Nephrol Dial Transplant (2008) 23: Editorial Comments
most important goal to protect from progressive vascu-
lar calcification. The prescription of very high doses of
calcium-containing phosphate binders, such as those given
in the recent past, should not still be advocated.
Conflict of interest statement. M.K. received grant support and honoraria
(lecture fees, advisory tasks) from Genzyme, Fresenius Medical Care and
Shire.
(See related article by Phan et al. Effect of oral calcium carbonate on aortic
calcification in apolipoprotein E-deficient (apoE−/− ) mice with chronic
renal failure. Nephrol Dial Transplant 2008; 23: 82–90.)
References
1. Phan O, Ivanovski O, Nguyen-Khoa T et al. Sevelamer prevents
uremia-enhanced atherosclerosis progression in apolipoprotein E
deficient (apoE-/-) mice. Circulation 2005; 112: 2875–2882
2. Phan O, Ivanovski O, Nikolov IG et al. Effect of oral calciumcarbonate
on aortic calcification in apolipoprotein E deficient (apoE-/-) mice
with chronic renal failure. Nephrol Dial Transplant 2007 in press
3. Jono S, McKee MD, Murry CE et al. Phosphate regulation of vascular
smooth muscle cell calcification. Circ Res 2000; 87: E10–E17
Nephrol Dial Transplant (2008) 23: 19–24
doi: 10.1093/ndt/gfm673
Advance Access publication 28 September 2007
Steal syndrome—strategies to preserve vascular access and extremity
Volker Mickley
Department of Vascular Surgery, Clinical Centre Mittelbaden, Kreiskrankenhaus Rastatt, Germany
Keywords: ; access banding; arteriovenous access; DRIL
procedure; PAVA procedure; review; steal syndrome
Introduction
In access-related steal syndrome, four stages can be distin-
guished (Table 1, [1]). Steal syndrome stage I (retrograde
inflow of blood into the access during diastole without com-
plaints) is a frequent finding in arteriovenous (AV) fistulae
and grafts [2] and needs no intervention. Patients with pain
on exercise or during dialysis (stage II), however, require
Correspondence and offprint requests to: Dr Volker Mickley, Depart-
ment of Vascular Surgery, Clinical Centre Mittelbaden, Kreiskrankenhaus
Rastatt, Engelstrasse 39, D-76437 Rastatt, Germany. E-mail:
v.mickley@klinikum-mittelbaden.de
19
4. Yang H, Curinga G, Giachelli CM. Elevated extracellular calcium lev-
els induce smooth muscle cell matrix mineralization in vitro. Kidney
Int 2004; 66: 2293–2299
5. Reynolds JL, Joannides AJ, Skepper JN et al. Human vascular smooth
muscle cells undergo vesicle-mediated calcification in response to
changes in extracellular calcium and phosphate concentrations: a po-
tential mechanism for accelerated vascular calcification in ESRD.
J Am Soc Nephrol 2004; 15: 2857–2867
6. Murshed M, Harmey D, Millan JL et al. Unique coexpression in
osteoblasts of broadly expressed genes accounts for the spatial restric-
tion of ECM mineralization to bone. Genes Dev 2005; 19: 1093–1104
7. Stubbs JR, Liu S, Tang W et al. Role of hyperphosphatemia and
1,25-dihydroxyvitamin d in vascular calcification and mortality in
fibroblastic growth factor 23 null mice. J Am Soc Nephrol 2007; 18:
2116–2124
8. Block GA, Klassen PS, Lazarus JM et al. Mineral metabolism, mor-
tality, and morbidity in maintenance Hemodialysis. J Am Soc Nephrol.
2004; 15: 2208–2218
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9. Kalantar-Zadeh K, Kuwae N, Regidor DL et al. Survival predictability
of time-varying indicators of bone disease in maintenance hemodial-
ysis patients. Kidney Int 2006; 70: 771–780
10. Russo D, Miranda I, Ruocco C et al. The progression of coronary
artery calcification in predialysis patients on calcium carbonate or
sevelamer. Kidney Int 2007 (Epub ahead of print)
Received for publication: 9.10.07
Accepted in revised form: 15.10.07
permanent attention in order to early detect deterioration to
stage III (rest pain) or stage IV (necrosis).
