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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

Investigation in a patient aged 46 years with decompensated heart failure and severe renal insufficiency demonstrated a small, poorly functioning right kidney and severe stenosis of the left renal artery. Cardiac decompensation was corrected and the left kidney revascularised by autotransplantation. Renal function recovered considerably (FG 75/min) and the severe hypertension was reduced. In hypertension patients by main renal artery stenosis, renal autotransplantation is recommended, since it is a safe method without technical difficulty and has given good results. The mutual dependence of hypertension and renal insufficiency is reviewed. When renal function is poor, revascularisation of the stenosed kidney will lead to recovery. The hypertension will usually improve but will always become more responsive to drug therapy.
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PMID:Severe renal insufficiency and renovascular hypertension. 78 49

In rats with unilateral renal artery stenosis, the malignant phase of hypertension is characterized by: systolic blood pressure above 180-190 mm Hg; sodium and water loss; polyuria and polydipsia; markedly activated renin-angiotensin-aldosterone system; impairment of renal function and malignant nephrosclerosis in the contralateral kidney; some rats exhibit signs of cerebral hemorrhage, heart failure, acute renal failure, and some rats die. After such a phase of malignant hypertension, a period of remission may occur, which is followed by another malignant phase, etc. When malignant hypertensive rats are offered, in addition to water, saline as drinking fluid, they compulsively drink the saline, BP falls transiently, and all signs of malignant hypertension nearly or completely disappear. These observations indicate that, at a critically high BP level, it is salt and water loss which, by activating the renin-angiotensin system, trigger the vicious circle of malignant renal hypertension in rats.
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PMID:Pathogenesis of malignant hypertension: experimental evidence from the renal hypertensive rat. 119 18

Treatment with angiotensin-converting enzyme (ACE) inhibitors can begin at any time when a left ventricular dysfunction has been diagnosed. In the absence of rare contra-indications (renal artery stenosis, connective tissue disease, severe renal failure), all patients with asymptomatic or, a fortiori, symptomatic chronic heart failure can benefit from ACE inhibitors, whatever the origin of the heart failure. Among the ACE inhibitors now available, the benefits of captopril (3 daily doses) and of enalapril (2 daily doses) on all the targets of cardiac failure treatment are now well established. The effects of lisinopril on mortality are not yet known, but the haemodynamic and symptomatic benefits of this drug are also well established (with the advantage of once daily administration). Other ACE inhibitors with less numerous and less convincing trial reports can be used or rejected depending on the physician's faith in the effects of this pharmaceutical class. With all ACE inhibitors the initial dose must be very low, to be gradually increased over several days or even weeks until the highest dose tolerated is reached. ACE inhibitors can be associated with the classical treatment of cardiac failure. A previous diuretic treatment with sodium depletion may increase the risks of first dose effect and renal intolerance due to the introduction of the ACE inhibitors. Theoretically, the combination of ACE inhibitors and spironolactone is to be avoided for fear of hyperkalaemia and renal deterioration. Yet, provided some precautions are taken this combination may improve the benefits of ACE inhibition when the renin-angiotensin-aldosterone system inhibition is not optimal. However, this has yet to be demonstrated by prospective clinical trials.
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PMID:[Management of the treatment with converting enzyme inhibitors in chronic heart failure]. 129 41

During a 4-year period, acute renal failure was observed in 27 patients (mean age 65 years) treated by various angiotensin-converting-enzyme (ACE) inhibitors for hypertension, heart failure, or a combination of both. None had significant renal artery stenosis on angiography. Overt volume depletion was present in 21 and hypotension in 12 cases. All patients received diuretic therapy and/or a low-salt diet. Other facilitating factors included cardiac failure, pre-existing chronic renal insufficiency, combined therapy with non-steroidal anti-inflammatory drugs, and diabetes mellitus. Twenty-two patients had two or more of these factors at presentation. A renal biopsy performed in 10 cases showed severe arteriosclerosis of small renal arteries in eight and acute tubular necrosis in five instances. Therapy comprised volume expansion, and withdrawal of diuretics and, except in two patients, of ACE inhibitors. Twenty-one patients recovered normal renal function, two died, and permanent renal damage remained in four. These results suggest that sodium depletion has a critical role in inducing acute renal failure, whose outcome is not always benign. A combination of diuretics and ACE inhibitors should be prescribed with caution, especially in older patients with small as well as with large renal vessel disease.
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PMID:Acute renal failure after the use of angiotensin-converting-enzyme inhibitors in patients without renal artery stenosis. 131 66

In a decade from 1980, 11 children aged 3 to 11 years presented with Takayasu's arteritis (TA). All were severely hypertensive. Operative correction was offered to 10 of 11 children presenting with renovascular hypertension (RVH) including cardiac failure alone in 1 and both renal and cardiac failure in 8, a result of TA involving renal arteries by stenosis or occlusion. Nine patients had renal autotransplantation to an heterotopic site in the pelvis. Seven of 12 kidneys were salvaged by autotransplant with relief of RVH. Renal artery stenosis was successfully corrected by this procedure in 5 patients. Autotransplantation failed in 4 patients, 1 of whom subsequently had a successful allograft transplant. One patient was treated primarily by cadaver allograft transplantation. One patient whose autotransplant failed had a functioning contralateral kidney and is well with controlled RVH. One patient died prior to any treatment. Patient survival improved with the use of total lymphoid irradiation in the most recent 7 patients.
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PMID:Management of renal hypertension in children with Takayasu's arteritis using renal autografting or allograft transplantation in selected circumstances and total lymphoid irradiation. 135 25

