Documenti di Didattica
Documenti di Professioni
Documenti di Cultura
to
manage
renovascular
hypertension
An
article
from
the
e-journal
of
the
ESC
Council
for
Cardiology
Practice
Vol.
13,
N
8
-
09
Dec
2014
Dr.
Emma
Tintea
Dr.
Elisabeta
Badila,
FESC
Renal
artery
stenosis
must
be
considered
in
any
patient
with
a
history
of
severe
or
resistant
hypertension,
especially
in
those
associating
a
decline
in
renal
function
or
significant
atherosclerosis
in
other
vascular
territories.
Detailed
here
are
the
initial
work-up,
evaluation
and
imaging
that
should
be
performed
in
all
those
suspected
of
renal
artery
stenosis,
as
well
as
the
intensive
medical
therapy,
monitoring
and
possible
revascularisation,
according
to
the
latest
trials,
that
will
be
necessary.
Table
of
contents
INTRODUCTION
BACKGROUND
Stenosis
Etiology
Pathophysiology
Clinical
clues
Diagnostic
testing
Other
diagnostic
tools
Treatment
Medical
management
Surgical
revascularisation
Angioplasty
Clinical
trials
CONCLUSIONS
REFERENCES
NOTES
TO
EDITOR
Hypertension
INTRODUCTION
A
suspected
case
of
renal
hypertension's
holds
relative
simplicity
in
theoretical
terms
yet
it
masks
a
rather
complicated
situation
in
clinical
practice.
In
theory,
renal
artery
stenosis
results
in
increased
blood
pressure
values
and
declined
renal
function;
as
a
consequence,
removal
of
the
obstruction
(the
stenosis)
should
allow
proper
hypertension
(HTN)
control
and
good
restoration
of
renal
function.
In
clinical
practice,
however,
the
physician
must
make
difficult
decisions,
personalised
for
each
patient.
Questions
are:
BACKGROUND
Renovascular
hypertension
(RVH)
is
the
most
frequent
form
of
secondary
hypertension.
It
is
most
often
diagnosed
among
elderly
patients
and
has
significant
effects
on
prognosis
and
patient
outcomes.
An
increased
risk
of
cardiovascular
(CV)
events
and
death
(16%
per
year,
six
times
more
than
end-stage
renal
disease)
in
patients
67
years
of
age
and
older
with
a
new
diagnosis
of
RVH
was
revealed
on
examination
of
Medicare
records
(1).
Renal
artery
stenosis
causes
clinical
syndromes
that
go
from
asymptomatic
obstruction
(incidental
renal
artery
stenosis)
to
RVH
and
ischemic
nephropathy.
In
turn,
thes
syndromes
are
often
complicated
by
accelerated
CV
disease
-
congestive
heart
failure,
stroke
and
secondary
aldosteronism.
Strictly
speaking
though,
renovascular
hypertension
can
only
be
diagnosed
in
retrospect,
based
on
the
reaction
of
blood
pressure
(BP)
values
to
a
given
therapeutic
intervention
-
to
remove
the
stenosis.
Thus,
RVH
is
correctly
and
properly
diagnosed
6
to
12
weeks
after
an
intervention,
when
BP
is
lower
than
it
was
prior
to
the
intervention,
with
the
patient
taking
the
same
or
fewer
antihypertensive
medications.
STENOSIS
In
contrast
to
the
pathophysiology-based
definition
of
RVH
seen
above,
the
diagnosis
of
renal
artery
stenosis
(RAS)
takes
into
account
several
anatomical
criteria;
classically,
RAS
is
diagnosed
when
a
>75%
narrowing
of
the
diameter
of
a
main
renal
artery,
or
>50%
luminal
narrowing
with
a
poststenotic
dilatation
are
found
(2).
The
distinction
between
RVH
and
RAS
is
important.
There
are
patients
with
advanced
RAS
in
whom
BP
values
are
normal,
and
RVH
patients
who
due
to
ischemic
nephropathy
presumably,
necessitate
surgical
small
kidney
removal
yet
who
do
not
reach
normalisation
of
BP
values
-
only
25%
of
these
patients
do.
Atherosclerotic
disease
of
renal
arteries
may
progress
to
complete
arterial
occlusion.
