Systemic Effects of Hemodialysis Access

Anil K. Agarwal
Patients with advanced chronic kidney disease are at a high risk of cardiovascular events. Patients with end-stage renal disease
have a particularly high morbidity and mortality, in part attributed to the complications and dysfunction related to vascular access
in this population. Creation of an arteriovenous access for HD is considered standard of care for most patients and has distinct advantages including less likelihood of infections, less need for intervention, and positive impact on survival as compared with usage
of a catheter. However, creation of an arteriovenous shunt incites a series of events that significantly impacts cardiovascular and
neurohormonal health in both positive and negative ways. This article will review the short- and long-term effects of dialysis access on cardiovascular, neurohormonal, and pulmonary systems as well as a brief review of their effect on survival on HD. Presence
of other comorbidities in a patient with dialysis access can amplify these effects, and these considerations are of paramount importance in individualizing the approach to not only the choice of vascular access but also the modality of kidney replacement therapy.
Q 2015 by the National Kidney Foundation, Inc. All rights reserved.
Key Words: Systemic effects of dialysis access, High-flow fistula, Vascular access, Pulmonary hypertension

INTRODUCTION
Patients with ESRD suffer from failure of a vital organ
with diverse roles in maintenance of milieu interieur,
often with concomitant suboptimal function of other
vital organs, in the backdrop of multiple comorbidities
including diabetes mellitus, hypertension, heart failure,
and infections. Kidneys regulate cardiovascular hemodynamics through regulation of blood volume and BP as
well as mineral metabolism. Ineffective regulation of these
essential functions leads to cardiovascular consequences
including left ventricular (LV) hypertrophy, volume overload, and endothelial dysfunction. Consequently, the
patient with kidney dysfunction is considered to be at
the highest level of cardiovascular risk. AVF for HD
remains a singular important advance that made chronic
HD feasible.1 However, creation of AV access for HD
imparts another degree of complexity to this already complex physiology.
Aside from making obvious alterations in the vascular
anatomy, the AV accesses cause changes in cardiovascular
hemodynamics, including the systemic and pulmonary circulations that have been recognized for over half a century,
starting soon after the placement of the rst AVF.2,3 These
alterations result in adaptations and maladaptations of
cardiac structure, function, and pulmonary circulation
that impact normal function, quality of life, and survival
of patients on HD. Use of AV grafts and catheters has
been noted to be associated with higher levels of
circulating pro-inammatory cytokines. Vascular access
can lead to other systemic complications including ischemia
(steal), thromboembolic phenomenon, infections, and psychological complications. Dialysis catheters can cause central vein stenosis (CVS) in addition to a high incidence of
infections. This review will focus primarily on hemodynamic alterations associated with AV accesses and their
downstream effects because most studies have examined
AVF or mixed AV accesses. AV grafts are likely to cause
similar hemodynamic consequences as AVF. However, AV
grafts are associated with a higher level of inammation
than AVF. Systemic effects of central venous catheters
(CVCs) will be briey mentioned, primarily related to infectious and mechanical effects not related to physiologic
changes, because of their adverse impact on survival and
quality of life of patients on HD.

