Renal Artery Stenosis Flashcards
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)