Renovascular Hypertension Flashcards
2 main causes of renal artery stenosis?
atherosclerosis (almost always caused by smoking)
fibromuscular dysplasia
What is renovascular disease? Is it always symptomatic?
Any occlusion of renal arteries. No, it’s not always symptomatic, nor does it always cause HTN.
(lots of people only learn they have it when they’re being evaluated as potential kidney donors)
How does location of occlusive lesion vary between atherosclerotic and fibromuscular dysplasia causes of renal artery stenosis?
Atherosclerotic: lesion usually proximal to aorta.
Fibromuscular: lesions distal to aorta.
Is renovascular diasease a common cause of HTN?
How do you know if renal artery stenosis is causing secondary HTN?
(important!)
No - only 1-3% of HTN in the U.S. is caused by renovascular disease.
You don’t know that renal artery stenosis is causing secondary HTN until you fix the stenosis and the HTN goes away!
Important: What is a huge risk factor for atherosclerotic type renovascular disease?
Smoking.
Important: Why should you look for atherosclerotic disease in other organs before you do anything about somebody’s atherosclerotic renovascular disease?
It’s likely there. If you drop somebody’s BP by revascularizing the renal artery, you might cause ischemia of affected organs (eg. brain).
Why does renal artery stenosis increase BP? (you know this)
Renin
3 things that control renin release?
Baroreceptors.
Sympathetic nerves.
Macula densa.
What adrenergic receptor governs sympathetic-driven renin release?
Beta-1
Can antagonize this with beta-blockers.
If renal artery disease is unilateral, how does the unaffected kidney respond? How does this affect the affected kidney?
Normal kidney sees high BP -> pressure natriuresis.
Na+ / volume loss further decreases perfusion of the affected kidney -> more renin release.
On what main factor is the HTN of unilateral renal artery disease dependent? (important!)
Angiotensin II.
If you give an ACE inhibitor or ARB, you’ll drop the BP significantly.
(diuretics won’t help much, as this is a slightly hypovolemic HTN)
How does bilateral renal artery stenosis differ from unilateral in terms of mechanism of HTN?
There’s no normal kidney to cause a pressure diuresis, so renin just causes volume just accumulate.
Increased volume -> increased perfusion of kidneys -> new steady state.
On what factor is bilateral renal artery disease most dependent?
(important!)
Hypervolemia.
Giving an ACE inhibitor / ARB won’t lower BP much until the volume is brought down. Renin is low to normal!
Why is hypervolemia in bilateral renal artery disease bad?
Most worrisome would be pulmonary edema.
Why is medical treatment of HTN secondary to bilateral renal artery disease tricky?
If you give diuretic + ARB, you’ll drop the BP. But the kidneys were dependent on that higher BP for perfusion, so you can see a rapid drop in GFR.
(drop in GFR with anti-hypertensive treatment can be an indication for renal artery revascularization)
Example of an iatrogenic cause of renal artery occlusion?
Aortic stent (for AAA) can occlude one or both renal arteries.
It’s difficult to know when you should revascularize someone with renal artery disease.
it’s true
What’s one common difficulty with knowing if revascularization of a renal artery is indicated?
Degree of stenosis is often overestimated with imaging.
What is potentially a better way to assess the significance of someone’s renal artery stenosis than percent occlusion?
Kidney oxygenation with fancy MR stuff.
How does kidney oxygenation / hypoxia correlate to what you’d see on histology of a biopsy?
More hypoxia -> more scarring, inflammation, badness.
When looking at doppler ultrasound of kidney, is pulsatility in the vessels good or bad? How is this quantified?
Pulsatility is bad.
Pulsatility can be expressed as resistance index… high resistance index = more pulsatility.
What’s the potential utility of calculating the resistance index in a patient with renal artery disease?
Low resistance index may predict improved kidney function revascularization.
Patients with high resistance index don’t have improved kidney function after revascularization.
Hypothesis for why high resistance index predicts poor response to revascularization?
In these kidneys, inflammatory and fibrotic changes may already have permanently impaired kidney function (and also caused increased pulsatility).