When
the
entire
renal
parenchyma
is
affected
(i.e.,
in
bilateral
stenosis
or
stenosis
to
a
solitary
kidney),
renal
artery
stenosis
may
cause
severe
deterioration
of
renal
function,
often
referred
to
as
ischemic
nephropathy.
This
represents
an
important
consequence
of
atherosclerotic
renovascular
HTN,
which,
in
many
cases,
may
remain
undetected.
It
is
a
frequent
cause
of
end-
stage
renal
disease
and
is
associated
with
a
poor
prognosis
even
after
initiation
of
renal
replacement
therapy.
ETIOLOGY
Causes
for
renovascular
HTN
are:
Atherosclerotic
RAS
is
the
predominant
lesion
detected
in
patients
over
50
years
of
age;
it
frequently
affects
the
ostium
and
the
proximal
one-third
of
the
renal
artery's
main
branch.
Atherosclerosis
accounts
for
nearly
90%
of
renovascular
hypertension.
Many
individuals
with
atherosclerotic
renal
artery
lesions
have
years
of
preexisting
essential
hypertension,
active
smoking
history,
and
coexisting
diabetes
mellitus.
The
true
prevalence
of
atherosclerotic
renal
artery
disease
in
the
general
population
is
unknown.
In
selected
populations
displaying
atherosclerotic
disease
of
other
vascular
territories,
prevalence
is
around
10-30%
(4).
One
must
note
that
even
among
those
in
whom
RAS
is
documented,
only
in
some
of
these
patients
does
the
stenosis
have
pathophysiological
significance,
thus
explaining
the
highly
heterogeneous
outcomes
of
studies
investigating
benefits
of
renal
revascularisation.
Fibromuscular
dysplasia
(FMD)
is
a
noninflammatory,
nonatherosclerotic
vascular
disease
that
preferentially
affects
small
-
to
medium
-
sized
arteries.
Most
FMD
lesions
are
caused
by
medial
fibroplasia,
consisting
of
banded
lesions
in
the
mid
portion
of
the
renal
arteries.
Fibromuscular
dysplasia
may
generally
occur
in
any
vascular
territory,
including
the
coronary
bed,
but
usually
affects
the
renal
arteries.
Most
frequently
fibromuscular
dysplasia
is
located
in
the
distal
two-thirds
of
the
renal
arteries,
their
secondary
or
distal
branches.
Screening
angiography
in
potential
kidney
donors
indicates
that
such
lesions
can
be
asymptomatic
and
may
be
detected
in
up
to
3%
to
6%
of
normotensive
individuals
(5).
When
they
reach
sufficient
hemodynamic
severity
to
produce
renovascular
hypertension,
they
most
commonly
affect
women
between
15
and
50
years
of
age.
Screening
angiography
of
a
population
with
resistant
HTN
showed
a
FMD
prevalence
of
16%
(6).
Revascularisation,
in
most
cases,
restores
blood
pressure
values,
and
thus
cures
HTN.
Fibromuscular
dysplasia
occurring
as
an
isolated
disease
does
usually
not
associate
with
renal
failure.
PATHOPHYSIOLOGY
To
make
a
renovascular
hypertension
diagnosis,
RAS
evaluation
is
required
but
not
sufficient.
When
stenosis
is
severe
enough
(i.e.,
when
it
causes
at
least
75%
reduction
in
diameter),
renal
hypoperfusion
and
functional
changes
in
the
affected
kidney
may
ensue,
leading
to
activation
of
the
renin-angiotensin-aldosterone
system,
which
plays
a
central
role
in
the
development
of
RVH.
When
the
stenosis
is
due
to
atherosclerosis,
however,
it
is
sometimes
difficult
or
impossible
to
establish
whether
it
is
the
stenosis
that
is
causing
the
hypertension,
or
whether
the
hypertension
is
preexisting
essential
hypertension.
Under
these
circumstances,
it
may
be
difficult
to
predict
whether
the
revascularisation
procedure
will
lower
blood
pressure.
The
mechanism
is
different
in
unilateral
or
bilateral
renal
artery
stenosis:
In
significant
unilateral
stenosis
the
plasma
renin
activity
increases
as
a
result
of
ischemia
in
the
affected
kidney.
