NDT Advance Access originally published online on November 17, 2005
Nephrology Dialysis Transplantation 2006 21(2):254-257; doi:10.1093/ndt/gfi276
© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Editorial Comment
Arteriovenous fistula after renal transplantation: utility, futility or threat?
Philippe Unger1 and
Karl Martin Wissing2
1 Department of Cardiology and 2 Department of Nephrology, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium
Correspondence and offprint requests to: Philippe Unger, MD, Department of Cardiology, Erasme Hospital, 808 route de Lennik, B-1070 Brussels, Belgium. Email: punger{at}ulb.ac.be
Keywords: arteriovenous fistulas; left ventricular morphology; renal transplantation
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Introduction
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Creation of an arteriovenous (AV) fistula for haemodialysis
therapy provides convenient access to the circulation in patients
with end-stage renal disease. However, the chronic volume overload
induced by the AV fistula induces structural and functional
cardiac changes, including left ventricular remodelling, which
may be deleterious. The balance between the need for vascular
access and the deleterious effects of a patent AV fistula on
cardiac function and morphology obviously favours the former
in patients requiring long-term haemodialysis. After renal transplantation,
however, the value of keeping an AV fistula patent is more uncertain
and whether it should be closed after successful renal transplantation
remains a matter of debate. Since recent studies have provided
more insight into the cardiac and haemodynamic changes induced
by the procedure, this review aims to summarize the pros and
cons of AV fistula closure.
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Determinants of left ventricular morphology after renal transplantation
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Left ventricular hypertrophy is highly prevalent among patients
with end-stage renal disease [
1]. Hypertension and chronic anaemia
appear to be the main stimuli for the development of left ventricular
hypertrophy in dialysis patients, although age, diabetes and
metabolic factors may also play a role. Left ventricular dilatation
is also frequent and is associated with anaemia, hypertension,
hypoalbuminaemia, ischaemic heart disease and plasma volume
expansion [
2]. In addition, left ventricular adaptation to the
chronic volume overload induced by AV fistulas is characterized
by increased stroke volume and cardiac output and by left ventricular
enlargement; the resulting left ventricular hypertrophy is predominantly
eccentric (i.e. characterized by increased left ventricular
mass with normal relative wall thickness) [
2,
3]. Renal transplantation
improves left ventricular volume, paralleling the correction
of uraemia and volume status, the normalization of the haemoglobin
level and the rise in serum albumin and may reduce left ventricular
hypertrophy [
4,
5]. However, the prevalence of left ventricular
hypertrophy remains high, with uncontrolled hypertension and
anaemia as main contributing factors. Strict blood pressure
control contributes to the regression of left ventricular hypertrophy
[
6]. The effect of a patent AV fistula on left ventricular morphology
after renal transplantation had received little attention until
recent data suggested a significant contribution to residual
hypertrophy [
7–11].
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Deleterious effects of AV fistulas
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Complications of AV fistulas are not uncommon and include steal
syndrome, arm oedema, thrombosis and, rarely, traumatic bleeding.
Furthermore, patients frequently consider the presence of a
dilated and pulsatile fistula as non-aesthetic. In addition
to local complications, a haemodynamically significant role
of the fistula is supported by numerous case reports showing
high output cardiac failure subsiding after AV fistula closure.
Obviously, these reports involved patients with large AV fistulas
and it is difficult to extrapolate the detrimental effects of
AV fistulas to larger samples of patients with smaller AV access.
Even when heart failure is not evident, the creation of an AV
fistula stimulates brain natriuretic peptide (BNP) release in
response to myocardial tension and increased intravascular volume
[
12], an interesting observation in light of the fact that raised
BNP may predict survival even in patients with asymptomatic
heart failure [
13]. In addition, AV fistula creation may adversely
affect the balance between cardiac oxygen supply and demand
[
14] and may predispose to a risk of myocardial ischaemia by
reducing subendocardial perfusion [
15]. Creation of an AV fistula
increases left ventricular volume [
12,
16] and left ventricular
mass is higher in transplanted patients when there is a patent
AV fistula [
11]. As in patients with hypertension, left ventricular
mass is an independent risk factor for adverse outcomes in patients
with chronic kidney disease [
17] and after renal transplantation
[
18,
19]. In uraemic patients with left ventricular dilatation,
normal systolic function and a low mass-to-volume ratio, a condition
that is a hallmark of volume overload and the presence of an
AV fistula, the clinical outcome may be more dependent on the
degree of LV dilatation than the degree of hypertrophy [
5].
