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Query: UMLS:C0034063 (pulmonary edema)
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To evaluate the prevalence of clinically significant renal artery stenosis (RAS) in patients referred for coronary angiography, we analyzed data on 2,439 consecutive patients. Patients underwent selective renal angiography in conjunction with coronary angiography if refractory hypertension (blood pressure > 140/90 on two drugs) or flash pulmonary edema was present. A total of 1,089 renal arteries of 534 patients were evaluated. Twelve percent (137/1,089) of the renal arteries in 19% (101/534) of patients had > 70% diameter stenosis in at least one vessel. Bilateral renal artery stenosis was present in 26% (26/101) of patients. One hundred and thirty-two of the 137 vessels underwent stent revascularization due to clinical renovascular hypertension. Acute clinical success (< 20% diameter stenosis without death or urgent surgery) was 98% (99/101). Due to high prevalence and effective available treatment, we recommend routine screening for RAS in all patients with refractory hypertension referred for coronary angiography.
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PMID:Prevalence of renal artery stenosis requiring revascularization in patients initially referred for coronary angiography. 1259 12

We describe a patient with a clinical presentation of moderate renal dysfunction, recurrent hospitalizations for congestive heart failure, and an episode of abrupt-onset pulmonary edema (flash pulmonary edema). Diagnostic angiography revealed triple-vessel coronary artery disease (CAD) and bilateral severe renal artery stenosis. This patient underwent successful bilateral renal artery stent implantation with marked improvement in his functional class without further recurrence of pulmonary edema.
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PMID:Renal artery stent implantation in a patient with bilateral renal artery stenoses presenting with flash pulmonary edema. 1262 14

The clinical diagnosis of renal artery stenosis relies on a high index of suspicion and confirmation by noninvasive imaging modalities. There are three distinct clinical syndromes associated with renal artery stenosis: renin-dependent hypertension, essential hypertension, and ischemic nephropathy. Clinical features that should heighten suspicion for renal artery stenosis include abrupt-onset or accelerated hypertension at any age, unexplained acute or chronic azotemia, azotemia induced by angiotensin-converting enzyme (ACE) inhibitors, asymmetric renal dimensions, and congestive heart failure with normal ventricular function. Patients with true renin-dependent (renovascular) hypertension are typically young or middle-age women with renal fibromuscular dysplasia (FMD). Initial therapy for renovascular hypertension associated with FMD is an ACE inhibitor; refractory hypertension responds readily to balloon angioplasty without stenting. Elderly patients with generalized atherosclerosis and hypertension often have atherosclerotic renal artery stenosis (ARAS); hypertension in these patients is usually not renin dependent (ie, essential hypertension). Hypertension alone, even if treated with multiple medications, is not a compelling indication for renal artery revascularization; these patients should be treated aggressively with antihypertensive medical therapy. Renal artery revascularization with stenting may be considered for refractory severe hypertension, and would be expected to improve blood control and modestly reduce medication requirements. Renal revascularization rarely cures hypertension in patients with ARAS. Patients with ARAS, hypertension, and end-organ injury should be considered for renal revascularization. Manifestations of end-organ injury include nonischemic pulmonary edema; hypertensive crisis associated with acute coronary syndrome, aortic dissection, or neurologic impairment; and renal insufficiency. Ischemic nephropathy is best treated before the development of advanced renal failure. The best candidates for revascularization are those with baseline serum creatinine less than 2.0 mg/dL, bilateral renal artery stenosis, normal renal resistive indices, no proteinuria, and one or more manifestations of end-organ injury. In these patients, renal revascularization is best accomplished by stenting, although surgical revascularization may be considered in patients with concomitant severe aortic aneurysmal or occlusive disease.
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PMID:Atherosclerotic Renal Artery Stenosis. 1268 6

Renal artery stenosis (RAS) may cause hypertension, azotemia, episodes of flash pulmonary edema and congestive heart failure. Renal artery angioplasty and stenting was performed in 207 patients from 1991 to 1997. Thirty-nine of these patients (19%) underwent renal artery stenting for the control of recurrent episodes of congestive heart failure and flash pulmonary edema. All patients had angiographic evidence of severe (>70%) bilateral RAS (n = 18) or severe RAS to a solitary functioning kidney (n = 21). Sixteen patients (41%) were male and 23 (59%) were female, mean age 69.9 years (range 50-85 years). Of the 18 patients with bilateral RAS, 12 (66.6%) underwent bilateral stenting. Mean blood pressure decreased from 174/85 +/- 32/23 mmHg to 148/72 +/- 24/14 mmHg (p < 0.001). Mean number of blood pressure medications decreased from 3 +/- 1 to 2.5 +/- 1 (p = 0.006). Twenty-eight patients (71.8%) had improvement in blood pressure control. The mean serum creatinine decreased from 3.16 +/- 1.61 to 2.65 +/- 1.87 (p = 0.06). Six of 39 patients (15.4%) used angiotensin converting enzyme (ACE) inhibitors prior to stenting whereas 19 of 39 patients (48.7%) used ACE inhibitors poststenting (p = 0.004). Twenty of 39 patients (51.4%) demonstrated improvement in serum creatinine, 10 of 39 patients (25.6%) had stabilization of serum creatinine and nine of 39 patients (23%) demonstrated worsening. The number of hospitalizations due to congestive heart failure in the year preceding renal artery stenting was 2.4 +/- 1.4 and poststenting was 0.3 +/- 0.7 (p < 0.001). The New York Heart Association Functional Class decreased from 2.9 +/- 0.9 prestenting to 1.6 +/- 0.9 poststenting (p < 0.001). Thirty of 39 patients (77%) had no hospitalizations for congestive heart failure during a mean follow-up period of 21.3 months. Nine patients expired during the course of follow up; eight of the nine patients died within the first year after renal artery stenting. Renal artery stenting decreased the frequency of congestive heart failure, flash pulmonary edema, and the need for hospitalization in most patients. Blood pressure was markedly improved in the majority of patients with improved or stabilized renal function. Evaluation for RAS is important in hypertensive patients who present with recurrent congestive heart failure or flash pulmonary edema.
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PMID:Clinical benefit of renal artery angioplasty with stenting for the control of recurrent and refractory congestive heart failure. 1271 Aug 43

