Overview
Renal Artery Stenosis
1. Clinical Overview
Summary
Renal artery stenosis (RAS) is narrowing of one or both renal arteries leading to renal hypoperfusion, activation of the renin-angiotensin-aldosterone system (RAAS), and secondary hypertension. The two main causes are atherosclerosis (most common) and fibromuscular dysplasia (FMD).
Key Facts
| Aspect | Detail |
|---|---|
| Primary Mechanism | Renal hypoperfusion → RAAS activation → Hypertension |
| Most Common Cause | Atherosclerosis (90%) - proximal renal artery |
| Classic Patient (Athero) | Elderly male with diffuse atherosclerotic disease |
| Classic Patient (FMD) | Young female, "string of beads" on imaging |
| Prevalence | 1-5% of all hypertension cases |
Clinical Pearls
- Flash Pulmonary Oedema: Sudden, severe pulmonary oedema in hypertensive patient - think bilateral RAS
- ACE Inhibitor Test: Acute renal failure after starting ACEi/ARB suggests bilateral RAS or RAS in solitary kidney
- Abdominal Bruit: Present in ~50% of significant RAS - listen for it!
- Resistant HTN: RAS is a key secondary cause to exclude in resistant hypertension
2. Epidemiology
Prevalence & Demographics
| Population | Prevalence |
|---|---|
| General hypertensive population | 1-5% |
| Resistant hypertension | 10-20% |
| Patients with PAD | 25-30% |
| Elderly with CKD | Up to 40% |
Risk Factors by Aetiology
| Atherosclerotic RAS | Fibromuscular Dysplasia |
|---|---|
| Age >50 years | Age <50 years |
| Male predominance | Female predominance (9:1) |
| Smoking | Genetic predisposition |
| Diabetes | Often bilateral |
| Dyslipidaemia | May affect other arteries |
| Known PAD/CAD/CVD |
3. Pathophysiology
RAAS Activation Mechanism
Renal Artery Stenosis
↓
Reduced Renal Perfusion Pressure
↓
Juxtaglomerular Cells Sense ↓ Pressure
↓
↑ Renin Release
↓
Angiotensinogen → Angiotensin I
↓ (ACE)
Angiotensin II
↓
┌────────────┬────────────┐
↓ ↓ ↓
Vasoconstriction Aldosterone Sympathetic
Release Activation
↓ ↓ ↓
HYPERTENSION (Secondary)
Atherosclerotic vs Fibromuscular Dysplasia
| Feature | Atherosclerotic | FMD |
|---|---|---|
| Location | Proximal/ostial (within 1cm of aorta) | Mid-distal renal artery |
| Appearance | Eccentric plaque | "String of beads" |
| Progression | Progressive | Usually stable |
| Associated conditions | Diffuse atherosclerosis | May affect carotid, iliacs |
| Treatment response | Variable | Excellent with angioplasty |
Compensatory Mechanisms
- Contralateral kidney compensates (if unilateral)
- GFR maintained by efferent arteriolar constriction (Angiotensin II)
- ACEi/ARB removes this compensation → acute GFR drop
4. Clinical Presentation
Suggestive Clinical Features
| Feature | Significance |
|---|---|
| Resistant hypertension | HTN despite 3+ drugs including diuretic |
| Malignant hypertension | Severe HTN with end-organ damage |
| Flash pulmonary oedema | Sudden onset, bilateral RAS |
| Unexplained azotaemia | Progressive renal impairment |
| Hypertension onset <30 or >55 years | Atypical age |
| Abdominal bruit | Present in ~50% with significant RAS |
Classic Scenarios
| Scenario | Think... |
|---|---|
| Elderly male, resistant HTN, PVD | Atherosclerotic RAS |
| Young woman, HTN, abdominal bruit | FMD |
| Flash pulmonary oedema, HTN | Bilateral RAS |
| Creatinine rises on ACEi | RAS (especially bilateral) |
5. Clinical Examination
Key Examination Findings
| Finding | Location/Method |
|---|---|
| Blood pressure | Often severely elevated, may have asymmetry |
| Abdominal bruit | Epigastric/flank, systolic-diastolic |
| Signs of atherosclerosis | Peripheral pulses, carotid bruits |
| Fundoscopy | Hypertensive retinopathy |
| Fluid status | Pulmonary oedema, peripheral oedema |
Differential Diagnosis of Secondary Hypertension
| Condition | Distinguishing Feature |
|---|---|
| Primary aldosteronism | Hypokalaemia, ↑aldosterone:renin ratio |
| Phaeochromocytoma | Episodic HTN, palpitations, sweating |
| Cushing syndrome | Body habitus, striae, proximal weakness |
| Coarctation | BP difference arms/legs, rib notching |
| OSA | Snoring, daytime somnolence |
6. Investigations
Screening Tests
| Test | Notes |
|---|---|
| U&E | Renal function, hypokalaemia (secondary hyperaldosteronism) |
| Urinalysis | Proteinuria |
| Renal ultrasound | Size discrepancy (>1.5cm difference suggests RAS) |
Imaging Studies
| Modality | Sensitivity | Advantages | Disadvantages |
|---|---|---|---|
| Duplex US | 85-90% | Non-invasive, no contrast | Operator-dependent, obesity limit |
| MRA | 90-95% | No radiation | Gadolinium risk in CKD, overestimates stenosis |
| CTA | 95% | Accurate | Contrast nephrotoxicity, radiation |
| Renal Angiography | GOLD STANDARD | Definitive, allows intervention | Invasive, contrast load |
Diagnostic Criteria
- Haemodynamically significant stenosis: ≥60-70% luminal narrowing
- Or peak systolic velocity ratio >3.5 on Doppler
7. Management
Management Algorithm
Suspected Renal Artery Stenosis
↓
Screening: Duplex US / MRA
↓
┌────┴────┐