Cardiovascular and Neurohormonal Effects

Creation of AVF has immediate and late effects on systemic
circulation.26 The procedure is followed by an increase in
cardiac contractility and decrease in peripheral resistance,
which result in increased cardiac output (CO). There is
also an increase in blood volume and LV end-diastolic volume along with restrictive physiology in diastole. At the
same time, vascular endothelium undergoes structural
and functional changes responding to the shear stress
and increase in blood ow. There is production of nitric oxide and vasorelaxation. The diameters of the artery and the
vein increase as a result of increased ow through this
newly created low-resistance parallel circuit.
Short-term effects of AVF creation have been studied
extensively. An echocardiographic study of 16 patients
with chronic kidney failure assessed echocardiographic
changes before and 3, 7, and 14 days after creation of
AVF 4 Concentrations of atrial natriuretic peptide (ANP)
and brain natriuretic peptide (BNP) were also checked on
day 1, 3, 6, 10, and 14. The study showed that within
10 days to 2 weeks after creation of AVF, CO increased by
15%, fractional shortening increased by 8%, and LV enddiastolic diameter increased 4%. There was shortening of
the deceleration time of the early diastolic lling wave
(212%) and the ratio of the peak velocity of early diastolic
to atrial lling (E-A ratio) increased (118%). The difference
in duration of LV inow and pulmonary venous ow at
atrial contraction, a marker of LV end-diastolic pressure,
signicantly shortened by day 14 after the operation
(237%). The authors concluded that the creation of an
AV stula induced LV diastolic dysfunction and a restrictive lling pattern. There was an increase in ANP and
From the Section of Nephrology at University Hospital East, The Ohio State
University Wexner Medical Center, Columbus, OH.
Financial Disclosure: The author declares that he has no relevant nancial
interests.
Address correspondence to Anil K. Agarwal, MD, FACP, FASN, FNKF,
Section of Nephrology at University Hospital East, The Ohio State University
Wexner Medical Center, Columbus, OH 43210 E-mail: Anil.agarwal@osumc.
edu
2015 by the National Kidney Foundation, Inc. All rights reserved.
1548-5595/$36.00
http://dx.doi.org/10.1053/j.ackd.2015.07.003

Advances in Chronic Kidney Disease, Vol 22, No 6 (November), 2015: pp 459-465

459

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Agarwal

BNP levels with maximal increase after 10 days (ANP,

with no change in aldosterone levels. Plasma angiotensin
148%; BNP, 168%; Fig. 1). The increase in CO was associII, angiotensin-converting enzyme, and endothelin levels
ated with elevation of ANP levels but not BNP levels. The
did not change. The authors concluded that creation of
increase in E-A ratio correlated only with BNP level elevaAV access is independently associated with further protion.
gression of already existing LVH.
Acute and chronic hemodynamic changes at 24 hour and
AVF can affect cardiac load by increasing preload and
8 weeks after placement of a radiocephalic AVF were studdecreasing afterload. In 10 patients with AVF, a
ied in 17 subjects at 24 hours with a Swan-Ganz catheter.5
60-second compression and reconstruction of aortic presAt baseline, all patients had normal right atrial pressure;
sure waves from nger pressure recordings showed a
pulmonary artery wedge pressure, stroke volume index
small increase in LV oxygen demand, but a larger decline
(SVI), high normal heart rate (HR), and systemic vascular
in cardiac oxygen supply.7 During stula compression,
systolic, diastolic, and mean arterial pressures increased,
resistance index (SVRI). The PAP, MAP, cardiac index (CI),
and HR decreased signicantly. Although stroke volume
and pulmonary vascular resistance index (PVRI) were
decreased slightly, there was a signicant decrease in CO
high at baseline. At 24 hours after the AV stula creation,
and increase in SVR.
there was an insignicant rise in HR, CI, PAP, and PVRI,
It is well recognized that arterial stiffness, as measured
and a fall in SVRI and MAP with no change in right atrial
by carotid-femoral pulse wave velocity, is increased in
pressure, pulmonary artery wedge pressure, and SVI. A
dialysis patients and causes increased central BP and
rising trend of HR and CI with a fall in SVRI was observed
myocardial hypoperfusion. In a small study of 43 patients,
in 10 of 17 patients. At the sixth week, the 8 patients stud30 of the 43 patients with successful AVF showed
ied showed a signicant increase in the systolic pressure
decreased total peripheral
and MAP and PVRI. Also,
resistance, increased SV and
there was a rise in SVI in all
CLINICAL SUMMARY
CO with decreased systolic
patients and CI in 6 patients,
and diastolic BP 2 weeks afwith insignicant change in

Arteriovenous access for hemodialysis is preferred over
ter placement of AV stula.8
the cardiac lling pressure.
catheter access due to the less likelihood of infections and
This study demonstrated
None of the patients develinterventions and a positive impact on survival as
potential benets of AVF
oped congestive heart failure
compared to using a catheter.
creation in HD patients
due to AVF. Increase

Access creation leads to changes in heart rate, blood
although overall benets of
(although insignicant) in
pressure, blood volume, cardiac output, pulmonary and
AV access have to be considCI after AVF despite a
systemic resistance, changes in natriuretic peptides as
ered in an individual patient.
decrease in preload after
well as structural changes in vascular endothelium and
AVF was not well explained
left ventricular mass.
Heart Failure
by these ndings. The au
Access flow to cardiac output ratio .0.3 may predict heart
thors concluded that the crePresence of AVF, especially
failure.
when associated with high
ation of an AVF for HD does
access ow, has been obnot lead to a signicant

