Hypertension was said to be cured or improved after additional treatment in 90% of the patients after angioplasty and 86% after operation. Renal function FK506 improved or remained unchanged in 83% of the patients after angioplasty and 72% after surgery. Although 17% of the patients initially treated with angioplasty required subsequent surgery, BP, renal function and the renal artery patency rate did not differ between the angioplasty and surgery arms 24 months
after treatment. Critics of this study have argued that surgical patency may produce better outcomes in the long term (5–10 years) although this remains to be reproduced in other studies and probably depends on surgical expertise. Since the first description of a patient with RAS responding to revascularization by Pickering et al.,16 many studies have confirmed ‘flash pulmonary oedema’ as a clinical entity. All of these studies are case reports or case series that show a reduction of the ‘flash pulmonary oedema’ (recurrent pulmonary oedema with normal left ventricular function associated with renovascular disease)
by the use of angioplasty with/without stenting of the renal artery. No prospective data exist, the data are descriptive, and there are no long-term follow-up data. Prior to any studies in angioplasty PCI-32765 mouse in this area, a few case reports have suggested surgical revascularization of the renal artery may lead to people coming off dialysis. Dwyer et al.17 demonstrated in a case series that there was improvement in renal function in dialysis-dependent patients submitted to percutaneous transluminal coronary angioplasty (PTCA). In these and the surgical patients, urine output was established immediately without the need for further dialysis. The authors recommended urgent investigation Epothilone B (EPO906, Patupilone) with Doppler ultrasound and TechneScan MAG3 before angiography to determine
which kidney is to be targeted based on viability of renal tissue. Since that case series, a few additional case reports have been published but no prospective series with long-term follow up. Fibromuscular dysplasia is a non-atherosclerotic, non-inflammatory vascular disease of largely unknown pathogenesis that primarily affects the renal and cerebral arteries. Because FMD is not common, no large controlled studies exist to help guide therapy. The disease can present in a number of ways, ranging from asymptomatic to a multisystem disorder with a clinical picture that mimics necrotizing vasculitis, involving mesenteric ischemia, renal vascular hypertension, renal failure, claudication, transient ischemic attack or stroke. Commonly, for FMD of the kidneys, the presentation is that of a young woman with sudden onset of hypertension. Currently, the mainstay of intervention is PTCA for patients with difficult to control hypertension, renal insufficiency or arterial dissection.