic peptide
(ANP) concentrations to help assess the extracellular volume [87,88]. One study, for example,
measured predialysis and postdialysis ANP values [87]. Predialysis levels were markedly elevated
in the hypertensive patients compared to those who were normotensive; in addition, the
postdialysis ANP concentrations normalized in those with dialysis-sensitive hypertension but were
unchanged in those with dialysis-resistant hypertension. In general, although predialysis ANP
values may correlate with volume overload, postdialysis levels are unreliable in determining dry
weight [81].
Two other factors may limit the degree of fluid removal by predisposing to episodes of
hypotension (and therefore the need for volume replacement) during the hemodialysis procedure:
antihypertensive drugs; and rapid fluid removal required by shorter dialysis times. Thus, tapering
drug therapy and gradual fluid removal may be beneficial in patients in whom hypotension during
dialysis prevents the attainment of dry weight and a normal BP.
Chronic volume overload also may be due to the chronic dialysate sodium prescription. Dialysate
sodium prescriptions are relatively higher than that observed in most dialysis patients, leading to
decreased sodium loss during dialysis and mild increases in serum sodium values post-dialysis
[89]. This results in volume overload and increased thirst, thereby increased blood pressure. To
help avoid these, some advocate an individualized approach to the dialysate sodium prescription.
Among patients initiated on dialysis, a period of time must ensue between the attainment of dry
weight and adequate control of blood pressure, a property termed the lag phenomenon [90]. This
reflects the time required to convert the patient from a catabolic to an anabolic state, a period in
which the extracellular fluid space slowly stabilizes [90]. A similar phenomenon has been
observed with the use of diuretics for the treatment of hypertension in the patient without renal
failure [91].
Prolonged and/or more frequent hemodialysis Patients in a large dialysis center in Tassin,
France and some home hemodialysis patients undergo long, slow hemodialysis in which the
standard regimen is eight hours, three times per week. This regimen is associated with the
maintenance of normotension without medications in almost all patients [41,62,92,93]. Although
these results have been largely attributed to optimal volume control, other factors may also
contribute, such as more complete control of uremia [62] which, as noted above, may decrease
afferent renal nerve activity and efferent sympathetic activation [46]. A subset of these patients,
for example, are normotensive despite the presence of increased extracellular fluid volume while
having achieved clinical dry weight [94]. The reason for this observation is unclear. This regimen,
which is not widely used, is also associated with a high patient survival rate [41]. (See "Patient
survival and maintenance dialysis", section on 'Adequacy of dialysis'.)
Nocturnal hemodialysis, a procedure in which dialysis is performed six or seven nights a week
during sleep for a variable amount of time based upon the length of sleep desired (usually 6 to 12
hours in total), is also associated with excellent blood pressure control [95]. Almost all patients
become normotensive without medications. To achieve this, the "target weight" is progressively
decreased until all antihypertensive agents are discontinued. (See "Technical aspects of nocturnal
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hemodialysis".)
Some studies also suggest that more frequent hemodialysis treatments, via short daily
hemodialysis, may also be associated with normotension without medications and with regression
of left ventricular hypertrophy. (See "Short daily hemodialysis", for a detailed review of this
issue).
The 2007 European Best Practice Guidelines recommend that the treatment time and/or
frequency of dialysis should be increased in patients with hypertension despite optimal volume
removal [96].
Antihypertensive medications Therapy with antihypertensive drugs is primarily indicated in
the 25 to 30 percent of dialysis patients in whom hypertension persists despite seemingly
adequate volume control. Some evidence suggests that the administration of such agents may
provide significant clinical benefits, including improved mortality.
A 2009 systematic review and meta-analysis of eight randomised controlled trials (three with and
five without hypertensive patients) that enrolled 1679 dialysis patients found that lowering blood
pressure with antihypertensive therapy was associated with decreased risks of cardiovascular
events (RR of 0.71, 95% CI 0.55-0.92), all cause mortality (RR 0.80, 0.66-0.96) and
cardiovascular mortality (0.71, 0.50-0.99) [97]. Although there was significant variation in
attained blood pressure, the overall mean decrease in systolic and diastolic blood pressure with
active therapy was 4 to 5 mmHg and 2 to 3 mmHg, respectively. There were no studies that
compared the efficacy of different antihypertensive agents; the relative effects of ARBs, ACE
inhibitors, beta blockers, and calcium blockers were largely compared with placebo or
conventional therapy. Additional limitations included the low number of patients (including those
with hypertension), lack of information concerning volume control, and marked variations in blood
pressure reduction (due in part to absence of firm criteria for measurement) [98].
