michigan hypertension core curriculum - State of Michigan

trial, angioplasty resulted in significant reduction in BP and antihypertensive medications in patients
with bilateral ARAS. 61 In a third, 28 % of medical patients crossed over to angioplasty. A contemporary
review of 2 randomized trials, 8 comparative studies, and 34 cohort studies concluded that angioplasty
leads to greater reduction of BP than medical therapy, particularly in patients with bilateral RAS. 63
Several prospective studies and meta analysis documented reduction in BP after renal stenting
16,51,64-72 In the only prospective randomized trial of angioplasty versus stenting in 85 patients, 19
revascularization resulted in significant reduction of systolic (19 mmHg) and diastolic (12 mmHg)
BP. There may be a relationship between renin-angiotensin activation and renal production of brain
natriuretic peptide (BNP), and BNP may predict the hypertension response to renal stenting. 73,74
After ARAS revascularization, hypertension cure (normal BP no medication) is observed in < 10 % of
patients, regardless of revascularization techniques.
RAS and malignant hypertension. The augmented renin and angiotensin II levels in some patients
with stenosis of a solitary kidney or that may occasionally occur in patients with bilateral ARAS may
promote acute volume loading and vasoconstriction, flash pulmonary edema, and other manifestations
of malignant hypertension. 6,75-79 Prevention of recurrent pulmonary edema is a Class I recommendation
for renal revascularization 6 , based on several small studies. 77,79,80,27
Failure of renal revascularization to cure hypertension. The explanations for why renal
revascularization does not cure hypertension are somewhat speculative (Table 8). There is a persistent
misperception that ARAS patients have renovascular hypertension, and contemporary reviews continue
to use this terminology. 2,20 While the experimental Goldblatt models are compelling demonstrations
of renin-angiotensin activation due to RAS 81 , the mechanisms of hypertension in humans with and
without RAS are far more complex, and include sympathetic and cerebral nervous system activation,
vasoactive oxygen species, abnormalities in endothelial dependent relaxation, and ischemic and
hypertensive intra-renal injury. 82-86 Patients with ARAS do not have renovascular hypertension, as
evidenced by similarities in the extent of renin activation compared to hypertensive patients without
RAS 87,88 and the low cure rate of hypertension after successful revascularization. Although lumen
enlargement after balloon angioplasty for ARAS is clearly suboptimal, observational studies do not
suggest different cure rates after renal artery bypass or stenting. 89-100 The most likely explanations
are that patients with ARAS have essential hypertension, many do not have renal ischemia, and
unrecognized hypertensive nephropathy leads to self-perpetuating hypertension.
NKFM & MDCH 113