Renovascular disease

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. 

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

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. 

Angiotensin-converting enzyme inhibitors should be used with caution in patients taking diuretics because of an enhanced hypotensive effect. Angiotensin-converting enzyme inhibitors should also be used with caution in patients with renal impairment. Renal function needs to be monitored in patients with renovascular disease. 

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. 

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... 

Three contraindications are (a) patients with a hypersensitivity to ACE inhibitors (including angioedema), (b) patients with known or suspected renovascular disease, and (c) pregnancy. 

Watson ML, Bell GM, Muir AL, Buist TA, Kellett RJ, Padfield PL. Captopril/diuretic combinations in severe renovascular disease a cautionary note. Lancet 1983 2(8346) 404-5. 

J-M. Halimi, J Ribstein, G. Du Cailar, et al. Nephrotic-range proteinuria in patients with renovascular disease. American Journal of Medicine 108, 120(2000). 

Chronic kidney disease Cushing s syndrome Coarctation of the aorta Obstructive sleep apnea Parathyroid disease Pheoc h ro mocyto ma Primary aldosteronism Renovascular disease Thyroid disease... 

A reduction in GFR has been reported in the presence and absence of renal artery stenosis. The rise is often minimal in renovascular disease if only one renal artery is stenotic, but is more apparent in patients with a single kidney with renovascular disease, congestive heart failure, volume depletion, or bilateral renal small vessel disease. Up to one-third of patients with bilateral renal artery stenosis demonstrate a rise in serum creatinine >30% after starting ACEI therapy. 

Acute decreases in renal function and hyperkalemia usually resolve over several days after ACEl or ARB therapy is discontinued. Occasional patients will require management of severe hyperkalemia, usually with sodium polystyrene sulfate (see Chap. 50). ACEl or ARB therapy may frequently be reinitiated, particularly for patients with congestive heart failure, after intravascular volume depletion has been corrected or the diuretic doses reduced. The development of mild renal insufficiency (serum creatinine concentration of 2 to 3 mg/dL) may be an acceptable trade-off for hemodynamic improvement in certain patients with severe congestive heart failure or renovascular disease not amenable to invasive management. Congestive heart failure patients with greater renal insufficiency may be best treated by substitution of hydralazine and nitrates for afterload reduction. 

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. ... 

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. 

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... 

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... 

Gift of Life Donor Program (2004) History of organ and tissue donation and transplantation, www.donorsl.org Hiramoto J, LaBerge J, Hirose R (2003) Live donor renal transport using kidney with arteriographic evidence of mild renovascular disease. Clin Transplant 16 24-29 Houston Chronicle (2004) A brief history of transplants. www.chron.com/content/chronicle/special/transplant/ history.html... 

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