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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renovascular disease appears to be increasing in prevalence, particularly in older subjects with atherosclerotic disease elsewhere. Its clinical manifestations and presentation are changing because of rapid advances in medical therapy and other comorbid events. Although fibromuscular dysplasia and other diseases affecting the renal artery can produce the syndrome of renovascular hypertension, atherosclerotic renal artery stenosis is the most common clinical entity. It can produce a spectrum of manifestations, ranging from asymptomatic ("incidental"), identified during angiographic evaluation of other conditions, to progressive hypertension to accelerated cardiovascular disease with pulmonary edema and advanced renal failure. With the widespread application of drugs which block the renin-angiotensin system, including angiotensin-converting enzyme inhibitors and angiotensin antagonists, many cases of renovascular hypertension remain unsuspected and never produce adverse effects. Clinicians need to be alert to the potential for disease progression, with the potential for total renal artery occlusion and/or loss of viable renal tissue. Selection of patients for renal revascularization depends on individual balance of risks and benefits regarding the likely outcomes regarding both improvements in blood pressure control and preservation of renal function.
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PMID:Epidemiology and clinical presentation. 1102 94

We report the case of a 70-year-old hypertensive man with a solitary kidney and chronic renal insufficiency who developed two episodes of transient anuria after losartan administration. He was hospitalized for a myocardial infarction with pulmonary edema, treated with high-dose diuretics. Due to severe systolic dysfunction losartan was prescribed. Surprisingly, the first dose of 50 mg of losartan resulted in a sudden anuria, which lasted eight hours despite high-dose furosemide and amine infusion. One week later, by mistake, losartan was prescribed again and after the second dose of 50 mg, the patient developed a second episode of transient anuria lasting 10 hours. During these two episodes, his blood pressure diminished but no severe hypotension was noted. Ultimately, an arteriography showed a 70-80% renal artery stenosis. In this patient, renal artery stenosis combined with heart failure and diuretic therapy certainly resulted in a strong activation of the renin-angiotensin system (RAS). Under such conditions, angiotensin II receptor blockade by losartan probably induced a critical fall in glomerular filtration pressure. This case report highlights the fact that the angiotensin II receptor antagonist losartan can cause serious unexpected complications in patients with renovascular disease and should be used with extreme caution in this setting.
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PMID:Repeated transient anuria following losartan administration in a patient with a solitary kidney. 1125 25

Although the dehydration-rehydration problem in end-of-life care is one of the most important issues, clinical indications of hydration therapy have not been clarified because the pathophysiology is poorly understood. To explore the physiological changes of fluid status in terminally ill cancer patients, a prospective observational study was performed. We obtained 9 pairs of blood samplings from hospice inpatients with irreversible bowel obstruction who underwent two or more laboratory examinations during the admission periods. The plasma renin activity (PRA) and brain natriuretic peptide (BNP) were measured, in addition to basic laboratory tests performed as clinically required. A chart review evaluated the degree of fluid retention symptoms. In 7 patients receiving intravenous rehydration of 700-2200 ml/day, the mean PRA level significantly increased from 3.5+/-2.5 ng ml(-1) h(-1) to 11+/-8.2 ng ml(-1) x h(-1) ( P=0.047), and the mean BNP level significantly decreased from 52+/-34 pg/ml to 22+/-14 pg/ml ( P=0.047). Edema, ascites, and pleural effusion/pulmonary edema deteriorated in 5, 3, and 5 patients, respectively. In 2 patients without rehydration therapy, peripheral edema deteriorated with increased PRA levels (0.5 to 20 ng ml(-1) x h(-1), 0.4 to 8.7 ng ml(-1) x h(-1), respectively). In conclusion, intravenous volume depletion with fluid retention symptoms was observed in terminally ill cancer patients with intestinal obstruction both receiving and not receiving intravenous hydration. The pathological mechanism hypothesized is the fluid shift from the intravascular compartment to the interstitial spaces.
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PMID:Fluid status of terminally ill cancer patients with intestinal obstruction: an exploratory observational study. 1235 26