The
activation
of
the
renin-angiotensin-aldosterone
system
(RASS),
leads
to
excessive
secretion
of
angiotensin
II,
with
secondary
vasoconstriction
and
aldosterone,
resulting
in
water
and
sodium
retention.
The
mechanism
was
described
in
1971
and
has
been
referred
to
since
as
"angiotensin-dependent
hypertension
(7).
The
reaction
in
the
contralateral
kidney,
the
pressure
diuresis,
is
however
insufficient
to
counterbalance
the
increase
in
BP
values.
In
the
case
of
bilateral
renal
artery
stenosis,
the
increase
in
angiotensin
II
and
aldosterone
levels
results
in
water
and
sodium
retention;
in
the
absence
of
a
healthy
kidney
to
balance
it,
volume-dependent
HTN
develops
and
suppresses
renin
secretion.
This
hypertension
can
be
converted
back
to
angiotensin
II
dependency
by
sodium
and
volume
depletion.
For
example,
excessive
diuretic
therapy
may
reduce
volemia,
but
restores
renin
secretion,
activates
the
RASS,
which
further
inhibits
sodium
excretion,
thus
leading
to
resistance
to
diuretic
therapy.
CLINICAL
CLUES
Clinical
settings
in
which
RVH
should
be
considered
in
the
differential
diagnosis:
Significant
atherosclerosis
in
other
vascular
territories
(is
associated
with
atherosclerotic
RAS);
Onset
of
HTN
before
the
age
of
30
(consider
FMD)
or
after
55
years
old
(especially
if
there
is
no
family
history
of
hypertension);
Abdominal
bruit
(especially
diastolic
component);
Worsening
of
previously
controlled
hypertension;
History
of
accelerated/malignant
hypertension
or
refractory
hypertension
to
an
appropriate
three-drug
regimen;
Unilateral
small
kidney;
difference
of
>1.5
cm
in
length
between
the
two
kidneys
(renal
ultrasound);
Rapid
deterioration
in
renal
function
(spontaneous
or
in
response
to
ACE
inhibitor
or
ARB);
Recurrent
congestive
heart
failure
or
flash
pulmonary
edema
in
a
hypertensive
patient,
especially
when
left
ventricle
ejection
fraction
is
preserved;
Keith-Wegener-Barker
grade
III
or
IV
fundi;
Angina
without
significant
coronary
artery
disease
in
hypertensive
patients.
DIAGNOSTIC
TESTING
The
screening
tools
developed
for
diagnosis
of
renovascular
HTN
are
either
based
on
physiological
parameters
(e.g.
renin
activity
or
blood
flow
to
each
kidney),
or
on
anatomic
parameters
(CT
angiography
and
MR
angiography),
while
others
combine
some
of
each
(Doppler
ultrasound,
captopril
scintigraphy).
Useful
noninvasive
tools
frequently
used
in
clinical
practice
are:
duplex
ultrasonography
(DUS),
CT
angiography
(CTA)
and
MR
angiography
(MRA).
Arteriography
remains
the
gold
standard
to
RAS
diagnosis,
however
with
a
degree
of
invasiveness
which
prevents
it
from
becoming
a
screening
tool.
Duplex
ultrasonography
It
has
high
sensitivity
(82%)
and
high
specificity
(90%),
and
is
relatively
inexpensive.
It
also
has
its
limits
the
operator
dependent
variability
and
the
technical
difficulties
in
the
case
of
obese
patients
or
in
those
with
overlying
bowel
gas.
There
are
significant
renal
artery
stenoses
of
accessory
renal
arteries
which
may
lead
to
renovascular
hypertension
and
are
difficult
to
identify
in
ultrasound
studies.
Furthermore,
it
may
be
negative
in
patients
with
FMD,
making
other
imaging
modalities
mandatory.
It
is
often
difficult
to
differentiate
using
Doppler
studies
between
a
50-70%
vs
a
>70%
stenosis,
and
thus
the
majority
of
ultrasonographers
use
a
cut-off
value
of
50%
for
significant
stenoses.
In
general
however,
DUS
is
a
reasonable
screening
solution
for
patients
in
whom
there
is
a
clinical
suspicion
of
atherosclerotic
RAS.