Potential short and long term effects of AV access should
change in the cardiac hemoserved to be associated with
be carefully considered in individualizing the approach
dynamic parameters and is
heart failure, which is generto the choice of vascular access and the modality of
renal replacement therapy, especially in patients with
ally attributed to an increase
not an appreciable factor
preexisting cardiovascular morbidity.
leading to circulatory conin CO.9 However, relatively
gestion or pulmonary edema
uncommon occurrence of
heart failure with such AVF
in these patients.
suggests presence of intrinsic heart disease in those who
Timing of various changes was also studied in another
prospective echocardiographic and neurohormonal study
develop heart failure. It is also likely that many cases of
heart failure due to AVF are missed and attributed to other
of 12 predialysis patients before and 1 and 3 months after
risk factors. Upper arm AV access is more likely to have
creation of a primary AV access.6 After creation of access,
the weight, BP, or hemoglobin level did not change, but
higher access ow and result in heart failure as compared
CI increased and SVR decreased. LV mass corrected to
with an access in forearm although there is no difference
height signicantly increased from 63.8 6 5.5 to
between AVF and AV graft (Fig. 3).10
2
2
68.9 6 4.9 g/m at 1 month and 72.5 6 8.9 g/m at 3 months
There are many AV accessassociated risk factors for
(Fig. 2). The increase in mass was mostly due to an increase
occurrence of heart failure. It is well known that a highow AVF can cause signicant adverse changes in CO, BP,
in interventricular septal thickness. LV end-diastolic diamand HR. An access ow (Qa) over 2 L per minute is a risk
eter and posterior wall thickness did not change. The incidence of LV hypertrophy (LVH) increased from 67% at
factor for occurrence of heart failure.10 Another risk factor
is the occurrence of a high degree of cardiopulmonary
baseline to 83% and 90% at 1 and 3 months, respectively.
recirculation. One study showed a strong positive correlaLeft atrial area increased, and early diastolic transmitral
ow increased. Inferior vena cava diameter increased at
tion between Qa, CO, and CI and a negative correlation
with SVR (Fig. 4).11 There was an average Qa:CO ratio of
1 month and did not change at 3 months. A remarkable in14% to 20% in stable long-term HD patients, but a ratio
crease in ANP was seen 2 weeks after creation of AVF associated with increased contractility, CO, and decrease in
higher than 0.3 was associated with high output heart
peripheral resistance. There was decreased renin activity
failure.

Systemic Effects of Hemodialysis Access

461

Figure 1. Percentage of increase in plasma concentrations of (A) atrial natriuretic peptide (ANP) and (B) brain natriuretic peptide (BNP) after the AVF operation. Values given as mean 6 standard error of the mean. *p , .05. **p , .01 compared with
control (pre) for each peptide.4

Similar association of high Qa with heart failure was

noted in a surgical study, and the symptoms of heart failure resolved with ow reduction.12 A study of 31 patients
undergoing ow reduction surgery showed intraoperative
increase in systolic blood pressure (111 6 6-123 6 6 mm
Hg, p , .05) and diastolic blood pressure
(57 6 4-63 6 5 mm Hg, p , .05) after 15-second clamping
of access.13 Mean access ow in these patients was approximately 3000 mL/min. Such increases were modest (16 6 3
and 12 6 2 mm Hg, respectively, p .37) in control
patients with access-associated hand ischemia, who had
mean access ow just above 1000 mL/min. Both groups
experienced modest reduction in heart rate of approximately 3 beats/min with compression. Authors suggested
that an incremental increase in access ow might cause
poor cardiac performance.
Impact on Myocardial Ischemia and Valvular Disease
In patients with preexisting coronary artery disease, creation of an AVF can incite silent subendocardial myocardial