Depending on the type and location of AV access for
HD, the risk of severe access-related peripheral ischaemia
(steal syndrome stage III or IV) varies between 1–2% (in
distal radio-cephalic AV fistulae) and 5–15% (in brachio-
cephalic/basilic fistulae and grafts) [3–6]. Following the
creation of a femoral (autogenous or allograft) access,
an even higher incidence of steal syndrome (16 to 36%,
[7,8]) has been reported. Women, diabetics and patients
with known coronary or peripheral arterial occlusive dis-
ease are at higher risk than the remaining HD population
[3,9–11].
The steal syndrome is likely to disappear when the access
is abandoned but creation of a new AV access on another
extremity is burdened with a significant risk of recurring
peripheral ischaemia. Therefore correction of the steal
syndrome must aim at the double goal of preserving the
access and at the same time, improving peripheral arterial
circulation.
20
Table 1. Classification of steal syndrome (modified from [1])
Stage I Retrograde diastolic flow without complaints; steal
phenomenon
Stage II Pain on exertion and/or during haemodialysis
Stage III Rest pain
Stage IV Ulceration/necrosis/gangrene
Pathophysiology
AV fistulae in general are constructed in a side of artery-to-
end of vein (or graft) fashion. Under resting conditions, the
high resistance of muscle-feeding arteries in the diastole
causes a retrograde flow in the artery distal to the AV anas-
tomosis and into the AV access. This ‘physiologic’ steal
phenomenon can be observed in 73% of AV fistulae and in
91% of access grafts [2]. Approximately 75% of the blood
flow through distal radio-cephalic fistulae is supplied by
the proximal radial artery, but 25% comes from a patent ul-
nar artery via the distal radial artery and palmar arch [12].
In elbow fistulae, the periarticular arterial collaterals have
the same impact.
When an AV fistula is created using healthy vessels,
dilatation of the proximal and distal arteries, as well as di-
latation of the collaterals around the anastomosis, compen-
sates for enhanced systolic AV flow and also for diastolic
retrograde inflow into the fistula. Any vascular pathology
affecting one or several of these adaptive mechanisms can
cause distal ischaemia by a steal mechanism. Arterial steno-
sis upstream of the anastomosis prevents the necessary flow
increase in the feeding artery; severe peripheral arterial oc-
clusive disease (PAOD) or vasculitis enhance the resistance
of distal arteries and simultaneously impair the function
of natural collaterals [13]. Under these conditions, during
diastole virtually all blood coming from the collaterals is
drained into the access [14]. Instead of a steal syndrome
stage I (also named steal phenomenon), the further dreaded
stages II to IV develop, with clinical signs of peripheral
ischaemia. The likelihood that a steal syndrome develops
depends more on the severity of arterial pathology and less
on the volume of intra-access blood flow.
Clinical findings
Access-related peripheral ischaemia is primarily diagnosed
on the basis of the patient’s complaints and clinical findings.
Similar to Fontaine’s classification of PAOD, four stages can
be distinguished (Table 1, [1]). In critical ischaemia stage III
or stage IV, transcutaneous oxygen partial pressure (tcpO2 )
is lower than 30 mmHg, wrist or digital arterial pressures
are below 50 mmHg and the digital(wrist)/brachial pres-
sure index is below 0.6 [13]. With access compression,
the respective values rise significantly, sometimes even to
normal. These tests help to distinguish steal syndrome from
other conditions causing the constellation of dystrophy, pain
and necrosis, such as carpal tunnel syndrome, Sudeck’s dys-
trophy or calciphylaxis.
A rare but potentially devastating complication of steal
is the so-called ischaemic monomelic neuropathy (IMN)
Nephrol Dial Transplant (2008) 23: Editorial Comments
[15,16]. In uraemic diabetics with pre-existing neuropathy,
a reduction of the blood flow in the vasa nervorum caused
by the steal phenomenon can cause severe sensorimotoric
dysfunction of the ulnar, radial and median nerves without
obvious tissue loss and with pressure indices above critical
values. Symptoms often occur immediately after creation
of the access. When the ischaemia is not reversed immedi-
ately and sufficiently, irreversible neural damage and per-
manent impairment of the afflicted extremity can be the
consequences.
Diagnostic evaluation
Access flow measurements—either with colour-coded
duplex-ultrasound or with one of the dilution methods—are
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of minor relevance for the diagnosis of steal syndrome
because—depending on the severity of arterial disease—
symptoms can occur at any rate of access flow. In a recent
German series [17], two-third of patients with an AV
fistula and access-related ischaemia had access flows
≤250 ml/min. Preoperative access flow measurements,
however, are indispensable in planning the optimal
treatment of a steal syndrome (see below).