Significant
RAS
stenosis
is
diagnosed
in
the
presence
of
a
velocity
ratio
between
the
renal
artery
and
aorta
larger
than
3.5.
The
resistivity
index
can
be
used
to
appreciate
the
benefit
of
possible
future
renal
revascularisation
therapy:
an
index
over
0.8
suggests
renal
parenchymal
disease,
which
will
not
improve
with
revascularisation.
Furthermore,
patients
with
kidneys
8
cm
or
less
in
length
have
a
low
probability
to
benefit
from
revascularisation
therapy.
A
more
recent
study
concluded
that
the
resistivity
index
(and
not
post-procedural
HTN)
represents
an
independent
predictor
of
renal
function
and
all-cause
mortality
in
patients
with
RVH
(8).
According
to
European
Guidelines,
DUS
is
recommended
as
the
first-line
imaging
test
to
establish
the
diagnosis
of
RAS
(class
I,
LOE
B)
(9).
A
hypertensive,
diabetic
insulin-dependent
female
patient
with
coronary
heart
disease
70%
stenosis
on
first
segment
of
left
anterior
descending
coronary,
with
uncontrolled
hypertension.
CTA
reveals
an
abdominal
aorta
with
severe
parietal
calcifications.
Main
right
renal
artery
ostial
and
juxtaostial
calcification,
without
significant
stenosis.
Left
renal
artery
presents
a
3
mm
in
length
severe
stenosis,
9
mm
from
its
emergence
from
the
aorta,
with
a
75%
obstruction
on
CT
evaluation,
with
mild
post-stenotic
dilatation.
(Images
from
authors'
personal
collection)
Figure
2.
Digital
substraction
renal
angiograms
from
the
same
patient
as
Fig.
1.
A
Before
angioplasty.
B
After
left
renal
angioplasty.
(Images
from
authors'
personal
collection)
Angiography
Renal
angiography
is
the
gold
standard
for
renal
artery
imaging.
Nearly
all
authorities
also
agree
that,
presuming
all
other
criteria
are
met,
individuals
who
have
a
very
high
absolute
risk
of
renal
artery
stenosis
or
renovascular
hypertension
should
proceed
directly
to
renal
angiography,
rather
than
undergo
an
imperfect
screening
test.
The
limitations
come
from
the
degree
of
invasiveness,
which
prevents
it
from
becoming
a
screening
tool,
and
the
use
of
iodine
contrast
which
have
the
risk
of
inducing
renal
failure
and
anaphylaxis.
When
the
clinical
index
of
suspicion
is
high
and
the
results
of
non-invasive
tests
are
inconclusive,
digital
subtraction
angiography
is
recommended
as
a
diagnostic
test
(prepared
for
intervention)
to
establish
the
diagnosis
of
RAS
(class
I,
LOE
C).
TREATMENT
The
purpose
of
therapy
in
patients
with
renal
artery
disease
is
to
control
blood
pressure
and
preserve
renal
function.
Currently,
there
is
ongoing
controversy
regarding
therapeutic
management
of
patients
with
RAS,
both
regarding
the
method
used
for
revascularisation
and
its
actual
benefit
in
practice.
If
HTN
control
cannot
be
achieved
or
a
decline
in
renal
function
is
evident,
revascularisation
should
be
more
strongly
considered.
The
table
below
shows
the
clues
that
may
help
with
this
decision,
personalised
according
to
characteristics
of
each
patient.
Table
1.
Factors
influencing
patient
selection
for
revascularisation
(2)
Positive
(favorable)
response
expected
after
revascularisation
Recurrent
flash
pulmonary
edema
Refractory
hypertension
despite
appropriate
three-drug
regimen
MEDICAL
MANAGEMENT
Publication
of
results
from
most
recent
clinical
trials
indicate
the
intensification
of
antihypertensive
therapy
and
the
control
of
additional
risk
factors
(smoking
cessation,
glycemic
control,
pharmacologic
therapy
using
aspirin,
statins)
(13).
All
patients
with
atherosclerotic
RAS
should
be
treated
according
to
the
European
Guidelines
on
Cardiovascular
Disease
Prevention
(14).
Medical
therapy
remains
the
cornerstone
of
treatment
for
renal-artery
stenosis
(15).
