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Stents are typically deployed to the extent of 1�C2 mm into the aortic lumen in order to completely eliminate ostial lesions. Figure 1 78-year-old woman with medically refractory hypertension and renal artery stenosis. (a) Abdominal aortogram exhibits stenosis of proximal renal arteries bilaterally (arrowheads). (b) Right renal arteriogram better delineates stenosis Akt inhibitor (arrowheads). (c) ... Procedure clinical outcomes Technically successful intervention is defined by less than 30% residual stenosis at the narrowest point of the vascular lumen and restoration of the pressure gradient to below the selected threshold for intervention.[1] Technical success rates vary based on the chosen intervention. A meta-analysis by Rees reported 99% technical success following stent placement, compared with 55% for ostial and 70% for non-ostial stenoses treated by angioplasty.[5] Clinical success following renal revascularization depends, in part, on the etiology, location, and extent of the underlying stenosis. Only a small percentage of patients with atherosclerotic RAS are reported as cured following treatment. In a recent multicenter randomized controlled trial, Cooper et al., found no difference in the occurrence of adverse renal or cardiovascular Selleckchem EPZ 6438 events among patients randomized to medical therapy alone or in conjunction with renal artery stenting.[6] Outcomes are more favorable in patients with FMD, however. A meta-analysis by Martin et al., found a mean cure rate of 44% following transcatheter treatment of RAS secondary to FMD (majority with the"medial fibroplastic" type).[1] Davidson et al., reported that younger age, milder hypertension, and shorter duration of hypertension were statistically significant independent variables predicting clinically successful results from angioplasty in patients with FMD.[7] Complication rates following transcatheter treatment of RAS range from 5 to 15%. Minor access site complications such as hematoma and pseudoaneurysm formation are the most common (3�C5%), while uncommon complications include renal artery dissection (5%), renal failure (5%), cholesterol embolization syndrome (1%), need for salvage surgical intervention (Montelukast Sodium and death (0.5%).[2] RENAL ARTERY (PSEUDO) ANEURYSM Epidemiology and pathophysiology A true renal artery aneurysm (RAA) is defined as an expansion of all layers of the arterial wall, whereas a renal artery pseudoaneurysm (RAP) is an expansion of the renal artery with focal disruption of the arterial wall.[8] RAAs are uncommon, with an incidence of ��1%. In women with FMD, however, the incidence may approach 10%.[9] Other etiologies of RAAs and/or RAPs include degenerative aneurysms, vasculitis, trauma, and percutaneous renal interventions.[10] RAAs are typically asymptomatic. Symptoms arise from rupture, embolization of the peripheral arterial bed, arterial thrombosis, or renal failure. RAAs are associated with hypertension in up to 73% of cases and hematuria in up to 30% of cases.