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

High-altitude pulmonary oedema (HAPE) is a potentially fatal condition affecting fit and previously well individuals at altitudes in excess of 3000 m. This article discusses the mechanisms of HAPE, considers the contribution of hypoxic pulmonary vasoconstriction and alterations in sodium transport to the pathological process. It discusses the various biochemical mediators such as nitric oxide (NO), endothelin-1 (ET-1), and the renin-angiotensin-aldosterone system (RAS) that may be involved and considers possible oxygen-sensing mechanisms involved in hypoxic adaptation such as hypoxia-inducible factor-1 (HIF-1). Those who have had HAPE once run an unpredictable but significant risk of recurrence; therefore, there may be a constitutional or genetic component in its aetiology. This paper considers the possible involvement of genes that may be involved in physiological adaptation to hypoxia (e.g., angiotensin-1 [AT(1)]-converting enzyme [ACE], tyrosine hydroxylase, serotonin transporter [5-HTT], and endothelial NO synthase [eNOS] genes). As yet, no formal association has been identified between an identified genetic polymorphism and HAPE, but genetic variation provides a possible mechanism to explain interindividual variation in response to hypoxia and enhanced or reduced performance at altitude.
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PMID:The genetic basis of high-altitude pulmonary oedema. 1476 4

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

A 77 year old man with coronary artery disease was referred to our institution for recurrent (flash) episodes of pulmonary edema due to malignant hypertension. A selective contrast-enhanced angiography showed severe bilateral renal artery stenosis. We also found a high level of plasma renin production identifying intense renin-angiotensin system activation. We first considered revascularisation. Percutaneous intervention initially failed and thereafter the patient denied surgical revascularisation. We have then recommended medical therapy, namely a beta-blocker after adequate correction of fluid retention. We used CARVEDILOL which has no nephrotoxicity and effectively inhibit the renin-angiotensin system. The patient feels significant functional and clinical improvement with no fluid retention relapse with a follow-up of more than 18 months.
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PMID:[Benefits of a beta-blocking agent (carvedilol) on bilateral atherosclerotic renal artery stenosis. A case report]. 1522 46

Alcohol abuse markedly increases the risk of sepsis-mediated acute lung injury. In a rat model, ethanol ingestion alone (in the absence of any other stress) causes pulmonary glutathione depletion, increased expression of transforming growth factor-beta1 (TGF-beta1), and alveolar epithelial barrier dysfunction, even though the lung appears grossly normal. However, during endotoxemia, ethanol-fed rats release more activated TGF-beta1 into the alveolar space where it can exacerbate epithelial barrier dysfunction and lung edema. Ethanol ingestion activates the renin-angiotensin system, and angiotensin II is capable of inducing oxidative stress and TGF-beta1 expression. We determined that lisinopril, an angiotensin-converting enzyme inhibitor that decreases angiotensin II formation, limited lung glutathione depletion, and treatment with either lisinopril or losartan, a selective angiotensin II type 1 receptor blocker, normalized TGF-beta1 expression. The glutathione precursor procysteine also prevented TGF-beta1 expression, suggesting that TGF-beta1 may be induced indirectly by angiotensin II-mediated oxidative stress and glutathione depletion. Importantly, lisinopril treatment normalized barrier function in alveolar epithelial cell monolayers from ethanol-fed rats, and treatment with either lisinopril or losartan normalized alveolar epithelial barrier function in ethanol-fed rats in vivo, as reflected by lung liquid clearance of an intratracheal saline challenge, even during endotoxemia. In parallel, lisinopril treatment limited TGF-beta1 protein release into the alveolar space during endotoxemia. Together, these results suggest that angiotensin II mediates oxidative stress and the consequent TGF-beta1 expression and alveolar epithelial barrier dysfunction that characterize the alcoholic lung.
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PMID:Angiotensin II mediates glutathione depletion, transforming growth factor-beta1 expression, and epithelial barrier dysfunction in the alcoholic rat lung. 1590 76

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

Atherosclerotic renal artery stenosis (RAS) is relatively common and often associated with reversible hypertension, progressive renal insufficiency, and/or coronary-independent pulmonary edema. Not all RAS is associated with renovascular hypertension. Historical and physical findings may suggest renovascular hypertension and warrant investigation for RAS. Noninvasive diagnostic imaging options include renal artery duplex ultrasonography, magnetic resonance angiography, computed tomographic angiography, and CO2 angiography, with each method having its own advantages and limitations. Functional tests of renal flow, which characterize RAS significance, include captopril-stimulated plasma renin activity and captopril renography. To date, no single approach has shown clear superiority either in diagnosis or identification of patients most likely to benefit from revascularization. Revascularization of RAS is recommended for severe/drug-refractory hypertension, preservation of renal function, recurrent flash pulmonary edema, or recurrent severe heart failure. Intervention response is variable, but the ongoing Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL) trial, comparing medical therapy with and without stenting, should provide management guidance.
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PMID:Atherosclerotic renal artery stenosis and renovascular hypertension: clinical diagnosis and indications for revascularization. 1684 4


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