Despite these limitations, it generally appears that renin-angiotensin-system blockers, beta
blockers, and calcium-channel blockers provide similar efficacy in dialysis patients. Thus, the type
of antihypertensive therapy chosen is dictated in part by coexistent diseases [66].
In addition, several points about specific classes of antihypertensive drugs deserve emphasis, as
discussed in the following sections [66,99]:
Calcium channel blockers Calcium channel blockers are both effective and well tolerated
in dialysis patients, even in those who are volume expanded [64]. The only randomized
prospective study found that amlodipine, compared with placebo, improved overall mortality
among hypertensive dialysis patients [100].
Calcium channel blockers are particularly useful in patients with left ventricular hypertrophy and
diastolic dysfunction. Calcium channel blockers do not require supplementary postdialysis dosing.
ACE inhibitors ACE inhibitors are well tolerated and are particularly effective in patients
with heart failure due to systolic dysfunction and in many patients after an acute myocardial
infarction. The 2006 K/DOQI guidelines also suggest that these agents and/or angiotensin II
receptor blockers are preferred in dialysis patients with significant residual renal function [101].
These agents may help preserve native kidney function. (See "Overview of the therapy of heart
failure due to systolic dysfunction" and "Angiotensin converting enzyme inhibitors and receptor
blockers in acute myocardial infarction: Recommendations for use".)
ACE inhibitors (and angiotensin II receptor blockers [ARBs], see next section) are associated with
a decrease in left ventricular mass among hemodialysis patients [102,103]. There are conflicting
data concerning the effect of ACE inhibitors on mortality among hypertensive patients undergoing
maintenance dialysis.
A randomized prospective study found no survival benefit with fosinopril among hemodialysis
patients with left ventricular hypertrophy [104].
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A possible mortality benefit was shown in an observational study in which hypertensive

dialysis patients were administered antihypertensive regimens with or without ACE inhibitors (60
and 66 patients, respectively) at the discretion of the physician [105].
ACE inhibitors have unique side effects in end-stage renal disease: they can interfere with the
action of erythropoietin; and they can trigger an anaphylactoid reaction (possibly mediated by
kinins) in patients dialyzed with an AN69 dialyzer. (See "Major side effects of angiotensin
converting enzyme inhibitors and angiotensin II receptor blockers", section on 'Angioedema and
anaphylactoid reactions' and "Reactions to the hemodialysis membrane".)
The effect of ACE inhibitors on erythropoiesis has been best described in renal transplant
recipients with erythrocytosis. In this setting, an ACE inhibitor can lower the hematocrit toward
normal in almost all patients. This can occur by reducing the secretion or interfering with the
action of EPO, including those receiving EPO supplementation [106,107]. (See "Erythrocytosis
following renal transplantation".)
There are less consistent data concerning the effect of ACE inhibitors on erythropoietin doses in
dialysis patients. Increased dose requirements and no effects have been reported [108]. There is
also an increased risk of hyperkalemia among chronic hemodialysis patients treated with an ACE
inhibitor [108]. (See "Major side effects of angiotensin converting enzyme inhibitors and
angiotensin II receptor blockers".)
ARBs A number of angiotensin II receptor blockers (ARBs) are currently available. Among
hemodialysis patients, ARBs (and ACE inhibitors) are associated with a decrease in left ventricular
mass [103]. (See "Renin-angiotensin system inhibition in the treatment of hypertension".)
There is limited experience with ARBs in patients with hypertension and end-stage renal disease
[108,109]. In one open-label trial, 360 hypertensive dialysis patients were randomly assigned to
an ARB or no ARB [109]. After multivariate adjustment, ARBs significantly reduced fatal and
nonfatal cardiovascular disease events (hazard ratio 0.5, 95% CI 0.33-0.79). The most common
adverse event was heart failure (fatal and nonfatal), with ARBs lowering the rate by one-half.
The 2006 K/DOQI guidelines suggest that these agents and/or ACE inhibitors are preferred in
dialysis patients with hypertension and significant residual renal function [101]. These agents
may help preserve native kidney function.