To detect proximal arterial stenoses, duplex-ultrasound
is of limited value in patients with an AV access, as the typ-
ical post-stenotic flow pattern (bi-phasic signal) is masked
because of the high diastolic flow through access-feeding
arteries. However, when duplex-ultrasound is performed
with the access being compressed, the post-stenotic flow
pattern can be detected and thus permits the localization of
a potential stenosis interfering with the arterial inflow. A
pattern of minimal flow in stenotic forearm arteries suggest-
ing severe disease of the peripheral artery as the cause of a
steal syndrome can easily be demonstrated by ultrasound,
whereas the palmar arch and finger arteries are better visu-
alized angiographically [18].
In selected cases and when performed by an experienced
investigator, colour-coded duplex-ultrasound alone may be
sufficient to define the cause of steal syndrome and to def-
initely plan the corrective procedure. Most authors, how-
ever, demand angiographic visualization of the complete
arterial and venous trees of the extremity. When an arte-
rial stenosis proximal to the AV anastomosis is ruled out
by duplex-ultrasonography with access compression or by
MR angiography, the AV anastomosis and the venous out-
flow are easily visualized by a transbrachial angiography.
In cases with a severe steal syndrome, forearm, hand and
finger arteries can only be opacified when the access is
compressed during dye injection. As a less invasive alter-
native to arterial puncture, contrast media can be injected
directly into the access. With central compression of the ac-
cess, the AV anastomosis, the feeding segment of the artery
and the peripheral arterial tree can be visualized.
Treatment options
Arterial inflow obstruction
Proximal arterial stenoses are the cause of access dys-
function in more than 10% of patients [19] and they have
Nephrol Dial Transplant (2008) 23: Editorial Comments
been demonstrated to be present in 25 to 50% of patients
with access-related ischaemia [20,21]. Standard interven-
tions result in immediate relief of symptoms [21]. Arte-
rial inflow obstruction should be treated irrespective of the
severity of steal-induced complaints; not only do they im-
pair the peripheral circulation, they also cause dysfunc-
tion of the vascular access, thus reducing the efficacy of
haemodialysis.
‘Classical’ steal syndrome
Only when inflow stenoses have been ruled out or success-
fully treated, should one classify symptoms of ischaemia as
a steal syndrome in the strict sense. In AV fistulae without
graft, blood flow tends to rise over time. Therefore pa-
tients with fistulae presenting with stage II steal syndrome
require permanent attention by the nephrology team, in
order to detect progression to stage III or stage IV in time.
However, in diabetic haemodialysis patients with signifi-
cant neuropathy, early correction of stage II steal syndrome
should be considered in order to prevent the development
of IMN. Progressive stenosis of the venous anastomosis of
access grafts frequently causes flow reduction as a result of
increased venous resistance. When stage II steal syndrome
occurs early after the creation of a vascular access using a
graft, watchful waiting is justified because symptoms of a
steal syndrome will most likely disappear with time. How-
ever, if such a stenosis has to be treated in a late phase,
simultaneous prophylactic correction of steal should be
considered. The presence of a steal syndrome causing crit-
ical limb ischaemia (stage III or stage IV) or IMN is reason
enough for urgent imaging and treatment—irrespective of
the type of AV access.
Since the early 1970s, banding the access has been the
preferred therapy for the steal syndrome.
Meanwhile therapeutic decisions seem to have become
somewhat more difficult with the advent of surgical proce-
dures such as DRIL and DRAL, PAVA, RUDI and MILLER.
Despite being widely quoted, those techniques are not
necessarily well understood. The following algorithm hope-
fully helps to find the most adequate solution for the prob-
lem of each individual patient. Pre-therapeutic access flow
measurements, although not necessary for the diagnosis of
steal syndrome, have become more and more important for
a differentiated approach. Depending on the flow values
measured, (i) ‘high flow’ (>800 ml/min in native fistulae,
>1200 ml/min in access grafts), (ii) ‘normal flow’ and (iii)
‘low flow associated steal’ (<400 ml/min in native fistulae,
<600 ml/min in access grafts) can be distinguished [22,23].
