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HYPERTENSION
Dr. Villaflor
February 5, 2016
BLOCK
19
MODULE 04
LECTURE 05
SUMMARY/OUTLINE
I.
Etiology
IV. Diagnosis
a. Renal Artery Stenosis
a. Captopril Renography
b. Fibromuscular Dysplasia
b. Functional Studies
c. Nutcracker Syndrome
c. Anatomic Studies
II. Pathophysiology
V. Treatment
a. Unilateral RAS
VI. Conclusions
b. Bilateral RAS
c. Ischemic Renal Disease
III. Clinical Features
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LEGEND: Lecture Audio &/Box Harrisons 19 Ed Prev yr notes (SGD)
RENOVASCULAR HYPERTENSION
Defined as:
The presence of systemic hypertension due to a stenotic
or obstructive lesion within the renal artery
The mechanism of hypertension is generally related to
activation of the renin-angiotensin system.
Two patients are at risk for this disorder:
o Older arteriosclerotic patients
o Patients with fibromuscular dysplasia
Form of secondary hypertension, accounting for an
estimated 0.5% to 4% of cases in unselected
hypertensive patients
The simultaneous presence of renal artery stenosis (RAS)
and systemic hypertension should not lead to the
conclusion that the patient has RVH;
Strictly speaking, the definitive diagnosis of RVH can only
be made retrospectively when hypertension improves
upon correction of the stenosis
In practice, obtaining complete reversal of
hypertension is rarely possible
Important to recognize that renovascular disease
o Often accelerates preexisting hypertension,
o Can ultimately threaten the viability of the poststenotic kidney and
o Impair sodium excretion in subjects with
congestive heart failure
When to suspect RVH:
o Severe or refractory HPN
o Recent loss of hypertension control
o Recent onset of moderately severe HPN
o Unexplained deterioration of renal function
o Deterioration of renal function associated
with ACE inhibitor
If BP is adequately controlled with a simple antihypertensive
regimen and renal function remains stable, there may be little
impetus to pursue an evaluation for renal artery stenosis
m When we speak of renovascular hypertension, it should
be remembered that if you have RAS (renoarterial
stenosis) you will eventually have renal hypertension.
Page 1 of 9
Post stenotic
dilatation
main RA Branching
points
artery
Others (carotids)
Rare
Frequent
** Important: Please take note of this chart.
Atherosclerosis
FMD
>90%
<20 %
Age
After age 50
Young
More common in
More common in
Gender
males
females
Location
Proximal 1 cm of
Middle of renal
Nutcracker syndrome
A vascular compression disorder and refers to the
compression of the left renal vein between the superior
mesenteric artery (SMA) and aorta. This can lead to renal
Page 2 of 9
Renal Vein
Compression
Pathophysiology
Overview
Unilateral RAS
There seems to be three phases of hypertension in
patients with unilateral RAS:
1. High renin, low volume
2. High/normal renin, elevated plasma volume
3. Irreversible parenchymal HTN
m There is burden on the contralateral kidney
Page 3 of 9
Irreversible parenchymal HTN:
Prolonged exposure to high BP and high levels of ATII
causes widespread arteriolar damage and
glomerulosclerosis in the contralateral kidney
This is likely why RVH secondary to ARAS does not
resolve after revascularization
Hughes et al. showed that corrective surgery for
unilateral RVH was successful in 78% of those with HTN
of less than 5 years duration but in only 25% of those
with HTN of a longer duration
Bilateral RAS
Much less is known about the mechanisms of RVH in
bilateral RAS
The overall picture is a mixed one with both renin and
volume factors playing a role
Evidence suggests there is an increase in effective
circulating blood volume owed to elevated aldosterone
levels and a blunted pressure natriuresis effect
Clinical Features
These patients do not exhibit specific clinical findings and
it is therefore particularly important to identity high-risk
groups in which suspicion of this condition should be
heightened
There are two important ischemic renal syndromes to
consider
1. ARF after the institution of an ACEI
m In a patient with CKD (e.g. those who have a
creatinine (Cr) of 1.2 or CKD 3-4), when you
give ACE inhibitors, it is a must that we
monitor the Cr about 5 days or 1 week after
institution because when there is elevation
of Cr, you have a sign that there is AKI -- you
might be dealing with an ARF or an ischemic
kidney.
This is your worry if you give ACEI/ARBs in
patients with CKD:
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Page 5 of 9
Diagnosis
There are two groups of diagnostic studies used to evaluate
RAS.
Anatomic studies:
Renal angiography gold standard
m This is the gold standard because you want to
look and are looking at the vessels. We
delineate the vessels the renal artery- as it
supplies the kidneys.
Doppler ultrasonography
Spiral CT angiography
MR angiography
Functional studies:
Renal-vein-renin measurement
m Because your arteries are constricted, you
expect that your renin is high. There is actually
measurement of your renal vein renin but it is
invasive.
125
Nuclear imaging with I iothalamate or DTPA to
determine GFR
Conventional renography
ACEI renography
Captopril Renography
Captopril renography is a nuclear study which takes
advantage of the fact ACEI can abruptly reduce function in
an ischemic kidney.