Figure 2. Changes in left ventricular mass indexed to height

after creation of an AV access. Each line represents 1 patient.
Filled squares represent mean 6 standard error of the mean
for the corresponding period.6

ischemia due to increase in sympathetic demand and

contractility, which causes an imbalance between subendocardial oxygen supply and increased oxygen demand.14
Also, AVF can potentially steal blood ow from an ipsilateral internal mammary artery bypass graft predisposing to
myocardial ischemia and cause decompensation in presence of critical aortic stenosis.1518
Pulmonary Hypertension
Pulmonary hypertension (PH) is quite prevalent in patients
with ESRD (40%-50%) but remains an underappreciated
cause of cardiovascular morbidity and mortality.19,20 PH is
dened as pulmonary artery pressure greater than 25 mm
of Hg at rest and 30 mm of Hg during exercise.21 The pathogenesis of PH and possible management have been extensively reviewed, and potential mechanisms of development
of PH in dialysis patients have been hypothesized (Fig. 5).22
PH in ESRD patients is generally attributed to increase in
pulmonary ow especially in patients with high-ow AVF

Figure 3. Comparison of the cardiac output values among

the patients subdivided according to the vascular access
flow cutoff values. The horizontal line represents the
median, upper, and lower limits of the box including the first
and third quartiles, and capped bars indicate minimum and
maximum value. The 1-way ANOVA followed by the Tukeys
posthoc test was performed to compare the mean cardiac
output values in each access blood flow category identified
by the cutoff points previously calculated.10

462

Agarwal

PD, which also supports the theory of high pulmonary

ow with HD and AV access. PH and CO decrease significantly after compression of AVF.23 Furthermore, kidney
failure itself may be a contributing factor as demonstrated
by resolution of PH after transplantation despite a patent
AV access.27 Prevalent uncontrolled systemic hypertension
also contributes to secondary PH in many instances.
Treatment of PH includes use of anticoagulants,
diuretics, oxygen, vasodilators, and antiproliferative
agents. The efcacy of these therapeutic modalities, however, has not been studied in patients with ESRD. PH may
reverse after kidney transplantation. Flow reduction in a
high-ow AV access should be considered. PD provides
an alternative therapy in appropriate patient.
Figure 4. Relationship between access flow and cardiac
index.11 The dots represent the cardiac index at different access flow. This is how it is in the original article and does not
need to be expanded.

and elevation of pulmonary systolic pressure after the creation of AV access.23 Pulmonary artery vasoconstriction
can occur due to hormonal and metabolic derangements,
whereas increase in pulmonary artery pressure can be a
result of anemia, uid overload, and hemodynamic
changes due to AV access. A study of 180 patients with
HD, PD, and kidney transplant analyzed demographic,
clinical, and echocardiographic ndings to create a multivariable linear regression model to nd factors associated
with pulmonary artery pressure.24 PH was detected in
31.6%, 8.3%, and 5% of the patients on HD, PD, and transplant recipients, respectively (p , .001). In multivariate
analysis, HD, age, smoking, systolic cardiac dysfunction,
and diastolic cardiac dysfunction were associated with
systolic pulmonary artery pressure. Decreased nitric oxide
production, presence of inhibitors of nitric oxide, and
endothelial dysfunction in HD patients with AVF and
PH and elevated levels of inammatory cytokines such
as IL-1 beta, TNF-alpha, and IL-6 have been implicated
as well.25 After closure of AVF, improvement has been
demonstrated that implicates AV access as a cause of PH
in this population.26 PH is uncommon in patients with

Reversing Changes of AV Access Creation: Impact of

Kidney Transplantation, AVF Ligation, or Banding
Interestingly and importantly, LVH can regress after kidney transplantation and once AVF is nonfunctional. In patients with high-ow AVF, banding of the AVF to reduce
the ow, distalization of anastomosis, complete ligation,
and abandoning of the access can resolve symptoms and
reversal of cardiac changes toward normal.28,29 Ligation
of access has the potential to reverse the hemodynamic
changes; however, it leaves the patient with no
functional access. Reduction of ow in such an access
can be achieved using banding or distalization of inow.
Ultrasound-guided banding of AVF in 30 patients with
high-ow AVF and cardiac failure or steal syndrome led
to expected reduction in ow, size of anastomosis and resolution of symptoms, and no need of reintervention.30 CO
was reduced from 8.5 6 2.9 L/min to 6.1 6 1.9 L/min
(p , .01). During the median 1-year follow-up, AVF and
AV graft patency rates were 100% and 80%, respectively,
and there was resolution of clinical complaints. Such banding can be achieved using a variety of techniques that are
out of the scope of this article. Distalization of inow by
disconnecting the existing high-ow anastomosis and
creating another anastomosis using a smaller distal inow
has been shown to be successful as well.31
There has been a debate about the utility of an AVF after a
successful kidney transplant. In a rare case scenario, a lower