Ligation
Access ligation will lead to an immediate improvement of
steal syndrome and also to the loss of the access with the
need to create another one, again running the risk of pro-
voking a steal syndrome. Access ligation may be consid-
ered in severe ischaemia or IMN to gain time for a thorough
diagnostic work-up and preferably in a way that later reac-
tivation of the access with simultaneous treatment of the
steal syndrome is possible. However, after ligation, reacti-
21
vation of the fistula will not be possible in many cases due
to thrombosis. Thus a better alternative to ligation seems to
be to quickly perform the examinations needed for planning
the treatment, and to treat the steal syndrome immediately
afterwards with one of the procedures described below.
Access ligation can of course be performed when a steal
syndrome develops after successful kidney transplantation.
It is imperative when other corrective procedures are not
suitable or have failed.
Banding
Access banding aims at creating a narrow vessel segment
within the access, close to or at the AV anastomosis. Native
fistulae can be banded by non-absorbable sutures, small
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caliber interposition grafts or by narrowing the vein with
a tight Dacron or polytetrafluoroethylene (PTFE) cuff. In
prosthetic accesses, interposition of a short tapered graft
segment has been suggested [5,6,17,20,22,24].
Banding aims at a reduction of access flow. Thus it
can successfully be performed only in patients with a high
flow associated steal syndrome. Banding a low flow access
to a degree where steal syndrome disappears will result
in inefficient dialysis or even access thrombosis. In some
earlier series, banding was controlled only by intraoperative
tcpO2 measurements. Steal was cured in 90 to 100% of
patients, but only 10 to 40% of the banded accesses re-
mained patent (Table 2 , [5,6,20]). When the use of band-
ing is restricted to high flow associated steal syndromes
and when the degree of banding is controlled by intraoper-
ative flow measurements (aiming at ∼400 ml/min in native
fistulae and ∼600 ml/min in access grafts), postoperative
access patency rates are obviously much better (Table 2,
[22,25]).
DRIL and DRAL
In 1988, Schanzer et al. introduced the distal
revascularization-interval ligation (DRIL) procedure [26]
to the treatment of access-associated steal syndrome. The
artery distal to the access anastomosis is ligated. Thereby
retrograde diastolic inflow into the fistula—the pathophys-
iologic principle of steal—is stopped. This first part of the
DRIL procedure is completely sufficient for the treatment
of steal syndrome in distal radio-cephalic fistulae (distal
radial artery ligation, DRAL), as long as the ulnar artery
and the palmar arch are patent, thereby providing sufficient
blood flow to the hand [27]. In brachial AV fistulae and
grafts, a (vein) bypass is additionally implanted, connecting
the brachial artery above the anastomosis with the antecu-
bital artery (or one of the forearm arteries) distal to the
ligation, which now is situated in the ‘interval’ between
the access anastomosis and the distal bypass anastomo-
sis. Functioning vein valves in the graft and a reasonable
distance (>5 cm) between the proximal bypass anastomo-
sis and the access anastomosis prevent retrograde diastolic
flow in the graft. The DRIL procedure has been shown to
result in immediate relief of signs and symptoms of the steal
syndrome in the great majority of patients, and provides
22 Nephrol Dial Transplant (2008) 23: Editorial Comments
Table 2. Treatment results of steal syndrome

Author, year [ref.] Number of patients Free of symptoms (%) Access patent (%)

Banding Odland et al., 1991 [6] 16 100 40

DeCaprio et al., 1997 [20] 11 91 10
Morsy et al., 1998 [5] 6 100 33
Aschwanden et al., 2003 [25] 3 100 100
Zanow et al., 2006 [22] 77 86 91a 58b
DRIL Schanzer et al., 1992 [11] 14 93 82
Haimov et al., 1996 [14] 23 96 73
Katz et al., 1996 [28] 6 83 100
Berman et al., 1997 [9] 21 100 94
Lazarides et al., 1998 [4] 7 94 –
Stierli et al., 1998 [31] 6 100 100
Knox et al., 2002 [10] 52 90 83
Korzetz et al., 2003 [29] 9 89 100
Sessa et al., 2004 [30] 18 100 94
PAVA Zanow et al., 2006 [23] 30 84 87

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a One-year patency rates of banded autogenous fistulae.
b One-year patency rates of banded access grafts.

excellent long-term patency rates for both vein bypasses
and accesses (Table 2, [4,9–11,14,28–31]).
From a pathophysiologic point of view, DRIL seems to
be the ideal treatment of steal syndrome. There are, how-
ever, several disadvantages. DRIL is a rather complex and
time-consuming procedure, which is possible only when a
suitable vein can be harvested. Blocking retrograde inflow
into the access and bypassing blood around it might reduce
access flow by 25% or even more. This makes the DRIL
procedure a valuable option only for patients with high flow
and normal flow associated steal syndrome. In low flow as-
sociated steal syndrome, it has been suggested to perform
the bypass without interval ligation [32]. Clinical results,
however, have not been published thus far.