Patients are given radio-labeled agents that are
99
exclusively filtered (Tc -DTPA) thus estimating GFR
99
or agents that are filtered and secreted (Tc -MAG)
131
or I -hippurate) thus estimating RBF
A baseline study is done on day 1 and 50 mg of
captopril is given 1 hr prior to the second study on
day 2
The difference between the left and right kidney
with regard to uptake, excretion, kidney size and
asymmetry can be determined by this study.
99
Either a slowing of the excretion of Tc -DTPA or a
99
reduction of the uptake of the Tc -MAG can be used
to identity the effect of the ACEI in removing the
protective action of high levels of ATII on the
autoregulation of GFR and on maintenance of renal
blood flow.
Diagnostic Study
Sens.
Spec.
PPV
NPV
Renal Vein Renins
62%
70-80%
Doppler
80-98%
98%
99% 88-97%
Ultrasonography
Conventional
75%
85%
33%
Renography
ACEI Renography
75-90%
94%
92%
88%
CT angiography
92%
98%
87%
99%
MRA
100%
93%
90%
100%
Page 6 of 9
CT angiography
MRA
Antihypertensive Drug Therapy
Blockade of the Renin Angiotensin System
o ACE Inhibitors
o Angiotensin Receptor Blockers
o Direct Renin Inhibitors (Aliskiren) [efficacy
questionable]
Calcium Channel Blocking Agents
Diuretics
Mineralocorticoid Receptor Blockade
Additional classes: Beta-blockade, alpha-receptor
blockade, sympatholytic agents, vasodilators
Cardiovascular Risk Reduction
Removal of tobacco use
Treatment of Dyslipidemia: Statins, Fibrates, Others
Treatment of Obesity: Obstructive Sleep Apnea
Management of Glucose Intolerance/ Diabetes
Renal Revascularization
Endovascular revascularization:
o PTRA: Primary Fibromuscular Dysplasia
o PTRA with Stenting: Atherosclerotic Disease
most commonly used treatment for renovascular
HPN
Surgical:
o Renal Artery Bypass/Endarterectomy (reserved
for complex aorto-renal disease, aneurismal
disease, failed endovascular stent procedures,
etc.)
Nephrectomy
Open or Laparoscopic removal of pressor kidney;
usually non-functional
Management for RVH caused by ARAS
No general consensus among physicians on the ideal
therapy for this condition
o Numerous randomized prospective studies have
found no evidence of improvement in BP control in
patients undergoing angioplasty over medical therapy
alone
One of the largest trials,
o The Angioplasty and Stenting for Renal Artery Lesions
(ASTRAL) study,
806 renal failure patients (mean serum creatinine
approximately 2 mg/dL) with atherosclerotic
renal vascular disease included
Randomized to receive either revascularization
and medical therapy or medical therapy alone
On average, patients had 75% RAS
At 1-year follow-up there were no differences in
the change in serum creatinine level (it rose by
0.2 mg/dL in both groups) or in rates of renal
events, including acute renal failure
Currently, at least three major studies are under way to
Excellent
High-contrast
visualization of the requirement
vessels in 3D
Less reliable for
visualizing distal
segments and
small accessory
arteries
Noninvasive
Expensive
Provides excellent Prior stents
images
produce artifacts
Non-nephrotoxic, Blood flow
thus useful in
turbulence can
patients with renal exaggerate
insufficiency
measured stenosis
m If you localize the anatomic lesion, the renal
arteriography is the gold standard because you actually
visualize the artery plus the accessory vessels.
You may see that your main renal artery stenosed
and because your main renal artery is stenosed, you
will develop collaterals because your collaterals will
supply the rest. You have accessory vessels and some
have intrarenal branches. This procedure entails the
use of contrast.
Treatment
To date, there has been no large randomized clinical
controlled trial comparing medical therapy to newer
stenting procedures or surgery
m When you say stent, you place a tube so that you
will be able to dilate the stenosed area. If it is
surgical and you repair it, you cut and you
anastomose.
m For medical therapy, you just control the BP.
In addition, most of the reported date as to therapy have
been non-experimental reports
As result, no improvements in survival, freedom from
dialysis or protection from adverse cardiovascular
disease events have been demonstrated relative to an
equivalent non-interventional comparison group
RENOVASCULAR HYPERTENSION (RVH): MANAGEMENT
Treatment options include
1. Pharmacological
therapy
with
various
antihypertensive medications,
2. Percutaneous angioplasty with or without stent
placement, and
3. Surgical revision of RAS
Availability of potent antihypertensive drugs and the
advances in endovascular techniques, as well as stents, has
made surgical treatment rarely necessary
Page 7 of 9
Conclusions
Natural History and Pathophysiology
ARAS is clearly a progressive disease
The initial degree of stenosis/burden of vascular
disease is most predictive of IRD progression
m So if it is atherosclerotic, since the formation takes a
long time, most likely there is ischemic renal disease.
Once patients with IRD are dialysis dependent, their
prognosis is extremely poor.
The pathogenesis of IRD is multifactorial and predicting
the degree of reversible vs irreversible disease in a
particular patient is challenging.
High RI, slow progression of IRD, significant
proteinuria and advanced age seem to be predictors
of irreversible disease
Normal RI, minimal proteinuria and fast progression
of renal insufficiency seem to be predictors of
reversible disease
m Multifactorial because there is renin, volume,
cardiovascular events that will make the patient
prone to this complication.
2.
Juntado, R. | Lacson | Lagon | Lucero, S.
Pathophysiology of Renovascular Hypertension:
Page 9 of 9