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Atherosclerotic renal artery stenosis (ARAS) is an increasingly common cause of secondary hypertension and progressive chronic renal failure. Recent studies provide valuable information about the pathophysiology, natural history, diagnosis and treatment of ARAS. The pathophysiology of ARAS is more complex than experimental models using clipped renal arteries because the renal artery narrowing is gradual, may be bilateral, may affect smaller intra-renal arteries and other co-existing nephropathies are often present. Patients with ARAS have high mortality due to associated co-morbidity and progression of renal failure may be less common than previously thought. Magnetic resonance arteriography offers great promise for diagnosing of ARAS as it is non-invasive and can provide data on kidney function. In patients with ARAS, the co-existence of atherosclerotic disease in other vascular beds means that aspirin, blood pressure reduction, advice to stop smoking and lipid lowering therapy are likely to be associated with reduced vascular events. The effect of these approaches on the progression of ARAS is unclear but likely to be beneficial. Re-vascularisation of occluded renal arteries is an attractive option for treatment of ARAS but data from the few randomised controlled studies that have been published do not support its widespread application. Arterial stenting has a higher technical success rate than angioplasty while surgical revascularisation does not appear to improve outcome compared with angioplasty. Recent studies examining functional and histological features of kidneys supplied by atherosclerotic stenosed renal arteries may explain why revascularisation is not always beneficial. The results of on-going studies may identify sub-groups of patients with ARAS who gain a clear benefit from re-vascularisation. In the meantime it seems reasonable to attempt re-vascularisation in the following circumstances: severe hypertension resistant to medical therapy, rapidly progressive renal failure with no obvious cause other than ARAS and recurrent flash pulmonary oedema.
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PMID:Diagnosis and treatment of atherosclerotic renal artery stenosis (ARAS). 1191 84

Essential hypertension accounts for 95% of all cases of hypertension. A small number of patients (between 2% and 5%) have a reversible disease as the cause for raised blood pressure. Unilateral and bilateral renal artery stenosis may be responsible for secondary hypertension. Diagnosis and treatment of renal artery stenosis are of a great importance. Revascularization of ischemic kidney may correct blood pressure control and preserve renal function. Much data suggest close pathophysiological relation between renal artery stenosis, ischemic nephropathy and development of hypertension. However, it should be stressed that not every renal artery stenosis leads to hypertension and ischemic nephropathy. Therefore diagnosis of renal artery stenosis in hypertensive patient is not always equivalent with renovascular hypertension. The true prevalence of renal artery stenosis is unknown. In unselected population it accounts for less than 1% of hypertensive patients. Renovascular etiology of hypertension may be suggested by abrupt onset of hypertension, resistant and malignant hypertension or recurrent pulmonary edema of unknown etiology. Physical examination may reveal bruits over major vessels, including the abdominal aorta and renal arteries. The principle aim of the renal artery stenosis investigation is to confirm presence and size of vessel obstruction and its association with hypertension. Typical evaluation is based on imaging techniques and physiological studies. Former include: doppler duplex ultrasonography, conventional angiography, intraarterial and intravenous digital subtraction angiography, computed axial tomography, magnetic resonance angiography and intravascular ultrasonography. Functional studies are occasionally used. These are renal scintigraphy, evaluation of plasma renin activity in renal veins and evaluation of plasma rennin activity after ACE inhibition. Treatment of patients with renal artery stenosis and hypertension should restore vessel patency and inhibit its occlusion. Revascularization should elicit an improvement in or normalization of blood pressure control and renal function. Therapeutic approach include percutaneous renal artery angioplasty (PTRA), with or without stenting, revascularization by surgery and pharmacotherapy. PTRA is currently the first choice option. In general, it is simpler and similarly effective as surgical reconstruction. In some cases PTRA is completed with stent placement. It prevents immediate recoil but does not completely eliminate restenosis of revascularized artery. Surgical bypass is currently reserved for patients in whom PTRA and stenting fail and in patients with extensive atherosclerotic lesions. Patients with renal artery stenosis and hypertension should be provided with pharmacological treatment according to current recommendations. Specific procedures to limit associated risk factors of atherosclerosis should also be introduced.
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PMID:[Renovascular hypertension: is it only the top of the iceberg?]. 1497 69

