Renal Artery Stenosis Flashcards
(10 cards)
Define renal artery stenosis and the criteria that must be met
Narrowing of the renal artery lumen
It is considered angiographically significant if more than a 50% reduction in vessel diameter is present
State and briefly explain the key risk factors for RAS
Dyslipidaemia- leads to atherosclerosis/cholesterol deposition in vessel walls → inflammation and progression of plaque
Smoking- favours endothelial inflammation and dysfunction. Associated with both atherosclerotic and fibromuscular dysplasia (FMD)
Diabetes- causes endothelial dysfunction; major cardiovascular risk factor.
Female sex- less strong. FMD more frequent than in males, atherosclerotic RAS more likely to progress
State 2 key causes of RAS
Atherosclerosis 90% (older patients) -
- widespread aortic disease involving the renal artery ostia, often co-exists with CAD, IHD, stroke or PVD
Fibromuscular Dysplasia 10% (younger patients)
- Unknown aetiology- more common in females
- May be associated with collagen disorders, neurofibromatosis and Takayasu’s arteritis
- May be associated with micro-aneurysms in the mid and distal renal arteries (resembling a string of beads on angiography)
Explain the pathogenesis of RAS
- Renal hypoperfusion (due to the stenosis) stimulates RAAS
- Increased angiotensin II + aldosterone→ increased systemic vascular resistance and sodium retention.
- When the stenosis exceeds 50% reduction in vessel diameter, these regulatory mechanisms fail → worsening kidney function and difficult-to-control hypertension.
- Hypoperfusion, hypertension and AGT2 cause fibrosis, glomerulosclerosis and renal failure
Summarise the epidemiology of renal artery stenosis
- Prevalence unknown
- Accounts for 1-5% of all hypertension
- Fibromuscular dysplasia occurs mainly in women with hypertension < 45 yrs
Recognise the presenting symptoms of renal artery stenosis
- presence of key risk factors- smoking, dyslipidaemia, and diabetes.
- onset of hypertension age >55 years- atherosclerotic RAS.
- history of accelerated, malignant, or resistant hypertension refractory to Tx
- (which becomes worse on starting of ACE inhibitors)
- history of unexplained kidney dysfunction- due to progressive stenosis or hypertension-related end-organ damage
- History of multi-vessel CAD or PVD (suggests atherosclerotic RAS)
- History of flash pulmonary oedema
Recognise the signs of renal artery stenosis on physical examination
Identify appropriate primary investigations for renal artery stenosis
- serum creatinine + potassium
-
urinalysis and sediment evaluation-
- helpful in evaluating for glomerular source of kidney disease.
- In the absence of co-existent diabetic nephropathy or hypertensive glomerulosclerosis, RAS is not associated with proteinuria or abnormalities in the urinary sediment
-
aldosterone-to-renin ratio
- <20 excludes primary aldosteronism as cause of hypertension and hypokalaemia or low-normal potassium
Identify appropriate secondary investigations for renal artery stenosis
Non-Invasive
- Duplex ultrasound- shows the renal arteries and measures flow velocity as a means of assessing the severity of stenosis
- Ultrasound measurement of kidney size
Invasive
- Gadolinium-enhanced MR angiography (MRA): visualises the renal arteries and peri-renal aorta. Risk of contrast nephrotoxicity (contraindicated in stage 4/5 CKD)
- CT angiography- as for above
- Digital Subtraction renal Angiography = GOLD STANDARD (image) – but done after CT/MR as it is invasive
- Renal Scintigraphy
- Uses radio-agent that is either excreted by glomerular filtration or by the tubules
- Addition of an ACE inhibitor causes delayed clearance by the affected kidney (may not be useful in bilateral renal artery stenosis)