ACE
inhibitors,
angiotensin
II
receptor
blockers
and
calcium
channel
blockers
are
effective
in
the
treatment
of
hypertension
in
the
presence
of
unilateral
RAS
and
may
lead
to
slowing
of
the
progression
of
renal
disease
(class
I,
level
B).
The
major
risk
of
current
pharmacologic
therapy
resides
in
the
decline
of
renal
function,
a
clinical
situation
often
encountered
when
introducing
an
ACE
inhibitor
or
ARB.
These
drugs
are
efficient
antihypertensives
in
86-92%
of
RVH
patients,
usually
in
combination
with
a
calcium
antagonist
and
a
diuretic.
ACEIs
and
ARBs
are
generally
well
tolerated,
with
only
5%
of
cases
requiring
cessation
during
the
first
three
months.
A
significant
(over
30%)
fall
in
GFR
(or
an
over
0.5
mg/dL
rise
in
serum
creatinine)
may
be
an
indication
to
consider
renal
revascularisation.
ACE
inhibitors
and
ARBs
are
contraindicated
in
the
case
of
bilateral
RAS
and
when
this
lesion
affects
a
single
functional
kidney.
There
is
evidence
that
thiazides,
hydralazine,
and
beta-blockers
are
also
effective
in
achieving
target
blood
pressure
in
individuals
with
RAS
(16).
SURGICAL
REVASCULARISATION
Currently,
surgical
revascularisation
is
seldom
practiced
as
the
number
of
angioplasty
procedures
has
been
increasing.
By-pass
procedures
from
nonaortic
donor
sites
(splenic,
celiac,
mesenteric,
or
hepatic
artery)
are
more
agreeable
than
the
traditional
aortic-renal
by-pass
and
the
renal
endarterectomy
(for
technical
and
anatomic
reasons).
These
procedures
limit
aortic
manipulation
and
minimize
atherosclerotic
emboli
formation,
with
the
disadvantage
of
an
increased
perioperatory
mortality
rate
(2-6%)
mainly
secondary
to
graft
failures
or
other
complications
of
widespread
atherosclerotic
vascular
disease.
Surgical
revascularisation
may
be
considered
for
patients
undergoing
surgical
repair
of
the
aorta,
patients
with
complex
anatomy
of
the
renal
arteries,
or
after
a
failed
endovascular
procedure
(class
IIb,
level
C).
A
metaanalysis
of
47
retrospective
or
nonrandomized
studies
compared
the
outcomes
in
patients
subjected
to
surgical
revascularisation
vs
patients
subjected
to
endovascular
procedures.
The
results
showed
similar
technical
success
rates,
better
long-term
BP
control
and
renal
function,
but
slightly
higher
perioperative
mortality
(attributed
to
concomitant
aortic
surgery)
(17).
ANGIOPLASTY
The
renal
percutaneous
transluminal
angioplasty
(RPTA)
is
an
accepted
and
durable
treatment
strategy
when
the
etiology
of
RVH
is
fibromuscular
dysplasia.
The
rate
of
restenosis
varies
in
the
range
of
5
to
11%
after
one
year
(18).
In
atherosclerotic
renal
artery
disease
the
role
of
interventional
therapy
is
a
subject
of
controversy,
as
trials
so
far
have
not
proven
significant
clinical
benefits.
Angioplasty
for
an
ostial
lesion,
for
sequential
stenoses
of
a
single
artery,
or
for
stenoses
in
multiple
renal
arteries
on
the
same
side,
are
all
associated
with
an
even
poorer
response.
Expert
opinion,
especially
from
the
fields
of
Cardiology
and
Interventional
Radiology,
argue
that
revascularisation
offers
the
potential
to
improve
or
reverse
renovascular
hypertension,
to
salvage
or
preserve
the
renal
circulation
and
renal
function,
and
to
improve
the
management
of
patients
with
refractory
forms
of
congestive
heart
failure
(19).
Many
nephrologists
however
argue
that
renal
revascularisation
does
not
offer
major
benefits
in
the
control
of
HTN
and
that
the
periprocedural
risk
for
complications
is
larger,
including
the
less
frequent
renal
function
decline
secondary
to
atherosclerotic
embolization.
In
observational
series,
technical
failures
(~19%),
restenosis
(~13%),
and
persistently
elevated
BP
(~35%)
were
more
common.