Renal artery stenosis (RAS) is a common cause of secondary hypertension, with the activation of the renin-angiotensin-aldosterone system being the pathophysiologic hallmark of the disease. Renovascular hypertension, ischemic nephropathy, proteinuria, and flash pulmonary edema are the main clinical syndromes associated with RAS. The prevalence of RAS is on the rise, owing to an increasing prevalence of diabetes and atherosclerotic disease among our aging population. This rise in RAS prevalence poses major challenges for clinicians making diagnostic and treatment decisions. Although renal angioplasty is of proven benefit in fibromuscular dysplasia, randomized trials in atherosclerotic RAS have not shown any advantage for revascularization over medical therapy in terms of blood pressure control or renal function preservation. Angioplasty and surgical interventions should be reserved for patients with preserved kidney size and hemodynamically significant stenosis.
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PMID:Challenges in the diagnosis and management of renal artery stenosis. 1591 98

Fibromuscular dysplasia (FMD) and aortoarteritis are the most frequent causes of secondary hypertension induced by renal artery stenosis (RAS). Revascularization of this disease entity usually cures arterial hypertension. Demographic evolution leads to an increasing incidence of atherosclerotic RAS, one of the major causes of end-stage renal failure. Furthermore, atherosclerotic RAS leads to deterioration of primary hypertension, progression of atherosclerosis manifestation such as occlusive and aneurysmatic peripheral artery disease, and chronic or acute organ damage such as left ventricular hypertrophy and recurrent flash pulmonary edema. Despite the lack of sufficiently powered randomized controlled trials, each hemodynamically relevant RAS (eg, > or = 70%) should be considered for stent angioplasty in patients without end-stage ischemic nephropathy or limited life expectancy due to concomitant disease (eg, cancer). Drug-eluting stents will probably reduce the overall low in-stent restenosis rate of 10% to 20%. Interventions in patients with dialysis-dependent end-stage nephropathy are left to appropriate clinical study protocols.
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PMID:Renal artery stenosis. 1748 11

Hymenopterid stings and subsequent allergic reactions including fatal anaphylaxis are common indications for emergency department visits worldwide. Besides that, sting can cause death as a result of multi-system involvement ranging from intravascular hemolysis, rhabdomyolysis, acute renal failure, hepatic dysfunction and occasionally thrombocytopenia and coagulopathy. Eleven cases (all male, age 35.5 +/- 15.2 years) of wasp bites admitted in the Manipal Teaching Hospital (MTH), Pokhara during 01st February, 2006 to 30th October, 2007 were enrolled in this study. Mean wasp bites number was 48.7 +/- 7.1 (11-100) and mean time to reach the hospital from the bite time was 69.1 +/- 149.7 hours (1.5 h-12 days). Nine patients developed acute renal failure (ARF) and secondary hypertension. Eight patients underwent hemodialysis. Two patients stuck by more than 75 stings developed refractory pulmonary edema and died in the course of treatment. Victims with lesser numbers of wasp envenomation, who received quick initiation of alkaline diuresis and intensive dialytic support had shorter hospital stay and less severe complications.
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PMID:A study of wasp bites in a tertiary hospital of western Nepal. 1976 40

Renovascular hypertension (hypertension induced by renal artery stenosis) is a form of secondary hypertension caused by overactivation of the renin-angiotensin system by the ischemic kidney. Prevalence of renal artery stenosis (RAS) is estimated to be between 2% (unselected hypertensives) and 40% (older patients with other atherosclerotic comorbidities). Most cases of RAS are caused by atherosclerosis; other causes, including fibromuscular dysplasia, vasculitis, thromboembolism and aneurysms, are less frequent. The most frequent clinical presentation of RAS is hypertension. Acute kidney injury, rapid loss of kidney function and episodes of flash pulmonary edema are other symptoms of RAS, especially in bilateral disease. In current practice, RAS therapy includes antiplatelet (aspirin) and lipid-lowering (statin) therapy as well as angiotensin II receptor blockers or angiotensin-converting enzyme inhibitors as a first choice of antihypertensive agents. Angiotensin blockade, however, is contraindicated in bilateral RAS and in RAS of the solitary kidney. This review summarizes the current status and perspectives on the epidemiology and management of renovascular hypertension.
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PMID:Epidemiology and optimal management in patients with renal artery stenosis. 2302 22