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Rationale for AV fistula closure
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Several prospective studies have shown an early decrease in
left ventricular volume and mass after AV fistula closure [
7,
9],
although these studies involved a rather limited number of selected
patients with large and mainly symptomatic fistulas. A 6.4–8.6%
decrease in left ventricular mass was found 1 month after AV
fistula closure [
9,
10], reaching 11.1% and 15.8% at 3–4
and 21 months, respectively [
7,
10]. Not all patients responded
to surgical closure to a similar degree and the increase in
total peripheral resistance and in blood pressure during an
acute compression best predicted left ventricular diameter and
mass reduction [
9].
Left ventricular mass reduction of a similar magnitude during antihypertensive treatment is associated with a marked reduction in risk for subsequent cardiovascular disease in hypertensive patients [20]. But will the reduced left ventricular hypertrophy associated with fistula closure translate into a similar cardiovascular risk reduction? There are currently no data allowing this extrapolation, as this would require a large population sample. Moreover, after adjustment for left ventricular mass, hypertensive patients with the eccentric left ventricular hypertrophy pattern, which is frequently found in patients with large AV fistulas (Figure 1), have been show to experience a lower incidence of cardiovascular events compared with those patients with concentric hypertrophy (that is, increased left ventricular mass and relative wall thickness) [21]. Furthermore, in hypertensive patients, the concentric pattern, which is also the predominant geometry after AV fistula closure (Figure 1) [10], has been shown to confer a risk significantly higher than that conferred by normal left ventricular geometry [21]. Thus, beyond the net reduction in left ventricular mass, the expected beneficial effects of AV fistula closure may be hampered by the lack of normalization of left ventricular morphology. In addition to the effects on left ventricular morphology, patients often report exercise tolerance improvement (unpublished data), but this should be investigated further.
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Fig. 1. Left ventricular morphology at baseline (left panel) and a median of 16 months after surgical AV fistula closure (right panel). Patients are divided into four groups according to left ventricular mass index (LVMI) and relative wall thickness [RWT = (septal + posterior wall thickness)/left ventricular end diastolic diameter]: normal left ventricular geometry (lower left case); concentric remodelling (lower right case); eccentric hypertrophy (upper left case); and concentric hypertrophy (upper right case). At baseline, both concentric and eccentric hypertrophy patterns are predominant, whereas after surgical ligation of the AV access, left ventricular morphology fails to normalize and the concentric remodelling pattern is the most prevalent. Adapted from [10].
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Which patients should be considered for surgical closure?
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Should the renal graft deteriorate and graft loss occur, a return
to haemodialysis therapy would require creation of a new vascular
access, and ligation of an AV fistula carries the obvious disadvantage
of destroying a functioning vascular access. The ideal patient
for fistula closure should, therefore, have a minimal risk of
graft failure that would ultimately require a new functional
AV fistula and should expect significant long-term benefits
from fistula closure. Hence, fistula closure should be restricted
to patients with good graft function and without significant
proteinuria, no history of severe or multiple acute rejection
episodes and no signs of recurrence of the primary kidney disease
in the graft. In our centre, 41 renal transplant patients (20
male and 21 female) underwent surgical closure of a patent AV
fistula between September 1999 and April 2004. The fistula was
closed a median of 2.1 years (range: 0.7–16.5 years) after
transplantation and the mean age at fistula closure was 50.2±13.9
years. During a median follow-up of 45.8 months (range: 4.6–73
months), three patients returned to dialysis because of chronic
allograft nephropathy and one patient died of heart failure.
The overall actuarial graft survival was 84% and the death-censored
graft survival was 87.9% (
Figure 2). A new AV fistula could
be created in all three patients who needed to resume haemodialysis.
Our experience suggests that medium-term graft loss is low in
carefully selected renal transplant patients and that surgical
closure of an AV fistula does not seem to preclude the creation
of a new vascular access should the patient need to restart
dialysis. However, this low incidence of renal graft loss is
likely to increase with a longer follow-up period. Furthermore,
peripheral vascular status should be included in the decision
analysis, to avoid closure of a vascular access in patients
who have few suitable veins remaining.
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Fig. 2. Death-censored graft survival after closure of the AV fistula in 41 renal transplant patients. Censored observations are indicated as vertical lines on the survival plot.
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Conclusions
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AV fistula closure reduces left ventricular volume and mass
in renal transplant patients. Whether fistula closure will reduce
the associated high cardiac morbidity and mortality is unknown.
There are clearly insufficient data yet to promote systematic
closure of AV fistulas in kidney transplant patients with stable
renal function, unless symptoms are present. The balance might
favour closure in selected asymptomatic patients, with a large
AV fistula, a dilated left ventricle, a low probability of graft
loss and a high risk of cardiac events. Randomized large-scale
prospective studies are clearly needed and, potentially, will
better define the protective role of fistula closure.
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Acknowledgments
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P.U. has received a grant from the Fonds pour la Chirurgie Cardiaque.
Conflict of interest statement. None declared.
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Received for publication: 27. 9.05
Accepted in revised form: 25.10.05
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Introduction
Determinants of left ventricular...