Angioplasty
plus
stenting
would,
in
theory,
have
more
advantages,
especially
when
carried
out
in
locations
at
high
risk
for
restenosis.
The
largest
experience
published
to
date
comes
from
Durros
et
al.
In
this
study,
after
a
4
years
follow-up,
patients
treated
with
a
specific,
early
renal
artery
stent,
registered
a
significant
decrease
in
blood
pressure
values,
a
small
decrease
in
number
of
antihypertensive
drugs
needed
for
HTN
control,
with
an
overall
mortality
rate
of
26%.
Restenosis
rate
varied
from
10%
to
30%,
depending
on
the
type
of
stenosis
and
length
of
follow-up
(20).
According
to
the
current
ESC
Guidelines
on
the
management
of
PAD,
in
the
case
of
indication
for
angioplasty,
stenting
is
recommended
in
ostial
atherosclerotic
RAS
(Class
I,
LOE
B).
In
all
other
clinical
situations
discussed
within
the
Guidelines
the
level
of
recommendation
is
Class
IIb:
angioplasty,
preferably
with
stenting,
may
be
considered
in
the
case
of
>60%
symptomatic
RAS
secondary
to
atherosclerosis;
endovascular
treatment
of
RAS
may
be
considered
in
patients
with
impaired
renal
function.
Treatment
of
RAS,
by
balloon
angioplasty
with
or
without
stenting,
may
be
considered
for
patients
with
RAS
and
unexplained
recurrent
congestive
heart
failure
or
sudden
pulmonary
edema
and
preserved
systolic
left
ventricular
function.
CLINICAL
TRIALS
Three
studies
have
compared
initial
angioplasty
without
stenting
with
medical
therapy:
EMMA
(Essai
Multicentrique
Medicaments
vs
Angioplastie)
(21),
the
Scottish
and
Newcastle
Renal
Artery
Stenosis
trial
(22)
and
DRASTIC
(the
Dutch
Renal
Artery
Stenosis
Intervention
Cooperative)
(23).
After
combining
the
results
of
these
trials,
patients
subjected
to
angioplasty
had
a
small
decrease
in
BP
values
(6.3/3.3
mmHg,
p
0.02/0.03)
when
compared
to
those
receiving
pharmacologic
treatment,
with
a
less
than
significant
change
in
serum
creatinine
(p
0.06)
(24).
Since
2009,
results
have
been
published
from
new
trials
comparing
best
medical
therapy
versus
angioplasty
with
stenting.
However,
no
significant
benefits
were
seen
in
revascularisation
therapy
of
RAS.
The
ASTRAL
(Angioplasty
and
Stenting
for
Renal
Artery
Lesions)
trial,
published
in
2009,
was
based
on
the
hypotheses
that
interventional
therapy
delays
the
decline
in
renal
function.
Thus,
806
patients
were
randomised
to
either
receive
best
medical
treatment
plus
revascularisation,
or
best
medical
therapy
alone
(25).
Study
results
were
negative.
However,
it
should
be
noted
that
the
study
did
not
include
patients
with
flash
pulmonary
edema,
critical
RAS
and
very
severe
or
uncontrolled
hypertension;
intervention
in
these
subsets
of
patients
is
not
supported
by
a
high
level
of
evidence
but
is
often
performed
in
clinical
practice.
Moreover,
the
primary
goal
of
this
trial
was
to
follow-up
on
the
decline
rate
of
renal
function
and
not
HTN
control
after
the
intervention.
The
STAR
(Stent
Placement
in
Patients
With
Atherosclerotic
Renal
Artery
Stenosis
and
Impaired
Renal
Function)
trial
conducted
on
a
significantly
smaller
number
of
patients
(140)
offered
similar
results
(26).
The
most
recently
published
trial
on
this
topic,
the
CORAL
(Cardiovascular
Outcomes
in
Renal
Atherosclerotic
Lesions)
trial
included
947
patients
with
RAS
and
significant
HTN
(on
two
or
more
antihypertensive
drugs)
who
were
then
randomised
to
receive
either
medical
therapy
alone
or
medical
therapy
plus
renal
stenting
(27).