ARBS and ACE inhibitors have similar issues in terms of adverse effects, including hyperkalemia
and possible dampened erythropoiesis [108]. In addition, although ARBs do not affect bradykinin
levels, anaphylactoid reactions have been reported among patients receiving ARBS during
hemodialysis with AN69 membranes [110,111]. (See "Reactions to the hemodialysis membrane".)
Beta blockers Beta blockers are particularly indicated in patients who have had a recent
myocardial infarction. As in nonuremic subjects, patients with end-stage renal disease who have
heart failure due to systolic dysfunction may also benefit from therapy with a beta blocker. Such
therapy should be initiated at very low doses to minimize the risk of hemodynamic deterioration.
(See "Myocardial dysfunction in end-stage renal disease" and "Use of beta blockers in heart
failure due to systolic dysfunction".)
Potential side effects include central nervous system depression (an effect that may be more
prominent with lipid-soluble drugs that cross the blood-brain barrier), hyperkalemia (particularly
with non-selective beta blockers), bradycardia, and possible exacerbation of heart failure [108].
In addition, beta blockers should be used cautiously in patients also taking a calcium channel
blocker, since there are often additive negative chronotropic and inotropic actions.
Central sympathetic agonists The central sympathetic agonists, such as methyldopa and
clonidine, are used less frequently because of their adverse effects involving the central nervous
system. Some physicians have found clonidine patches to be effective and well tolerated, but this
is not a universal finding [108,112].
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Reduced dialysate sodium concentration A variable dialysate sodium concentration may

result in lower antihypertensive medication requirements and decreased postdialysis blood
pressure. A randomized crossover study, for example, evaluated the antihypertensive effects of a
programmed decrease in sodium dialysate concentration from 155 to 135 meq/L (the last half
hour was held constant at 135 meq/L) compared with the standard stable sodium dialysate
concentration of 140 meq/L [113]. Postdialysis blood pressure (133/69 to 126/66, p<0.05),
postdialysis standing blood pressure, and drug usage were all reduced when patients were
dialyzed with a variable sodium prescription. Although these benefits will require confirmation in
further studies, a variable sodium protocol may be tried in selected hypertensive patients who do
not respond well to other modalities.
A fixed lower dialysate sodium concentration in combination with dietary salt restriction may also
help control hypertension [114]. In a preliminary uncontrolled study, for example, eight
hypertensive hemodialysis patients were dialyzed against a gradually lowered sodium dialysate
concentration (140 to 135 meq/L at a rate of 1 meq/L every three to four weeks) and were
encouraged to limit salt intake to less than 6 g/day [114]. At study end, the mean arterial
pressure was significantly lower (98 versus 108 mmHg, p=0.02), and antihypertensive
medications were no longer required in four patients. However, adherence to this diet was difficult
and the frequency of muscle cramps during dialysis was increased. This regimen also engenders
the risk of episodic hypotension, and should be instituted very cautiously.
Refractory hypertension Some dialysis patients are resistant to both volume control and
antihypertensive medications. Factors to be considered in this setting are concurrent use of a
medication that can raise the BP (such as nonsteroidal antiinflammatory drugs), renovascular
hypertension, noncompliance to medical regimen, and expanding cyst size in polycystic kidney
disease. If a treatable cause cannot be found, minoxidil may be effective in reducing the BP. (See
"NSAIDs and acetaminophen: Effects on blood pressure and hypertension" and "Chronic kidney
disease associated with atherosclerotic renovascular disease" and "Hypertension in autosomal
dominant polycystic kidney disease".)
Chronically noncompliant hypertensive patients who refuse to take medications at home may
benefit by the administration of long-acting antihypertensive medications in the dialysis unit. This
was shown in a single center study of 16 patients in whom such a regimen (consisting of some
combination of lisinopril, amlodipine, and/or transdermal clonidine based upon patient clinical
characteristics) lowered the predialysis systolic and diastolic blood pressures by 15 and 12
mmHg, respectively [112].
Patients undergoing hemodialysis who are noncompliant and in whom volume status and
hypertension cannot be controlled may also benefit by switching to peritoneal dialysis. Nearly all
peritoneal dialysis patients can become normotensive with strict adherence to volume control
[43]. The efficacy of peritoneal dialysis in controlling blood pressure in refractory patients is
related to its smoother volume removal and its more consistent maintenance of dry weight
[43,45,115-117].