PAVA
especially in patients without a suitable bypass vein and in
patients with a graft access. A potential drawback of the
method is that when it is applied to an autogenous fistula,
the fistula is turned into a semi-prosthetic access with the
consecutive risk of stenosis at the graft-to-vein anastomo-
sis. On the other hand, there should also be a considerable
risk of stenosis at the distal anastomosis of the vein bypass
in DRIL. Comparative studies are lacking.
Haemodynamically, PAVA is very similar to DRIL be-
cause as in DRIL, a proximal diversion of flow is created.
However, when the central anastomosis of the interposition
graft in PAVA is created on the central brachial or axil-
lary artery and when the graft used for feeding the access
has a diameter of 5 or 6 mm, PAVA enhances access flow
[23,32]. Therefore in low flow associated steal syndrome,
PAVA seems to be the best if not the only option to preserve
both the access and the extremity.

Another method to treat the steal syndrome is to create

a new, markedly more proximal arteriovenous anastomo-
sis (PAVA). The original AV anastomosis is ligated and
an interposition graft is used to connect the access vein or
graft with the feeding artery far centrally, the distal brachial
artery in the case of a wrist fistula, the proximal brachial
or even the axillary artery in the case of an upper arm
access. Thereby larger collaterals from the upper arm are
recruited enhancing peripheral blood supply. Although the
PAVA procedure has been widely used to treat steal syn-
drome, systematic studies have rarely been published. In
their outstanding prospective series of 30 patients, Zanow
et al. [23] reported a complete relief of ischaemic symp-
toms in 84% of their patients with excellent access patency
rates (Table 2).
The PAVA procedure has several advantages over DRIL.
There is no need for vein harvesting because a PTFE graft
can be used for proximal feeding of the access. The anasto-
moses of the graft to the larger vessels are easier to suture
than those of the vein bypass to tiny and often calcified
forearm vessels in DRIL. Thus PAVA is a valuable alter-
native to DRIL in normal flow associated steal syndrome,
RUDI
In the case of high flow induced cardiac failure due to a
brachial AV access, closing the anastomosis in the antecu-
bital fossa and interposing a graft between the forearm ulnar
or radial artery has been shown to effectively reduce access
flow by more than 50% [33]. Minion et al. [34] recently
published a small series of four patients with brachial AV
access-induced steal syndrome, in whom they successfully
used the same technique, which they called ‘revision using
distal inflow’ (RUDI). Unfortunately pre- and postoperative
flow rates were not reported.
The RUDI procedure may be an alternative to banding
in high flow associated steal syndrome, but it should be
used only if the forearm artery not used for distal inflow is
patent; otherwise there would be a high risk of persisting
steal. RUDI is somewhat more invasive than most banding
procedures, and flow reduction cannot be tailored to the
individual patient’s needs, but it lengthens the needling area
of the access.
Nephrol Dial Transplant (2008) 23: Editorial Comments
MILLER
Minimally invasive limited ligation endoluminal-assisted
revision (MILLER) for the treatment of access-induced
steal syndrome was recently described by a group of
US interventional nephrologists [35]. In 16 patients with
brachial AV accesses, they exposed the access vein or
graft proximal to its anatomosis to the artery and per-
formed banding by tying a non-resorbable suture around
the access over an inflated 4 or 5 mm dilatation balloon
under fluoroscopic control to gain a defined reduction in
the vessel diameter. Pre- and postoperative flows were not
measured.
The MILLER procedure is no more than a simplified
banding procedure and should therefore (if at all) be used
only in high flow associated steal. It can be performed
quickly and easily in the radiology unit immediately after
diagnostic angiography for the evaluation of steal. Banding
an access to a defined diameter, however, bears the risk of
inadequate post-interventional access flow or inadequate
therapy of steal symptoms. As already stated above, pre-
and per-interventional flow measurements would enhance
therapeutic certainty.
Conclusion
Due to the rise in the median ages of incident and prevalent
haemodialysis patients and due to the growing percent-
ages of diabetics among them, access-related ischaemia
has become a growing problem. While arterial inflow ob-
structions causing ischaemia and access failure can often
be treated interventionally, the ‘classical’ steal syndrome
mostly requires surgery. Access-associated steal syndrome
in this strict sense is basically caused by a significant
rise in peripheral arterial resistance. Pre- and intraopera-
tive flow measurements are essential for differentiated and
successful therapy aiming at the preservation of access and
extremity.