↓ ↓
Negative Positive/Equivocal
↓ ↓
Consider other CTA or Renal Angiography
causes ↓
┌───────┴───────┐
↓ ↓
Atherosclerotic FMD
↓ ↓
Medical Therapy First Angioplasty
(CORAL trial) (± Stent rarely)
↓ ↓
Revascularisation if: Excellent
- Refractory HTN outcomes
- Flash pulmonary oedema
- Progressive CKD
Medical Management
| Drug Class | Notes |
|---|---|
| ACEi/ARB | AVOID if bilateral RAS or solitary kidney with RAS |
| CCBs | First-line for BP control |
| Beta-blockers | Safe, effective |
| Diuretics | Thiazides or loop diuretics |
| Statins | All atherosclerotic RAS patients |
| Aspirin | Cardiovascular risk reduction |
Indications for Revascularisation
| Indication | Evidence |
|---|---|
| Fibromuscular dysplasia | Good evidence for angioplasty |
| Flash pulmonary oedema | May benefit from revascularisation |
| Progressive CKD despite medical therapy | Selected cases |
| Refractory hypertension | Selected cases |
CORAL Trial Key Points
- Conclusion: Renal artery stenting + medical therapy NOT superior to medical therapy alone for atherosclerotic RAS
- Implication: Medical therapy is first-line for atherosclerotic RAS
- Exception: Flash pulmonary oedema, rapidly declining renal function may still benefit
8. Complications
Complications of RAS
| Complication | Mechanism |
|---|---|
| Chronic kidney disease | Ischaemic nephropathy |
| Hypertensive emergency | Uncontrolled RAAS activation |
| Flash pulmonary oedema | Bilateral RAS, no escape route for sodium/water |
| Cardiovascular events | Associated atherosclerosis |
| End-stage renal disease | Progressive nephron loss |
Complications of Treatment
| Treatment | Complications |
|---|---|
| ACEi/ARB | Acute renal failure (bilateral RAS) |
| Angioplasty | Renal artery dissection, atheroemboli, contrast nephropathy |
| Stenting | Restenosis (10-20%), stent fracture |
9. Prognosis & Outcomes
Natural History
| Type | Progression |
|---|---|
| Atherosclerotic | Progressive in 50% over 5 years |
| FMD | Usually stable, rarely progresses |
Outcomes with Treatment
| Intervention | Outcome |
|---|---|
| Medical therapy (athero) | BP control in majority, 50% stable renal function |
| Angioplasty for FMD | Cure/improvement of HTN in 60-80% |
| Angioplasty ± stent (athero) | No benefit over medical therapy alone (CORAL) |
Poor Prognostic Factors
- Bilateral disease
- Small kidneys (<8cm)
- Elevated creatinine at baseline
- Proteinuria >1g/day
10. Evidence & Guidelines
Key Guidelines
| Organisation | Guideline | Key Points |
|---|---|---|
| AHA/ACC | Renal Artery Disease (2017) | Medical therapy first-line for athero RAS |
| ESC | PAD Guidelines (2017) | Similar recommendations |
| NICE | Hypertension (2019) | Investigate for secondary causes if resistant HTN |
Landmark Trials
| Trial | Finding |
|---|---|
| CORAL (2014) | Stenting + medical therapy = medical therapy alone for atherosclerotic RAS |
| ASTRAL (2009) | Revascularisation no benefit over medical therapy |
| STAR (2009) | No benefit of stenting in atherosclerotic RAS |
11. Patient / Layperson Explanation
For Patients
What is renal artery stenosis? It's a narrowing of the blood vessel(s) that supply blood to your kidneys. When the kidney doesn't get enough blood, it releases hormones that raise your blood pressure.
Why does this happen?
- In older people: Usually caused by fatty deposits (atherosclerosis) - the same thing that causes heart attacks and strokes
- In younger people (especially women): Can be caused by an abnormality in the blood vessel wall called fibromuscular dysplasia
What are the symptoms? Often there are no specific symptoms, but clues include:
- Blood pressure that's hard to control despite multiple medications
- Sudden episodes of fluid on the lungs
- Worsening kidney function, especially after starting certain blood pressure medications
How is it diagnosed?
- Ultrasound scan of your kidney blood vessels
- Sometimes a CT or MRI scan
- Occasionally a dye test called an angiogram
How is it treated?
- Medications: Blood pressure tablets, cholesterol tablets, and aspirin to protect your heart and kidneys
- Balloon/stent procedure: In selected cases, we may recommend opening up the narrowed artery
- Lifestyle: Stop smoking, healthy diet, exercise
What's the outlook? With good blood pressure control, most people do well. Regular monitoring of your kidney function and blood pressure is important.
12. References
- Cooper CJ, et al. Stenting and medical therapy for atherosclerotic renal-artery stenosis (CORAL). N Engl J Med. 2014;370(1):13-22.
- Wheatley K, et al. Revascularization versus medical therapy for renal-artery stenosis (ASTRAL). N Engl J Med. 2009;361(20):1953-1962.
- Textor SC. Renal Arterial Disease and Hypertension. Med Clin North Am. 2017;101(1):65-79.
- Olin JW, Sealove BA. Diagnosis, management, and future developments of fibromuscular dysplasia. J Vasc Surg. 2011;53(3):826-836.e1.
- AHA Scientific Statement: Renovascular Hypertension. Hypertension. 2017.