Renovascular Hypertension
Definition

Anatomically evident arterial disease
 Elevated blood pressure
 Goldblatt (1934)
 Cinically atypical
 Secondary to:
– Renin-Angiotensin-Aldosterone
Pathophysiology

Renal artery stenosis
 Ischemia – release of renin
 Renin promotes conversion of angiotensin I
to Angiotensin II
 Angiotensin II – severe vasoconstriction
– Aldosterone release
Pathophysiology

One kidney model (diseased)
– Volume is handled properly
– Non-stenotic kidney
– Vasoconstriction

Two kidney model (both diseased)
– Volume is not handled properly
Unilateral renal ischemia

2 Kidney 1 clip model
 Hypersecretion of renin in one kidney,
suppressed in the other
 Heyperreninemia
 Angiotensin II – vasoconstriction
 Pressure diuresis (excess sodium and water)
Bilateral renal ischemia
1 kidney – 1 clip
 No pressure diuresis
 Aldosterone induced sodium and water
retention

Stages

Immediate
– Hyperreninemia – immediate rise in pressure

Days to weeks
– BP elevated
– Contralateral kidney +/-

Long term
– With other kidney
– Without other kidney
With other kidney….

Volume expansion avoided
 Renin remains high
 Stenotic kidney retains sodium/produces
renin
 Non-stenotic dumps sodium/water/
decreases renin
 Once long term defect reached – benefit of
flow reversal less
Without other kidney…

Sodium and water retention
 Vasopressor effects of angiotensin II
 Renal perfusion maintained
 Renin levels fall
 HTN more dependent upon volume
expansion
…third stage

HTN is unremitting
 Persists after removal of stenosis
 Ischemic nephropathy
Angiotensin II

Vasoconstrictive on both afferent and
efferent arterioles
 Efferent arteriole smaller basal diameter
 Increase in efferent resistance > afferent
 Angiotensin II – mediates release of PGs
and NO which dilate afferent arteriole

Angiotensin II

Reduces renal blood flow
 Decreases the mesangial surface area
– Decreases filtration

Increase in glomerular capillary pressure
– Tends to increase filtration
Healthy Kidney
Fall in BP – activates renin-angiotensin
 Decrease in renal blood flow secondary to
increased afferent resistance
 Preferential increase in efferent resistance

– Increases glomerular hydraulic pressure
– Maintains GFR
Ischemic Kidney

Reduced afferent flow
 Intraglomerular pressure depends upon
Angiotensi II mediated efferent
vasoconstriction
 ACE I – removes efferent vasoconstriction
– Decreases intraglomerular pressure and GFR
– ACE I – decreases renal function and azotemia
Incidence
Older males – proximal aortic disease
 Younger females – distal FMD
 Less common in African - Americans
 US

– 1-5% of HTN in unselected populations
– 30% of HTN in atheropaths
– <1% of all HTN

International
– Possibly less prevalent
Presentation

HTN with azotemia (>1.5 mg/dl) and
modest proteinuria (< 1.5 g/dl)
 HTN with progressive CRI,
 Severe HTN (diastolic > 120 mmHG)
 HTN with asymmetric kidney
 Paradoxical worsening of HTN with
diuresis / ACEI
Presentation

Onset of HTN < 30 y.o., w/o risk factors
 Abrupt onset severe HTN (>160/100)
 HTN resistant to > 3 agents
 Abrupt increase in BP
 HX of smoking, No family Hx
 Systemic PAD with moderate to severe
HTN, > 50 yo
Presentation

Recurrent pulmonary edema with modsever HTN
 Mod to sever HTN in a patient with an
atrophic kidney
Physical Exam

Abdominal bruit
– 46% of pts with RVHT
– 9% of pts with essential HTN

Advanced fundoscopic changes
 Recurrent flash pulmonary edema
Differential
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Arteriosclerosis
Fibromuscular dysplasia
Other congenital disorders
Cholesterol embolic disease
Acute arterial thrombosis
Aortic dissection
Renal artery trauma
Arterial aneurysm
AVM
Polyarteritis nodosa
Aortic stenosis
Takyasu’s arteritis
Renal Vein Renin

Renin release from each kidney
 Ischemic kidney – renal vein 1.5x non
ischemic renal vein
 <10% of healthy patients have a > 1.5 ratio
 ACE I – increases the accuracy
 False positive and false negatives are
common
 Of coures doesn’t work in bilateral disease
Screening

American College of Cardiology and the
AHA
– Screening for RAS
– Only if intervention would be offered
Imaging Studies

MRA
– 96-100% sensitivity, 71-96% specificity
– Not useful in distal disease, FMD

Spiral CT
– Sensitivity 98%, specificity 94%
– If Cr >1.7 mmg/dL 93% and 81%

U/S
– Seensitivity 72-92%
Imaging studies

U/S
– Renal resistance indices (1-end diastolic
velocity/maximum systolic velocity X 100)
– RRI > 80% low likelihood that intervention will be
effective

Renogram with Captopril
– Radioisotope 1)1 kideny accounting for < 40% of total
GFR 2)delayed peak uptake by > 10 minutes
– > 5 min washout in involved side

A\ngiogram
– RAS| > 70%
– Or 50% stenosis with post-stenotic dilation
SLRHC Algorithm

Doppler
 MRA
 DSA - Angiogram
Treatment

Appropriate anti-HTN (no ACE I)
 Smoking cessation
 Antidyslipidemic
 Superiority if surgical intervention vs
medical intervention - unproven
PTA with Stent

Non-total occlusions
 FMD – PTA (no stent)
 FMD “cured” 50-85%, 8-20% with
atherosclerosis
 These numbers are improved with stenting
 Restenosis does occurr
Surgical revascularization

Reserved for pts with occluded main renal
arteries
 Primarily a vein graft
 80-90% benefit with cure or improvement
 Peri-op mortality < 5%