Figure 5. Potential pathophysiologic mechanisms of pulmonary hypertension in patients on dialysis.22

Systemic Effects of Hemodialysis Access

extremity AV access has the potential to steal blood ow

from an ipsilateral kidney transplant.32 This can be ameliorated by ligation of access. However, there is more concern
about cardiovascular impact of continued functional AV access after transplantation. The risk of surgical closure relates
to a potential need of access for HD in case of allograft failure. This can be minimized by a careful selection of patients
who have stable allograft function with no signicant proteinuria, recurrent rejection, or evidence of recurrence of
primary kidney disease.33 An AVF closure after transplantation has the potential benet of decreasing LV volume and
mass. Studies have shown a 6.4% to 8.6% decrease in LV
mass 1 month after AVF closure, reaching 11.1% and
15.8% at 3 to 4 and 21 months, respectively.3436 In these
studies, not all patients responded to surgical closure to a
similar degree. An increase in SVR and BP during an
acute compression of AVF best predicted LV diameter and
mass reduction.34 Other similar studies have shown that
there is regression of LVH after occlusion of AVF in nontransplant patients. In a study of 25 HD patients with malfunctioning AVF who underwent AVF closure,
echocardiographic changes from the baseline were
compared at 6 months.29 LV mass decreased from
225 6 55 to 206 6 51 g (p , .001), and LV mass index
decreased from 135 6 40 to 123 6 35 g/m2 (p , .001). LV internal diastolic diameter, interventricular septum thickness,
and diastolic posterior wall thickness decreased signicantly, whereas LV ejection fraction increased from
56 6 7% to 59 6 6% (p , .001). No signicant changes
were observed in controls that did not undergo AVF
closure. In patients with AVF closure, LV morphologic characteristics showed a decrease in both eccentric hypertrophy
and concentric hypertrophy in favor of normalization or a
pattern of concentric remodeling.
AV Access and Mortality
Both high- and low-ow AVF can be of importance to survival of patients on HD. High-ow AVF, by causing
adverse cardiovascular changes described previously,
can contribute to mortality. On the contrary, a low-ow access will also cause under dialysis and impact survival and
quality of life. To compare extremes of access ow, a Canadian study of 820 incident dialysis patients with median
follow-up period of 28 months, observed 25.1% overall
mortality 37 The adjusted risk of mortality was similar between the low and high baseline Qa before and after
adjustment for demographic characteristics, comorbidity,
and access type. The ndings did not suggest an increased
risk of death at higher levels of Qa.
Despite systemic effects of AV accesses that might be
detrimental, such accesses are less inammatory than a
catheter used for dialysis. There is controversy about
quantitative associations between vascular access type
and clinical outcomes. A systematic review of cohort
studies to evaluate such an association identied 3965 citations of which 67 met inclusion criteria.38 The metaanalysis showed that those individuals using catheters
had higher risks for all-cause mortality (risk ratio 1.53
and 1.38), fatal infections (2.12 and 1.49), and cardiovascular events (1.38 and 1.26) as compared with those using
AVF and AV graft, respectively. Compared to those with

