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Course Sample:
Introduction Renovascular hypertension is one of the more common causes of secondary hypertension with reports of its frequency varying from less than 1% in unselected patient populations to as much as 20% of patients referred to special centers. By definition, renovascular hypertension refers to hypertension caused by renal hypoperfusion - a decrease in blood flow to the kidney. Therefore, the presence of a solitary stenotic renal artery lesion does not establish the diagnosis of renovascular hypertension. It is absolutely necessary for renal ischemia to occur and this happens when stenosis is greater than 75% of the luminal diameter. This, in turn, sets off a cascade of events that leads to the stimulus that raises blood pressure; hence the diagnosis of renovascular hypertension. Most importantly, renovascular hypertension is an important diagnosis to make in that it the most common curable form of hypertension and it is one of the few potentially reversible causes of chronic renal failure. The following describes pathophysiologic mechanisms in renovascular hypertension, clinical features of the disease, and staging of suspicion for disease to select appropriate diagnostic steps. New therapeutic options are reviewed and the advantages and disadvantages of each are delineated. Pathophysiology of Renovascular Hypertension Renovascular hypertension in humans is the result of a stenotic lesion leading to ischemia that, in turn initiates events that lead to hypertension (Figure 1). The pathophysiological state of ischemia serves as the stimulus for a release of renin. Resultant high levels of angiotensin II levels then readily increase renal vascular resistance causing a shift in the pressure-natriuresis curve. In this second phase of renovascular hypertension, volume is increased and quite often maintained despite markedly elevated blood pressure further accentuating the hypertension. The patient then exhibits the symptoms of sudden and significant hypertension such as that of a pounding headaches and palpitations. Figure 1  Renal ischemia can readily continue for several years undetected. After years of renal ischemia, many patients may then enter a third phase of the disease. In these patients, regardless of whether the stenotic lesion is relieved or not, hypertension continues unabated. It is at this stage that widespread arteriosclerosis with concomitant glomerulosclerosis has already occurred in the contralateral, or nonstenotic kidney. These pathophysiological changes, specifically glomerulosclerosis along with medial hyperplasia of the blood vessels, is the result of the prolonged exposure to high blood pressures (and consequently increased glomerular pressures) in addition to the high levels of angiotensin II. The clinical relevance of this is that the sooner the lesion responsible for the renal ischemia is relieved, the greater chance of alleviating the hypertension and thereby preserving renal parenchymal tissue. The pathophysiology of the patient with bilateral disease is a little different than that seen with a solitary lesion. In patients with bilateral disease, cardiac output is usually greater than those with unilateral disease. Therefore, the hypertension in the patient with bilateral renal artery disease is more dependent on volume. The most likely etiology for this difference is that stenosis does not develop symmetrically in the two kidneys. Presumably, most bilateral stenotic lesions are initially an undetected unilateral lesion. Thus, parenchymal disease will develop in the contralateral kidney during the years of prolonged hypertension prior to the development of a stenotic lesion on that unaffected side. The hypertensive kidney disease would then impair the pressure natriuresis by which the contralateral kidney (non-stenotic side) normally maintains the classic high-renin-normal volume pattern of unilateral renal artery stenosis. This volume retention would be further exacerbated when the second stenotic lesion develops in the contralateral kidney. During this phase of the renovascular disease, the stenotic kidneys then chronically continue to secrete excess renin with the resultant elevation in peripheral resistance and fluid volume. |
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