A 68-year-old man presented with renal failure, heart failure, gastrointestinal bleeding, and a pulmonary infiltrate. Serologic evaluation revealed a perinuclear antineutrophil cytoplasmic antibody (ANCA) at a titer of 1:1280, which on immunoblot and enzyme immunoassay showed antimyeloperoxidase specificity. Autopsy showed microscopic polyarteritis based on the presence of necrotizing alveolitis and crescentic glomerulonephritis. The extent and activity of the glomerular disease was modified by a right renal artery stenosis (RAS). Twenty percent of glomeruli on the right and 82% glomeruli on the left contained crescentic lesions. Furthermore, predominantly active lesions were associated with renal artery stenosis, while the contralateral kidney contained mostly organized crescents. This observation suggests that hemodynamic factors or its sequelae can influence the onset and severity of ANCA-associated disease.
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PMID:Renal artery stenosis modifies glomerular injury in antineutrophil cytoplasmic antibody-associated disease. 135 84

A 7-day old neonate presented with heart failure secondary to severe hypertension. The hypertension was discovered on day 9 of life. Control of his hypertension was a difficult problem eventually requiring continuous intravenous sodium nitroprusside therapy, and ultimately a nephrectomy. The nephrectomized specimen revealed renal artery stenosis, renal artery thrombosis and renal vein thrombosis. His eventual outcome was excellent.
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PMID:Renovascular hypertension in a newborn: necessity of assessing blood pressure routinely. 147 66

The RAS is part of an extremely powerful feedback system for long-term control of blood pressure and volume homeostasis. Disturbances that tend to lower blood pressure, such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due, in large part, to the combined actions of ANGII and reduced arterial pressure. In response to increased sodium intake, decreased ANGII formation greatly amplifies the effectiveness of pressure natriuresis, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium retaining effects of ANGII necessitate increased blood pressure to maintain sodium balance via pressure natriuresis. Because the RAS is so powerful in regulating blood pressure, blockade of the system with ACE inhibitors offers a powerful therapeutic tool in diseases such as hypertension and congestive heart failure. The control of sodium excretion and blood pressure by ANGII is exerted through multiple intrarenal as well as extrarenal effects, including stimulation of aldosterone secretion, which can influence renal excretion. Current evidence suggests that the intrarenal effects of ANGII are quantitatively more important than those mediated by aldosterone in controlling blood pressure and renal excretion. The most important intrarenal effects of ANGII include efferent arteriolar constriction as well as direct effects on sodium transport. The constrictor effect on efferent arterioles also is important in preventing reductions in GFR in circumstances associated with impaired renal perfusion. Therefore blockade of ANGII formation in circumstances such as renal artery stenosis may caused marked reductions in GFR. However, in many patients efferent arteriolar vasodilation caused by ANGII blockade may not lower GFR markedly because of other autoregulatory mechanisms that compensate by causing parallel reductions in afferent arteriolar resistance. In these individuals, chronic ACE inhibition may prove to be beneficial in slowing the progression of renal disease because a reduction in glomerular hydrostatic pressure may help to prevent glomerular damage.
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PMID:The renin-angiotensin system: renal actions and blood pressure regulation. 187 29

Modification of the renin-angiotensin system, part of a powerful feedback system for long-term control of arterial pressure and volume homeostasis, through use of angiotensin-converting enzyme (ACE) inhibitors, offers a powerful means of reducing blood pressure in many hypertensive patients. There is considerable evidence to suggest that the chronic renal and blood pressure actions of ACE inhibitors are mediated mainly by blockade of angiotensin II formation, rather than by other effects such as increased levels of kinins or prostaglandins. The long-term actions of angiotensin II and aldosterone on blood pressure are closely intertwined with their effects on volume homeostasis and the renal pressure natriuresis mechanism. In most instances, changes in angiotensin II and aldosterone act to amplify the effectiveness of pressure natriuresis and minimize changes in blood pressure needed to maintain sodium balance. When angiotensin II or aldosterone levels are inappropriately elevated, the antinatriuretic effects of these hormones shift pressure natriuresis to higher levels, thereby necessitating increased blood pressure to maintain sodium balance. Control of renal excretory function and modulation of pressure natriuresis by angiotensin II is mediated by intrarenal and extrarenal effects, including stimulation of aldosterone secretion. Current evidence indicates that the intrarenal effects of angiotensin II are quantitatively more important than changes in aldosterone in regulating renal excretion and arterial pressure. The intrarenal actions of angiotensin II include a direct effect on tubular sodium transport as well as a potent constrictor action on efferent arterioles, which increases reabsorption by altering peritubular capillary forces. The constrictor effect of angiotensin II on efferent arterioles also helps to stabilize glomerular filtration rate and therefore excretion of metabolic waste products, an action that may be particularly important when renal perfusion is impaired (e.g., in renal artery stenosis or heart failure).
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PMID:Control of blood pressure by the renin-angiotensin-aldosterone system. 189 44


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