Renal artery stenosis Flashcards
Define renal artery stenosis.
Typically due to atherosclerotic disease or fibromuscular dysplasia. Usually caused by over 50% reduction in vessel diameter.
Often presents with accelerated or difficult-to-control hypertension.
What are the causes of renal artery stenosis?
Atherosclerosis (older patients) - 80%- widespread aortic disease involving the renal artery ostia. Endothelial injury due to DM, dyslipidaemia, smoking.
Fibromuscular dysplasia (younger female patients)- 10% – medial fibroplasia in 90%; unknown aetiology. Can be focal or multifocal (“string of beads” appearance)
Other causes of renal artery disease:
- Post-transplant at anastomosis
- Miscellaneous renal arterial disease
- Renal artery aneurysm
- Accessory renal artery
- Takayasu’s arteritis
- Atheroemboli
- Thromboemboli
- Williams syndrome
- Neurofibromatosis
- Spontaneous renal artery dissection
- Arteriovenous malformations
- Arteriovenous fistulas
- Trauma
- Abdominal radiotherapy
- Retroperitoneal fibrosis
What is the pathophysiology of renal artery stenosis?
Renal hypoperfusion stimulates the RAAS leading to increased angiotensin II and increased aldosterone
This leads to increased blood pressure (from increased systemic vascular resistance + sodium retention)
The high blood pressure leads to fibrosis, glomerulosclerosis and renal failure when stenosis exceeds 50% → uncontrollable hypertension.
Bilateral renal artery stenosis causes volume overload and inappropriately high levels of renin.
How common is RAS? Who is affected?
Prevalence of 0.2-0.5% in all hypertensive patients
Depends on cause:
Atherosclerosis (90% of RAS) - 25% of patients undergoing cardiac catheterisation for CAD have RAS
Fibromuscular dysplasia (10% of RAS) - females are 2-10 times more likely to be diagnosed with this type of RAS typically before 30yrs
What are the risk factors for RAS?
- Dyslipidaemia
- Smoking
- PVD/CAD
- Diabetes
- Female sex - fibromuscular dysplasia (FMD) more frequent than in males. In addition, atherosclerotic RAS more likely to progress in this population
What are the signs and symptoms of RAS?
Exclude other causes; confirm RAAS activation with raised low potassium, hypertension, glomerular disease.
- ↑ ↑ ↑ BP refractory to Tx (1-5% of HTN)
- Hx of AKI following ACEi - accelerated HTN and renal deterioration on ACEi/ARB in bilateral RAS. ACEi remove the efferent arterial tone causing hypoperfusion so AVOID
- Hx of unexplained CHF - flash pulmonary oedema (sudden onset, without LV impairment on echo)
- PVD - abdominal ± carotid or femoral bruits, weak leg pulses
- Signs of renal failure in advanced disease
- Onset of hypertension <30yrs
What investigations would you do in RAS?
- Serum creatinine - N or high
- Serum potassium- hypoklaemia in overactivation of renin-angiotensin system
- Aldosterone:renin ratio - should be <20 in RAS; this excludes <20 excludes primary aldosteronism as the cause of HTN and hypokalaemia.
Other:
- Urinalysis/sediment evaluation - normal unless diabetic nephropathy/glomerulosclerosis
- Duplex ultrasound - >50% reduction in vessel diameter and measures flow. AFFECTED kidney is SMALLER.
- Digital subtraction renal angiography = GOLD STANDARD but invasive
- CT angiogram or MR angiography - but risk of nephrotoxicity
What is the management of RAS?
Medical
Antihypertensive therapy - ACEi or ARB; but monitor U&Es closely
Lifestyle modification
+/- Referral to cardiologist/nephrologist
+/- Statin and antiplatelet - in atherosclerotic RAS
Surgical
Renal artery stenting - if refractory to _>_3 medications or having CKD, pulmonary oedema or bilateral RAS.
Post-stent clopidogrel - for length determined by specialist
Percutaneous renal artery balloon angioplasty - for fibromuscular dysplasia associated RAS
What is the management of RAS?
- Progression of stenosis
- Progression of CKD
Medical therapy associated:
- Orthostatic hypotension
- Symptomatic bradycardia
Surgery associated:
- Inguinal haematoma
- Retroperitoneal bleed
- MI or stroke
- Renal artery occlusion
- Re-stenosis
- Atheroembolism
