Renal artery stenosis is a well-established cause of secondary hypertension resulting from the activation of the renin-angiotensin system in response to reduced renal blood flow. Atherosclerosis is the most common etiology and is usually suspected in patients over the age of 45, dyslipidemic patients, or smokers. However, other etiologies such as fibromuscular dysplasia in younger patients or Takayasu’s arteritis should be considered. Atherosclerotic stenosis typically affects the proximal main renal artery near the ostium compared to fibromuscular dysplasia which typically affects the distal segments.
Classic presentations include chronic refractory hypertension, recurrent flash pulmonary edema and renal insufficiency- notably after initiating an angiotensin converting enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB). Although rare, there have also been reported cases of pregnant patients presenting with new onset or superimposed preeclampsia secondary to renovascular hypertension [1, 2].
Of the different modalities used to investigate renal artery stenosis, doppler ultrasonography is the safest and has a sensitivity of at least 85%, though it frequently overestimates stenoses as in our case [3, 4]. Magnetic resonance or computerized tomography angiography have superior diagnostic accuracy with a sensitivity of 94% but the gold standard remains conventional catheter based angiography . Supplemental studies such as direct renal vein renin, captopril renography or plasma renin activity to aldosterone ratios may be helpful in diagnostic dilemmas, though not currently routinely recommended .
Treatment may involve aggressive medical therapy with statins, antiplatelets and antihypertensives and/or renal artery revascularization. Historically, ACE-I or ARB therapy has been cautioned especially in bilateral renal artery stenosis because of the possibility of reduced post-stenotic renal perfusion pressures and subsequent ischemic nephropathy and renal failure. However, there have been observational studies suggesting a mortality benefit to closely monitored ACE-I or ARB treatment .
In terms of invasive treatment, percutaneous transluminal renal angioplasty with or without stenting has become the standard versus surgical revascularization. Although a recent systematic review showed only marginal benefit to this approach compared to medical therapy alone, there is evidence that select patient do have significant benefits in blood pressure control [2, 8, 9]. Furthermore, studies have shown that usually at least 80% stenosis is required to produce any significant hemodynamic stimulus to the renin-angiotensin system and thus may be a threshold for invasive treatment [10, 11]. However, as in our case, few patients have been shown to benefit from revascularization at stenoses of as low as 50% [8, 11]. Additionally, these hemodynamic studies were performed in non-pregnant patients. Thus, whilst these data are important to avoid unnecessary procedures, clinical acumen remains necessary for select cases where revascularization of seemingly insignificant stenoses may yet produce a clinical response.
In women with preeclampsia due to renovascular hypertension, there is significant risk for obstetric and medical complications including death especially with severe preeclampsia (blood pressures more than or equal to 160/90 mmHg even without signs of end organ dysfunction or hemolysis). Prompt treatment is required. Yet, the teratogenic risks of radiological investigations and antihypertensive medications such as ACE-I/ARB’s limit diagnostic and management options and pose quite a dilemma. When possible, expedited delivery is beneficial. However, there has been some success with interventional treatment prior to delivery . The high mortality risk of eclampsia continues into the the post-partum period and it is uncertain when blood pressures can be expected to normalize in preeclampsia even in the absence of renovascular hypertension . Therefore, an urgent and aggressive management strategy should be pursued for these patients with consideration for early revascularization if a rapid clinical response is not seen with medical management.