Banding the access is only indicated in high flow associ-
ated steal syndrome. The DRIL procedure is very effective
in the treatment of high flow and normal flow associated is-
chaemia, but is rather complex and time-consuming. PAVA
is equally effective and at the same time less invasive and
easier to perform than DRIL. PAVA is the only option to
optimize both access flow and peripheral circulation in low
flow associated steal syndrome, which is becoming more
and more frequent among our haemodialysis population due
to the rising proportion of elderly and diabetic patients. A
potential drawback of the method is that when it is applied
to an autogenous fistula, the fistula is turned into a semi-
prosthetic access, with the consecutive risk of stenosis at the
graft-to-vein anastomosis. RUDI and MILLER are modi-
fications of the typical banding procedures. Their relative
importance in the treatment of steal syndrome remains to
be defined.
Conflict of interest statement. None to declare.
23
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Nephrol Dial Transplant (2008) 23: 24–26
doi: 10.1093/ndt/gfm827
Advance Access publication 1 December 2007
Serum intact parathyroid hormone in diabetic patients on
haemodialysis: what is the treatment goal?
Luigi Gnudi
Unit for Metabolic Medicine, Department of Diabetes and Endocrinology, Cardiovascular Division, King’s College London School of
Medicine, Guy’s Hospital, King’s College London, London, UK
Keywords: ; bone osteodystrophy; diabetes; iPTH;
vascular disease
In this issue, Murakami et al. describe an interesting asso-
ciation between intact parathyroid hormone (iPTH) circu-
lating levels and glycaemic control in diabetic patients on
haemodialysis [1]. The findingsdescribe an inverse corre-
lation between iPTH serum levels and glycaemic control.
Specifically, diabetic patients with poor glycaemic control
(HbA1c: 7–8%) are characterized by low circulating iPTH,
which is conversely found at higher levels in diabetic
patients with good glycaemic control (HbA1c: 5–6%).
Both elevated and low circulating iPTH levels have been
linked respectively to high and low bone turnover os-
teodystrophy (or ‘adynamic bone disease’) in patients on
Correspondence and offprint requests to: Luigi Gnudi. Unit for Metabolic
Medicine, Department of Diabetes and Endocrinology, Cardiovascu-
lar Division, King’s College London School of Medicine, Guy’s
Hospital, King’s College London, London, UK. Tel: +44-71881939;
E-mail: lugi.gnudi@kcl.ac.uk
Nephrol Dial Transplant (2008) 23: Editorial Comments
interval ligation technique with preservation of vascular access:
description of an 18-case series. Ann Vasc Surg 2004; 18: 685–
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“steal syndrome” induced by arteriovenous grafts for hemodialysis.
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ysis access-related ischemic steal phenomena. Ann Vasc Surg 2004;
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flow arteriovenous fistulas. In: Sommer BG, Henry ML (eds). Vas-
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ligation endoluminal-assisted revision (MILLER) for the treatment
Downloaded from https://academic.oup.com/ndt/article/23/1/19/1927360 by guest on 18 May 2021
of dialysis access-associated steal syndrome. Kidney Int 2006; 70:
765–770
Received for publication: 9.1.07
Accepted in revised form: 4.9.07
haemodialysis [2–6]; despite the fact that iPTH serum
levels are considered important for the understanding of the
mechanisms leading to renal-related bone disease, changes
in iPTH biological action play a significant role in the
pathogenesis of renal osteodystrophy [2]. To further com-
plicate the understanding of the exact pathogenesis of renal
osteodystrophy, studies have shown that high bone turnover
osteodystrophy may present with low PTH levels, and low
bone turnover may occur with a high PTH level.
Hence the rationale for some authors to suggest that bone
biopsy, which is considered by many the ‘gold standard’
diagnostic tool for renal osteodystrophy [2], is required for
the understanding of this complex medical condition.
In haemodialysis patients, diabetes per se has been
associated with lower iPTH levels when compared to non-
diabetic patients [3, 7]. In diabetic haemodialyzed patients,
impaired iPTH secretion appears to be the main determi-
nant responsible for decreased bone turnover and ‘adynamic
bone disease’, as reports have proposed similar degree of
iPTH biological action on bone in the diabetic and
non-diabetic population [3].