Renal aery stenosis: aCauses- Atherosclerotic disease(most common cause) - Fibromuscular Dysplasia(FMD) - Extrinsic compression of the vessel a It is considered a specifically treatable "secondary" cause of hypeension a Pathogenesis: Critical levels of stenosis - reduction in perfusion pressure - Activation of the renin-angiotensin system and sympathetic adrenergic pathways - systemic hypeensiona LVH and renal fibrosis (later stages) a Renal aery stenosis is also labelled ischemic nephropathy; ARAS and SHT tend to affect both the poststenotic and contralateral kidneys, reducing overall (GFR) in ARAS Fibromuscular Dysplasia(FMD Atherosclerotic renal aery stenosis (ARAS) - Occurs in 3-5% of normal subjects - Presents clinically with hypeension in younger individuals (age 15-50), most often women. - lesions are frequently bilateral and, tend to affect more distal poions of the renal aery. - Usually does not affect kidney function, but may cause total occlusion and can be associated with renal aery aneurysms - Common in the general population, prevalence increases with age and in patients with CAD, PAD. - obstruction most commonly at the origin - If untreated may progress to total occlusion in 50% cases - It is a strong predictor of morbidity- and moality-related cardiovascular events a Evaluation: -Captopril renography with technetium 99m Tc meiatide (99mTc MAG3) a Normal study excludes renovascular hypeension-Nuclear imaging with technetium meiatide or technetium-labelled pentetic acid (DTPA)a Allows calculation of single-kidney GFR -Duplex ultrasonographyaInexpensive, non-invasive - Magnetic resonance angiographyaExpensive; not nephrotoxic but gadolinium toxicity excludes use in GFR<30 ml/min, unable to visualize stented vessels -computed tomographic angiographyaExpensive, potentially nephrotoxic, stents do not cause aefacts -Intra-aerial angiographyaConsidered "gold standard" for diagnosis of large vessel disease; Expensive, associated risk of atheroemboli, contrast toxicity, procedure-related complications, e.g., dissection a Treatment: -blockade of the renin-angiotensin system, attainment of goal blood pressures, cessation of tobacco, statins, and aspirin -percutaneous transluminal renal angioplasty (PTRA) (for FMD), endovascular stenting or surgical renal revascularization(for ARAS) Ref: Harrison's 18/e p2048