Atherosclerotic renal artery stenosis (RAS) is the single largest cause of secondary hypertension; it is associated with progressive renal insufficiency and causes cardiovascular complications such as refractory heart failure and flash pulmonary edema. Medical therapy, including risk factor modification, renin-angiotensin-aldosterone system antagonists, lipid-lowering agents, and antiplatelet therapy, is advised in all patients. Patients with uncontrolled renovascular hypertension despite optimal medical therapy, ischemic nephropathy, and cardiac destabilization syndromes who have severe RAS are likely to benefit from renal artery revascularization. Screening for RAS can be done with Doppler ultrasonography, CT angiography, and magnetic resonance angiography.
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PMID:Renal artery stenosis. 2543 31

Renovascular hypertension (RVH) is one of the most common causes of secondary hypertension. In about 90% of cases it is due to atherosclerotic renal artery stenosis, often accompanied by severe occlusive disease in the other vessels, and as such carries a bad prognosis. In the remaining 10% patients (usually young women) the underlying vascular lesion is fibromuscular dysplasia. A presence of RVH should be suspected in patients with severe or resistant hypertension, sudden decline of renal function, sudden development or worsening of hypertension, flash pulmonary edema, impairment of renal function after treatment with renal-angiotensin-aldosterone system (RAAS) antagonists. Those patients should be screened with Doppler ultrasound, followed by computer tomography or magnetic resonance angiography. In most cases intensive and well-controlled medical treatment with RAAS blockers, aldosterone and/or calcium antagonists, with an addition of statins and platelet-inhibiting drugs is succesful. However in a selected cases renal revascularization may be necessary.
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PMID:[Renovascular hypertension]. 2716 97

Atherosclerotic renal artery stenosis is the leading cause of secondary hypertension; it can also cause progressive renal insufficiency and cardiovascular complications such as refractory heart failure and flash pulmonary edema. Medical therapy including risk factor modification, renin-angiotensin-aldosterone system antagonists, lipid lowering agents, and antiplatelet therapy is the first line of treatment in all patients. Patients with uncontrolled renovascular hypertension despite optimal medical therapy, ischemic nephropathy, and cardiac destabilization syndromes who have severe renal artery stenosis are likely to benefit from renal artery revascularization. Screening for renal artery stenosis can be done with Doppler ultrasonography, computed tomographic angiography and magnetic resonance angiography. Invasive physiologic measurements are useful to confirm the severity of renal hypoperfusion and therefore improve the selection patients likely to respond to renal artery revascularization. Primary patency exceeds 80% at 5 years and surveillance for in-stent restenosis can be done with periodic clinical, laboratory, and imaging follow-up.
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PMID:Renal Artery Stenosis: When to Revascularize in 2017. 2832 53

Renal artery stenosis may play a significant role in the pathogenesis of secondary hypertension, renal dysfunction, and flash pulmonary edema. Currently correction of renal arterial inflow stenosis is reserved for resistant hypertension patients who have failed maximal medical therapy, have worsening renal function and/or unexplained proximal congestive failure. With the recent advances in minimally invasive percutaneous stent placement techniques, open surgical revascularization has been largely replaced by renal artery stenting. The potential benefit of revascularization seemed intuitive; however, the initial enthusiasm and rise in the number of percutaneous interventions have been tempered by many subsequent negative randomized clinical trials that failed to prove the proposed benefits of the percutaneous intervention. The negative randomized trial results have fallen under scrutiny due to trial design concerns and inconsistent outcomes of these studies compared to pivotal trials undertaken under US Food and Drug Administration scrutiny. Treatment of atherosclerotic renal artery occlusive disease has become one of the most debatable topics in the field of vascular disease. The results from recent randomized clinical trials of renal artery stenting have basically limited the utilization of the procedure in many centers, but not every clinical scenario was covered in those trials. There are potential areas for improvement focusing mainly on procedural details and patient selection with respect to catheter based treatment of atherosclerotic renal artery stenosis. We believe, limiting patient selection, enrollment criteria and outcomes measured functioned to reduce the benefit of renal artery stenosis stenting by not enrolling patients likely to benefit. Future studies incorporating potential procedural improvements and that include patients more likely to benefit from renal stenting than were included in ASTRAL and CORAL are needed to more carefully examine specific patient subgroups so that "the baby is not thrown out with the bath water." We also discuss several other concerns related to renal artery stenting which include diagnostic, procedure, indication, and reimbursement issues.
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PMID:Issues related to renal artery angioplasty and stenting. 2878 53


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