Indications and timing of revascularization for atherosclerotic renal artery stenosis are topics of considerable controversy. Labile hypertension, progressive renal failure, and flash pulmonary edema may be strong indications for revascularization, yet revascularization may carry significant morbidity and mortality risks. Medical therapy alone, however, may also risk deterioration of renal function with worsening morbidity and mortality. We report a case of renal artery stenosis illustrating some of the complexities of decision-making, the limitations of angiography, and the importance of physiologic testing.
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PMID:Renal artery stenosis: when to intervene? 1294 3

Atherosclerotic renal artery stenosis (RAS) is an increasingly important cause of end-stage kidney disease, and may cause hypertension, progressive renal failure, and recurrent pulmonary edema. Herein, we report two episodes of anuria and acute pulmonary edema associated with losartan treatment in a hypertensive patient with preexisting severe renal artery stenosis in a solitary kidney. After successful percutaneous renal balloon angioplasty procedure, urine flow was started immediately, despite 10 days of anuria. Blood pressure measurements were still at acceptable levels with a low dose Beta blocker, and serum creatinine levels were normal even after eight months. PTRA should be done in such patients, even with prolonged anuria. Physicians who recommend angiotensin receptor blockers in patients with RAS, especially in patients wih hypovolemia or a solitary kidney, should be careful about this complication.
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PMID:Two episodes of anuria and acute pulmonary edema in a losartan-treated patient with solitary kidney. 1468 57

One of the clinical manifestations of renovascular hypertension (RVH) may be a recurrent pulmonary oedema both in the absence or in the presence of systolic left ventricular dysfunction. This type of pulmonary oedema characterized as "flash" pulmonary oedema is ascribed to elevated angiotensin II concentrations with consequent hypertension as well as to volume overload resulting from decreased pressor natriuresis when there are significant stenoses of both or one renal arteries. The investigation included 30 patients with RVH treated by percutaneous transluminal angioplasty of the stenosed renal artery (PTRA) and/or stent implantation (PTR-ST) and 30 patients with surgical resection of the abdominal aortic aneurysm (AAA). The first group was divided in two subgroups according to the etiology of renal artery stenosis (RAS). In the subgroup with fibromuscular dysplasia (FMD) the mean age was 37.5 years, in the subgroup with atherosclerotic renal artery stenosis (ARAS) 54.8 years and in the group with operated AAA 68.6 years. There were more females than males only in the FMD subgroup (10:3). Two patients of the first group experienced pulmonary oedema, both in the subgroup with atherosclerotic renal artery stenosis associated with atherosclerosis of other arteries. Normalization of the blood pressure following PTRA in both and an uncomplicated course after a surgical myocardial revascularization in one of them illustrates the importance of renal revascularization. Pulmonary oedema occurred preoperatively in four out of 30 patients with abdominal aortic aneurysm in whom significant renal artery stenoses coexisted. Two patients died despite surgery, one patient is clinically stable and the medicament treatment of heart failure is inevitable in the fourth with a left ventricular aneurysm following myocardial infarction. The occurrence or recurrence of pulmonary oedema in the absence of other explanation should suggest the possibility of bilateral or unilateral renal artery stenosis requiring renal revascularization for blood pressure regulation as well as for elimination of other manifestations/complications.
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PMID:["Flash" pulmonary edema as a clinical manifestation of renovascular hypertension]. 1469 25

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 most commonly due to either fibromuscular dysplasia or atherosclerosis. The former predominates in young women while atherosclerosis is usually encountered in individuals over the age of 55. The most common clinical manifestation of fibromuscular dysplasia is hypertension, which can frequently be cured or significantly improved with percutaneous balloon dilation. Atherosclerotic RAS may present with hypertension, renal failure (ischemic nephropathy), recurrent episodes of congestive heart failure and flash pulmonary edema or may be discovered incidentally during an imaging procedure for some other reason. Screening tests for RAS have improved considerably over the last decade. While captopril renography was utilized almost exclusively in the past, duplex ultrasound of the renal arteries or magnetic resonance angiography have replaced other modalities as the screening test of choice in many centers. Rarely does an arteriogram have to be performed for diagnostic purposes only. Management of RAS consists of three possible strategies: medical management, surgical management or percutaneous therapy with balloon angioplasty and stent implantation. The treatment of choice to control hypertension in patients with fibromuscular disease is percutaneous angioplasty. Renal artery stenting has replaced surgical revascularization for most patients with atherosclerotic disease who meet the criteria for intervention.
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PMID:Renal artery disease: diagnosis and management. 1502 99

Renal artery stent implantation is associated with high rates of restenosis, particularly in vessels less than 4.5 mm in diameter. We describe 4-year follow-up results in the first patient to receive renal artery brachytherapy for this indication. A 68-year-old man who presented with flash pulmonary edema, hypertension and renal impairment was found to have severe bilateral renal artery stenosis and was treated with bilateral stent implantation. Following clinical deterioration due to severe in-stent restenosis, he underwent repeat angioplasty followed by intra-stent brachytherapy. To our knowledge, this is the first use of such therapy and hence the 4-year follow-up demonstrating excellent bilateral patency is the longest to date.
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PMID:A case of renal artery brachytherapy for in-stent restenosis: four-year follow-up. 1515 20


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