Approach

The evaluation of RAS includes consideration of factors in the patient's history and decisions on the appropriate imaging modalities.

History

Age of onset of hypertension may be suggestive of the underlying aetiology of RAS:

  • <30 years suggests fibromuscular dysplasia (FMD).[7][16]

  • >55 years suggests atherosclerotic RAS.[7][16]

Sudden or unexplained recurrent pulmonary oedema is suggestive of RAS:[7][16][17][18]

  • In patients with atherosclerosis, RAS may induce an acute or subacute acceleration of a pre-existing essential hypertension that may precipitate flash pulmonary oedema.

Hypertension (accelerated, malignant, or resistant)

  • Patients with either atherosclerotic or FMD form of RAS can present with severe, progressive, and/or difficult-to-control hypertension, sometimes causing end-organ damage.[7][16][19]

Kidney dysfunction or acute kidney injury:

  • Unexplained kidney dysfunction may result from progressive stenosis or hypertension-related end-organ damage.[2][7]

  • Acute kidney injury can be seen in some patients with bilateral RAS or RAS of a single functioning kidney after starting an ACE inhibitor or angiotensin II receptor antagonist.[2][7][19]

Clinical factors predisposing to atherosclerotic RAS include:[2][19]

  • Multivessel coronary artery disease (CAD)

  • Other peripheral vascular disease (PVD)

  • Unexplained congestive heart failure (CHF)

  • Refractory angina

  • Dyslipidaemia

  • Smoking (implicated in aetiology of both atherosclerotic and FMD types of RAS)[1][14]

  • Absence of family history of hypertension - may be suggestive of RAS as a cause of hypertension.[2][13]

Examination

Given that RAS can only conclusively be diagnosed with imaging, suggestive findings on examination include:

  • Hypertension on BP measurement

  • Abdominal bruit: the finding of an abdominal bruit should raise the suspicion for the presence of RAS[2][7]

  • Other bruits: bruits in other vessels are frequent due to the common pathophysiology and high prevalence of co-existent PVD.[13]

General investigations

  • Serum creatinine to estimate glomerular filtration rate.[1]

  • Serum potassium: hypokalaemia or low-to-normal potassium may suggest activation of the renin-angiotensin-aldosterone system.[7]

  • Urinalysis and sediment evaluation (to exclude glomerular disease): RAS, in the absence of co-existent diabetic nephropathy or hypertensive nephrosclerosis, is typically non-proteinuric without abnormalities in the urinary sediment.[4][20]

Evaluation of secondary causes of hypertension as indicated should be excluded and considered in the differential diagnosis: for example, aldosterone to renin ratio (ratio <20 excludes primary hyperaldosteronism).[7]

Choice of imaging

In addition to basic laboratory data, controversy remains as to what imaging modality is most appropriate. While ultrasonography offers a safe, non-invasive assessment, its sensitivity and specificity are lower than other modalities, and its use provides only indirect evidence of the presence of stenosis. Other non-invasive techniques (i.e., CT angiography or MR angiography) have a risk associated with the use of contrast media (radiocontrast nephropathy and nephrogenic systemic fibrosis, respectively). Conventional angiography, despite its procedural risk (e.g., atheroemboli, bleeding) and the risk of radiocontrast nephropathy, has the advantage of being able to determine the clinical significance of the lesions by measurement of the pressure gradient across a stenotic lesion, and the possibility of concurrently performing endovascular therapy. Alternative imaging modalities that experts might consider in patients with chronic kidney disease (CKD) include non-contrast magnetic resonance angiography[21][22][23] and invasive angiography with carbon dioxide (CO2).[24][25][26]

It is recommended to start with a non-invasive imaging test in patients with a high clinical probability of RAS.

A patient's risk is determined by the clinician's index of suspicion, based on the patient's demographics (onset of hypertension at age <30 years or >55 years), comorbid conditions (PVD, CAD, CVA), and clinical condition (hypertension refractory to >3 antihypertensive agents).

If the results of non-invasive tests are inconclusive and the clinical suspicion for RAS is high, invasive testing is recommended.[Figure caption and citation for the preceding image starts]: Magnetic resonance angiography (3-dimensional volume rendered reconstruction) in a patient with significant bilateral atherosclerotic renal artery stenosis. Arrows indicate proximal bilateral stenosesCourtesy of David J. Sheehan, DO; Radiology Department, University of Massachusetts Medical Center and Medical School [Citation ends].com.bmj.content.model.Caption@19edd4cf[Figure caption and citation for the preceding image starts]: Magnetic resonance angiography (maximum-intensity projection) in a patient with fibromuscular dysplasia of the renal arteries. Arrow indicates the characteristic irregular contour in the right renal arteryCourtesy of Raul Galvez, MD, MPH and Hale Ersoy, MD; Department of Radiology, Brigham and Women’s Hospital, Harvard Medical School [Citation ends].com.bmj.content.model.Caption@32ae206f[Figure caption and citation for the preceding image starts]: Digital subtraction angiography in a patient with significant atherosclerotic left renal artery stenosis. Panel A, prior to stent placement. Panel B, after successful stent deployment. Arrows indicate the site of stenosis and stent placement in their respective panelsCourtesy of Alvaro Alonso, MD and Scott J. Gilbert, MD [Citation ends].com.bmj.content.model.Caption@268eefa7

Non-invasive imaging

It is reasonable to begin with a renal duplex ultrasound, followed if necessary by CT angiography, MR angiography, or a captopril renal scan. Non-contrast MR angiography sequences can be considered in patients with CKD.[21][22][23]

  • Duplex ultrasound (sensitivity 84% to 98%, specificity 62% to 99%). Can identify discrepancy in kidney size and velocity of renal blood flow.[4][16][20] Ultrasound diagnostic criteria for significant renal artery stenosis are:[27]

    • Renal artery to aorta peak systolic velocity ratio (renal-aortic ratio) >3.5

    • Peak systolic velocity >200 cm/sec with evidence of post-stenotic turbulence

    • End-diastolic velocity >150 cm/sec (>80% renal artery stenosis) when present with a peak systolic velocity of >200 cm/sec

    • Renal resistive index >0.8 was used as a criterion historically, but as resistive index is now known to be influenced by extrarenal factors such as systemic haemodynamics, it is no longer routinely used in the diagnosis of RAS.[28][29]

  • Gadolinium-enhanced magnetic resonance angiography (sensitivity 90% to 100%, specificity 76% to 94%).[2][4][16][20] Noncontrast MR angiography sequences can be considered in patients with CKD.[21][22][23]

  • CT angiography (sensitivity 59% to 96%, specificity 82% to 99%).[2][4][20][30]

  • Captopril renal scan (sensitivity 45% to 94%, specificity 81% to 100%) has a less relevant contemporary role because of its complexity, poor sensitivity, and the availability of easier and more accurate tests.[2][4][20] The American College of Cardiology Foundation/American Heart Association and the European Society of Cardiology/European Stroke Association/European Society of Vascular Surgery do not recommend captopril renal scan for diagnosing RAS.[16][17]

Invasive testing

Conventional angiography:[2][4][20]

  • The most sensitive and specific test for assessing anatomical narrowing of the renal artery.

  • Also allows for therapeutic intervention at the same time.

  • Requires arterial catheterisation and contrast utilisation.

Additional diagnostic modalities may be used during invasive angiography (such as the evaluation of pressure gradients, the use of pressure wires to evaluate lesion physiology, or intravascular ultrasound). Likewise, carbon dioxide angiography may be performed in specialised centres in patients with CKD.[24][25][26]

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