463

stula, those using graft had increased all-cause mortality

(1.18) and fatal infection (1.36), but similar risk for cardiovascular events (1.07). The risk for bias, especially selection
bias, was high.
Considering recent increase in prevalence of AVF, it is
important to consider whether such change in access use
could have led to a higher mortality. A study of United
States Renal Data System Clinical Performance Measures
data comprising of 4854 patients who initiated dialysis between 1999 and 2004, analyzed risk of all-cause and cardiovascular death.39 AVF use was strongly associated with
lower all-cause and CV mortality. After adjustment for covariates, AVF use 90 days after dialysis initiation remained
signicantly associated with lower cardiovascular mortality
(hazard ratio 0.69, p .0004) compared with catheter use.
It is interesting to note that although AV access use at the
start of ESRD conferred a marginal reduction in CVrelated mortality, AVF use 90 days after dialysis initiation
conferred a 31% reduction in CV-related mortality, when
compared with CVC use at 90 days. Moreover, it is remarkable to note that the AVF use was protective given the
higher prevalence of hypertension among patients reporting AVF use at dialysis initiation, and the comparable prevalence of ischemic heart disease, myocardial infarction,
peripheral vascular disease, history of cardiac arrest, and cerebrovascular disease found among AVF, AVG, and CVC
patients in this nationally representative cohort.
Type of vascular access has been linked to survival on HD
with signicantly higher mortality with catheter as
compared with AVF and AV graft.40 Change in type of
vascular access can also affect clinical outcomes. A study
of 79,545 patients (43% stulas, 29% catheters, and 27%
grafts) showed unadjusted hazard ratios of death for grafts
(1.22, but 1.05 in adjusted models) and catheters (1.76)
compared with stulas.41 Compared with patients who
continued using a catheter, those who converted to either
a graft or stula had an hazard ratio of mortality of 0.69,
whereas those who converted from a graft or stula to a
catheter had increased hazard ratios to 2.12 (both p , .001).
Catheters are notorious for their predisposition to
become infected. Infection can often become disseminated and cause metastatic infections and death. There
is also a frequent risk of thromboembolism with
indwelling catheters. In addition to large vein and intracardiac thrombosis, the catheters can also cause brointimal proliferation and stenosis within the central veins.
CVS affects blood ow from the ipsilateral extremity
and compromises future vascular access on the same
side. In presence of bilateral upper extremity CVS, symptoms suggestive of superior vena cava syndrome can be
present. Recanalization of CVS is a possibility although
not always feasible or successful. However, in presence
of a high-ow AVF, recanalization of CVS can sometimes
result in precipitation of heart failure due to sudden volume overload. Furthermore, the catheters have been
observed to be associated with a high level of inammation and worse survival than AV accesses. A randomized
study of incident dialysis patients developing bacteremia
or sepsis requiring hospitalization showed increased risk
of subsequent heart disease and heart failure.42 As a high
level of inammation is associated with acceleration of

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Agarwal

atherosclerosis, occurrence of infection and inammation

due to vascular access may confer an increased risk of cardiovascular disease in patients with ESRD.43 In patients
with limited life expectancy (elderly, terminal illness)
and in those with poor peripheral vasculature, catheters
may be an appropriate choice or the only option when
HD is the chosen modality. Although catheters do not
induce striking changes in hemodynamics compared
with AV access, they do have a striking impact on patient
survival. These data compel consideration of overall evidence about pros and cons of vascular accesses rather
than simply looking at the changes in hemodynamics
associated with AV accesses.
Approach to Vascular Access: Considering
Hemodynamic Consequences
Consideration of the incipient hemodynamic changes after
creation of AVF is important, especially in those with preexisting cardiac conditions that are not uncommon in
ESRD population. The risks of AV access are especially
more relevant to those with advanced HF (New York
Heart Association class III and IV) and when an upper
arm AV access is created. It is reasonable to consider alternatives, including PD and placement of a planned
tunneled catheter if an AV access is not feasible or considered unsafe. It is also important to consider that catheters
are not necessarily devoid of adverse CV events due to
their impact on systemic inammation and their propensity toward infection and sepsis.
After creation of AVF, a high-risk patient, such as elderly
patient and the patient with HF, PH, valvular disease, and
upper arm AV stula should be monitored carefully for
adverse hemodynamic consequences. In case of symptoms
and evidence of high access ow, strategies to reduce ow
should be considered. Distalization of the anastomosis or
banding can be effective in many cases. In intractable
cases, ligation of the access may be necessary. The patient
should be closely monitored after the ligation of high-ow
AV stula because of the possibility of abrupt increase in
SVR and its adverse effect on cardiac performance. In presence of severe aortic stenosis, valve repair or replacement
should be considered before the placement of AV access.
Individualized approach to the dialysis access is essential
to improve outcomes.
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