Even
though
CORAL
included
only
patients
with
a
significant
renal
artery
stenosis
of
at
least
60%
of
the
diameter
(as
opposed
to
the
40%
cut-off
value
used
in
the
ASTRAL
and
STAR
trials),
no
clinical
benefit
was
proven
for
stenting.
This
trial
concludes
that
implanting
stents
for
moderately
severe
obstructive
renovascular
disease
is
no
better
than
medical
therapy
alone
in
preventing
the
primary
end
point
of
death
from
cardiovascular
or
renal
causes,
myocardial
infarction,
stroke,
hospitaliation
for
heart
failure,
progression
of
renal
failure,
or
the
need
for
renal-replacement
therapy.
In
canine
models,
only
stenoses
75%
of
diameter
determine
HTN
and
only
those
80%
are
associated
with
a
decline
in
renal
function
(28).
The
degree
of
stenosis
that
causes
a
switch
from
aerobic
to
anaerobic
metabolism
in
renal
tubular
cells
and
results
in
the
commonly
discussed,
but
poorly
defined,
condition
of
ischemic
nephropathy
has
not
been
determined.
In
clinical
practice,
results
after
intervention
vary
significantly
from
a
slight
improvement
to
a
lack
of
response
or
even
worsening
of
the
condition.
When
interpreting
these
results,
one
must
consider
the
causality
between
atherosclerotic
renal
artery
disease
and
hypertension
or
renal
failure
(or
even
both).
In
summary,
in
the
care
of
atherosclerotic
RAS
patients
with
refractory
HTN,
recurrent
or
refractory
congestive
heart
failure,
or
worsening
renal
function,
renal
revascularisation
may
be
considered,
keeping
in
mind
all
uncertainties
above
mentioned.
Until
new
treatments
are
found
to
be
safe
and
effective,
patients
in
everyday
practice
who
have
moderately
severe
atherosclerotic
renovascular
disease
and
either
hypertension
or
stage
3
chronic
kidney
disease,
should
receive
medical
therapy
to
control
blood
pressure
and
prevent
the
progression
of
atherosclerosis.
CONCLUSIONS
Renal
artery
stenosis
must
be
considered
in
any
patient
with
a
history
of
severe
or
resistant
HTN,
especially
in
those
associating
a
decline
in
renal
function
or
significant
atherosclerosis
in
other
vascular
territories.
Initial
work-up
must
include
renal
function
evaluation
and
lipid
profile,
followed
by
a
DUS
evaluation.
If
high-quality
duplex
imaging
is
not
available,
then
CTA
or
MRA
may
be
appropriate.
From
a
therapeutic
standpoint,
patients
with
FMD
benefit
from
angioplasty.
Intensive
medical
therapy,
including
tight
control
of
BP
with
a
regimen
that
includes
a
blocker
of
the
reninangiotensinaldosterone
system,
is
appropriate.
Serum
creatinine
and
serum
potassium
must
be
closely
monitored
especially
at
drug
therapy
initiation
and
at
drug
dosage
increments.
Furthermore,
patients
with
RAS
must
receive
maximal
medical
treatment,
including
an
antiplatelet
agent
and
a
statin,
with
care
given
to
the
treatment
of
diabetes,
if
present.
The
role
of
revascularisation
in
the
treatment
of
atherosclerotic
renal-
artery
stenosis
is
still
controversial.
Recently
published
trials
did
not
prove
superiority
of
interventional
therapy,
but
most
authors
recommend
angioplasty
with
or
without
stenting
when
HTN
control
cannot
be
achieved,
if
renal
function
is
declining
and
in
patients
with
flash
pulmonary
oedema.
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NOTES
TO
EDITOR
Elisabeta
Badila
MD,
PhD,
FESC
University
of
Medicine
and
Pharmacy
Carol
Davila
Emergency
Clinical
Hospital
of
Bucharest
Bucharest,
Romania
Emma
Tintea,
MD,
PhD
student.
University
of
Medicine
and
Pharmacy
Carol
Davila
Emergency
Clinical
Hospital
of
Bucharest
Bucharest,
Romania
Authors'
disclosures:
None
declared.
The
content
of
this
article
reflects
the
personal
opinion
of
the
author/s
and
is
not
necessarily
the
official
position
of
the
European
Society
of
Cardiology.