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Renovascular disease hypertension

Van Ampting JMA, Hijmering ML, Beutler JJ, van Etten RE, Koomans HA, Rabelink TJ, Stroes ESG. Vascular effects of ACE inhibition independent of the renin-angiotensin system in hypertensive renovascular disease. Hypertension 2001 37 40-45. [Pg.263]

Baseline hypokalemia may suggest mineralocorticoid-induced hypertension. The presence of protein, blood cells, and casts in the urine may indicate renovascular disease. [Pg.126]

More specific laboratory tests are used to diagnose secondary hypertension. These include plasma norepinephrine and urinary metanephrine levels for pheochromocytoma, plasma and urinary aldosterone levels for primary aldosteronism, and plasma renin activity, captopril stimulation test, renal vein renins, and renal artery angiography for renovascular disease. [Pg.126]

The aim of therapy is straightforward reduction of blood pressure to within the normal range. When hypertension is secondary to a known organic disease, such as renovascular disease or pheochromocytoma, therapy is directed toward correction of the underlying malady. Unfortunately, about 90% of cases of hypertension are of unknown etiology. The therapy of primary, or essential hypertension, as these cases are generally called, is often empirical. [Pg.226]

ACE inhibitors are used in the treatment of hypertension, heart failure, and diabetic neuropathy. These drugs should not be used in patients with renovascular disease. Anaphylactic reactions may occur in patients. It has been reported that ACE inhibitors affect the fetus when administered to pregnant animals.52 ACE inhibitors can cause injury and even death to the developing fetus in the second and third trimesters of pregnancy.53 55... [Pg.288]

The risk of ACE inhibitor-induced renal impairment in patients with or without renovascular disease can be potentiated by diuretics. " In an analysis of 74 patients who had been treated with captopril or lisinopril, reversible acute renal failure was more coimnon in those who were also treated with a diuretic (furosemide and/or hydrochlorothiazide) than those who were not (11 of 33 patients compared with 1 of 41 patients). Similarly, in a prescription-event monitoring study, enalapril was associated with raised creatinine or urea in 75 patients and it was thought to have contributed to the deterioration in renal function and subsequent deaths in 10 of these patients. However, 9 of these 10 were also receiving loop or thiazide diuretics, sometimes in high doses. Retrospective analysis of a controlled study in patients with hypertensive nephrosclerosis identified 8 of 34 patients who developed reversible renal impairment when treated with enalapril and various other antihypertensives including a diuretic (furosemide or hydrochlorothiazide). In contrast, 23 patients treated with placebo and various other antihypertensives did not develop renal impairment. Subsequently, enalapril was tolerated by 7 of the 8 patients without deterioration in renal function and 6 of these patients later received diuretics. One patient was again treated with enalapril with recurrence of renal impairment, but discontinuation of the diuretics (furosemide, hydrochlorothiazide, and triamterene) led to an improvement in renal function despite the continuation of enalapril. ... [Pg.21]

Secondary hypertension in childhood is predominantly caused by renal or renovascular disease. The details as well as the necessary imaging, the various imaging options, and diagnostic algorithms, and possible interventional and therapeutic approaches are discussed in Chapter 22 and 26. [Pg.358]

Renovascular disease (RVD) is an important but uncommon cause of hypertension in children, accounting for about 10% of cases (Gill et. al 1976 Deal et al. 1992 Wyszynska et al. 1992). Renal pathology is the cause of hypertension in over 90% of children after 1 year of age under 1 year of age, coarctation of the aorta is more common. The more severe the hypertension and the younger the child, then the more likely it is to be secondary hypertension. RVD is now well recognized in paediatrics, but... [Pg.415]

Gill DG, Mendes de CB, Cameron JS, Joseph MC, Ogg CS, Chantler C (1976) Analysis of 100 children with severe and persistent hypertension. Arch Dis Child 51 951-956 Goonasekera CD, Dillon MJ (2000) Measurement and interpretation of blood pressure. Arch Dis Child 82 261-265 Minty I, Lythgoe MF, Gordon I (1993) Hypertension in paediatrics can pre- and post-captopril technetium-99m dimercaptosuccinic acid renal scans exclude renovascular disease Eur J Nucl Med 20 699-702 Ng CS, de Bruyn R, Gordon 1 (1997) The investigation of renovascular hypertension in children the accuracy of radio-isotopes in detecting renovascular disease. Nucl Med Commun 18 1017-1028... [Pg.420]

In situations of known renin-angiotensin-aldosterone involvement, such as in hypertension secondary to renal disease (i.e., renovascular hypertension), diuretics probably should not be used because they further elevate plasma renin. [Pg.226]

The role of the sympathetic nervous system in renal injury, end-stage renal disease, and renovascular hypertension are discussed through a literature review accompanying sympathetic nerve mechanisms in hypertension and obesity. Relevant studies of sympathetic nerve activity and 32-adrenoceptor polymorphism might contribute to the onset and maintenance of renal injury in healthy subjects and in patients with chronic heart failure and cardiovascular events in ESRD patients. A better understanding of the relationships of sympathetic nerve activity with renal injury might help clinical implications (treatment) for renal injury in hypertensive patients and hypertension in patients with ESRD. Recently, the role of denervation of renal sympathetic nerve in refractory hypertension has been examined and showed its efficacy in humans. The outcome from the study have not been established, but a number of animal studies show theoretical benefits for those patients in the acute phase. Further studies are needed to clarify the relationships between the sympathetic nerve activity and renal injury. [Pg.76]

ACE inhibitors and AT -receptor blockers are most useful in hypertension when the raised blood pressure results from excess renin production (e.g. renovascular hypertension), or where concurrent use of another drug (diuretic or calcium blocker) renders the blood pressure renin-dependent. The fall in blood pressure can be rapid, especially with short-acting ACE inhibitors, and low initial doses of these should be used in patients at risk those with impaired renal function, or suspected cerebrovascular disease. These patients may be advised to omit any concurrent diuretic treatment for a few days before the first dose. The antihypertensive effect increases progressively over weeks with continued adminis-... [Pg.467]

Thus, in general, most hypertensive patients have essential hypertension or other better known forms of secondary hypertension that could include renovascular h5 ertension (due to renal artery stenosis), or chronic renal insufficiency (due to renal parenchymal disease), adrenal or steroid abnormalities (due to... [Pg.225]

Percutaneous treatment of diseases affecting the urinary tract most often begins with accessing a collecting system and placing a nephrostomy tube. Thus, nephrostomy insertion is the basic technique upon which percutaneous surgical procedures are built. This chapter discusses nephrostomy tube insertion, ureteral stent insertion, ureteral stricture dilatation, nephrostomy tract dilatation, percutaneous removal of calculi, endopyelotomy techniques used in the treatment of UPJ strictures and percutaneous renal angioplasty for treatment of renovascular hypertension. [Pg.473]


See other pages where Renovascular disease hypertension is mentioned: [Pg.275]    [Pg.124]    [Pg.210]    [Pg.275]    [Pg.111]    [Pg.228]    [Pg.1702]    [Pg.186]    [Pg.776]    [Pg.42]    [Pg.222]    [Pg.13]    [Pg.65]    [Pg.486]    [Pg.491]    [Pg.330]    [Pg.334]    [Pg.496]    [Pg.438]    [Pg.555]    [Pg.1059]    [Pg.164]    [Pg.493]   
See also in sourсe #XX -- [ Pg.186 , Pg.192 ]




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