|Classification and external resources|
Renovascular hypertension (or "renal hypertension") is a syndrome which consists of high blood pressure caused by the kidneys hormonal response to narrowing of the arteries supplying the kidneys (renal artery stenosis). When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increases blood pressure of the entire circulatory system. It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.
Cause: Narrowing of the arteries supplying the kidneys causes a low perfusion pressure which is detected by the juxtaglomerular apparatus (via the juxtaglomerular cells, which act as baroreceptors; located on the afferent arteriole wall). This leads to renin secretion that causes the angiotensinogen conversion to angiotensin I. Angiotensin I then proceeds to the lung where it is converted to Angiotensin II via Angiotensin Converting Enzyme (ACE). Angiotensin II causes vasoconstriction and aldosterone release leading to water and sodium retention and potassium depletion. The increased blood volume and vessel constriction contributes to increased blood pressure which can lead to hypertension.
Diagnosis and presentation
Techniques have been developed to diagnose renal hypertension using digital image processing of radiographs. Treatment may involve angioplasty and stenting of the renal arteries. The syndrome may be related to other diseases of the epithelium.
Suggestive clinical features include onset of hypertension <30 or >50 years of age, abdominal or femoral bruits, hypokalemic alkalosis, moderate to severe retinopathy, acute onset of hypertension or malignant hypertension, and hypertension resistant to medical therapy.
The "gold standard" in diagnosis of renal artery stenosis is conventional arteriography. Magnetic resonance angiography (MRA) is used in many centers, especially among patients with renal insufficiency at higher risk for contrast nephropathy. MRA may overestimate the severity of stenosis relative to angiography. In patients with normal renal function and hypertension, the captopril (or enalaprilat) renogram may be used. Lateralization of renal function [accentuation of the difference between affected and unaffected (or "less affected") sides] is suggestive of significant vascular disease. Test results may be falsely negative in the presence of bilateral disease.
Renal hypoperfusion activates renin-angiotensin-aldosterone (RAA) axis; ACE inhibitors and angiotensin II receptor blocker classes of antihypertensives are contraindicated as they might compromise the renal function especially if the stenosis is bilateral. Nitroprusside, labetalol, or calcium antagonists are generally effective in lowering blood pressure acutely, although inhibitors of the RAA axis [e.g., ACE inhibitors, angiotensin II receptor blockers (ARBs)] are most effective long-term treatment, if disease is not bilateral.
Surgical revascularization appears to be superior for ostial lesions characteristic of atherosclerosis. The relative efficacy of surgery compared with angioplasty (especially with stenting) for fibromuscular dysplasia or for non-occlusive, non-ostial atherosclerotic disease is unclear. Angioplasty (with or without stenting) tends to be temporarily effective for some cases. However, as of early 2011, six randomized controlled trials have failed to demonstrate any real benefit in blood pressure control or preservation of renal function when using endovascular (angioplasty or stenting) procedures compared to medical therapy alone. ACE inhibitors or ARBs are ideal agents for hypertension associated with renal artery stenosis, except in patients with bilateral disease (see "Ischemic Nephropathy" below) or disease in a solitary kidney (including an allograft).
- Harrison's Manual of Medicine: Renovascular Disease - Renal Artery Stenosis