Peritoneal dialysis is associated with lower systolic blood pressures than hemodialysis in most, but
not all, studies [25,51], except for the use of long hemodialysis sessions [41,62]. As previously
mentioned, long and slow hemodialysis and/or nocturnal hemodialysis have been associated with
the attainment of normotension on no antihypertensive medications in almost all patients [62].
These regimens lead to better fluid control and better removal of uremic metabolites, which might
decrease renal afferent nerve activity [46]. (See "Technical aspects of nocturnal hemodialysis".)
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Bilateral nephrectomy may be considered in the rare noncompliant individual with life-threatening
hypertension unable to be controlled with any dialysis modality. In one study, a significant
decrease in blood pressure was observed three to six months after nephrectomy with six patients
having a diastolic pressure of less than 90 mmHg [118]. One patient had persistent increases in
blood pressure due largely to excess fluid intake between dialysis treatments, thereby further
supporting the hypothesis that hypervolemia is highly significant in the pathogenesis of
hypertension among dialysis patients. Bilateral nephrectomy is now largely abandoned, but was
infrequently used for blood pressure control when potent antihypertensive agents were not yet
widely available.
HYPERTENSION DURING HEMODIALYSIS Although hypotension during hemodialysis is a
frequent complication, some patients develop paradoxical hypertension in the later stages of
dialysis, a time at which most of the excess fluid has already been removed. This problem is
intermittent in a given patient with a widely variable frequency. The pathogenesis is unclear,
although some evidence suggests that altered nitric oxide/endothelin-1 balance may contribute
[119].
The optimal therapy of this problem is not known. In our experience, various medical modalities
(such as the administration of an angiotensin converting enzyme inhibitor or an alpha-blocker at
the time of hypertension, or pretreatment with antihypertensive medications to lower the blood
pressure before dialysis) have not been predictably effective. We have had some success with the
administration of isotonic saline to presumably treat hypovolemia-induced but excessive reflex
sympathetic activation. Limited observational evidence suggests that this increase in blood
pressure is associated with adverse outcomes [120]. (See "Hemodynamic instability during
hemodialysis: Overview".)
SUMMARY AND RECOMMENDATIONS Despite a paucity of data concerning many aspects of
the evaluation and treatment of hypertension in hemodialysis patients, certain general
recommendations are appropriate [1]. All dialysis patients benefit by a comprehensive evaluation
of their cardiovascular status, such as the assessment for traditional risk factors associated with
adverse outcomes. Appropriate modalities may include ambulatory blood pressure monitoring and
cardiac echocardiography.
The target goals should generally be realized based upon individual patient characteristics, with
the lowest target BP values being consistent with patient well-being and the absence of
intradialytic hypotension [19]. For some patients on dialysis, the goal BP is a predialysis value of
less than 140/90 mmHg and a post-dialysis value of less than 130/80 mmHg [66]. If clinical
characteristics permit and ambulatory pressures are measured, a "normal" BP, defined as a mean
ambulatory BP less than 135/85 mmHg during the day and less than 120/80 mmHg at night, is
also a reasonable target goal.
To attain this level of control, the following measures may be utilized [1]:
Other than those drugs required for any underlying cardiac disease, antihypertensive
medications should be slowly withdrawn while uncovering the patient's true dry weight. This
process should be undertaken over 3 to 6 weeks among younger patients, and up to 12 to 14
weeks for older individuals and those with vascular pathology.
If the blood pressure remains elevated despite the attainment of dry weight, antihypertensive
medications should be administered. The choice of drug is based upon the benefits and adverse
effects previously delineated, but an antihypertensive agent is preferably administered during the
evening with a once per day dosing schedule. The K/DOQI guidelines suggest that ACE inhibitors
or angiotensin II receptor blockers are preferred because they may provide greater benefits, such
as relatively more LVH regression [66].
Patients should be adequately dialyzed. (See "Kt/V and the adequacy of hemodialysis" and
"Adequacy of peritoneal dialysis".)
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Large interdialytic weight gains must be discouraged. As delineated in the K/DOQI guidelines,
management of increased fluid accumulation should be accomplished by consultation with
dieticians, low sodium intake, increased ultrafiltration, and/or increased dialysis treatments [66].
Low initial doses of subcutaneous erythropoietin should be administered, and the target
hematocrit should be slowly obtained. (See "Erythropoietin for the anemia of chronic kidney
disease among predialysis and peritoneal dialysis patients" and "Erythropoietin for the anemia of
chronic kidney disease in hemodialysis patients".)
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