What is renovascular hypertension (RVH)?

Renovascular Hypertension (RVH)

Renovascular hypertension (RVH) is a form of secondary hypertension caused by renal artery occlusion or stenosis that decreases renal perfusion pressure, activating the renin-angiotensin-aldosterone system (RAAS) and thereby raising blood pressure. 1

Etiology

The main causes of renovascular hypertension include:

1. Atherosclerosis (90% of cases):

   • Most commonly affects the aorto-ostial segment and proximal 1 cm of the main renal artery
   • Typically occurs in older adults (>50 years)
   • Often associated with generalized atherosclerotic disease affecting other vascular beds 1

2. Fibromuscular Dysplasia (10% of cases):

   • Non-atherosclerotic, non-inflammatory disease
   • Typically affects middle and distal two-thirds of the renal artery and its branches
   • Most common in young women, though can occur in both genders at any age
   • Medial fibroplasia is the most common histological subtype (80-85% of FMD cases)
   • Often presents with characteristic "string of beads" appearance on angiography 1

3. Less common causes:

   • Renal artery aneurysms
   • Takayasu's arteritis
   • Atheroemboli and thromboemboli
   • Spontaneous renal artery dissection
   • Arteriovenous malformations
   • Trauma (including lithotripsy)
   • Retroperitoneal fibrosis 1, 2

Pathophysiology

RVH develops through the following mechanism:

1. Renal artery stenosis reduces perfusion pressure to the kidney
2. Juxtaglomerular cells release renin in response to decreased pressure
3. Renin catalyzes the conversion of angiotensinogen to angiotensin I
4. Angiotensin-converting enzyme converts angiotensin I to angiotensin II
5. Angiotensin II causes:
   • Peripheral arteriolar vasoconstriction
   • Increased renal tubular sodium and water reabsorption
   • Aldosterone release from the adrenal cortex
   • Increased sympathetic tone
   • Vasopressin release 3

These mechanisms collectively increase blood pressure through arteriolar constriction, enhanced cardiac output, and retention of sodium and water.

Clinical Features Suggesting RVH

• Abdominal bruit
• Malignant or accelerated hypertension
• Significant hypertension (diastolic >110 mmHg) in young adults (<35 years)
• New onset hypertension after age 50
• Sudden development or worsening of hypertension
• Refractory hypertension
• Deterioration of renal function after starting ACE inhibitors or ARBs
• Generalized atherosclerotic disease with hypertension 1

Diagnostic Approach

The diagnostic workup for suspected RVH includes:

1. Initial screening tests:

   • Renal artery Doppler ultrasound (highest recommendation for all patients, including those with decreased renal function) 1
   • MR angiography without contrast (especially in patients with reduced renal function) 1

2. Additional imaging options:

   • CT angiography (in patients with normal renal function)
   • MR angiography with contrast (in patients with normal renal function) 1

3. Definitive diagnosis:

   • Catheter angiography (when clinical suspicion is high and noninvasive tests are inconclusive) 1

4. Not recommended as screening tests:

   • Captopril renal scintigraphy
   • Selective renal vein renin measurements 1

Management Considerations

1. Medical therapy:

   • Calcium channel blockers (both dihydropyridine and non-dihydropyridine) are preferred as they don't interfere with aldosterone-to-renin ratio testing 1, 4
   • Alpha-receptor antagonists can also be used without interfering with testing 1
   • ACE inhibitors and ARBs should be avoided in bilateral renal artery stenosis or unilateral stenosis in patients with a single kidney due to risk of acute renal failure 4, 5

2. Revascularization may be considered for:

   • Refractory hypertension
   • Progressive deterioration of renal function
   • Options include angioplasty (with or without stenting) and surgical revascularization 4

3. Monitoring:

   • Close monitoring of renal function is essential, especially when using RAAS blockers
   • Blood pressure monitoring to ensure adequate control 4

Important Clinical Pitfalls

• RAS doesn't always cause RVH; bystander renal artery stenosis may be present in patients with essential hypertension 1
• A critical diagnostic challenge is determining the hemodynamic significance of RAS; most consider 50-60% stenosis significant, but perfusion pressure is generally not reduced until stenosis exceeds 70-75% 1
• The ultimate defining criterion for true RVH is a fall in blood pressure after intervention (angioplasty, stenting, or surgery) 1
• Bilateral renal artery disease complicates assessment as it's difficult to quantify the effect on blood pressure of one side versus the other 1

Understanding renovascular hypertension is crucial for appropriate management of affected patients, as successful treatment can significantly improve blood pressure control and mortality in selected cases.