Renal artery disease artery an intestinal artery disease
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Transcript Renal artery disease artery an intestinal artery disease
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
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%