Renal artery stenosis (RAS) is the main cause of “secondary” arterial hypertension. RAS is found in 0.5% to 5% of hypertensive patients. RAS is most often atherosclerotic in nature and less frequent due to fibromuscular hyperplasia.1 The prevalence of RAS is approximately 2% in unselected patients but reaches 40% in older patients or in patients with multiple risk factors for atherosclerosis or with documented atherosclerosis in other vascular territories.2,3 Due to improvements in vascular imaging by ultrasound, magnetic resonance imaging, computed tomography, and angiography and due to the larger proportion of elderly patients undergoing coronary angiography, the finding of a RAS on angiography is a frequent occurrence. “Drive-by” renal angiograms are frequently performed during coronary angiography procedures. However, as is the case in the coronary arteries, the relationship between anatomic findings and the functional repercussion of a given stenosis is poor.4
Thus, stenoses of the main trunk of the renal arteries are frequent and easy to identify, but their causative role in clinical manifestations is difficult to evaluate, and it is difficult to predict the effect of renal stenting
PATHOPHYSIOLOGY OF RENAL ARTERY STENOSIS
Renal artery stenoses contribute to arterial hypertension and/or to ischemic nephropathy.
Much modern thinking about the physiopathology of renovascular hypertension is influenced by the classical 1-kidney-1-clip animal model (analogous to a bilateral RAS)5 and the 2-kidneys-1-clip model6 (analogous to the unilateral RAS). A simplified scheme illustrating the pathophysiology of renovascular hypertension is shown in Figure 7-1. When the perfusion pressure decreases in the renal artery, especially in the afferent renal artery, an upregulation of renin production takes place in the juxtaglomerular apparatus. The decrease in glomerular filtration pressure will be partially counteracted by a constriction of the efferent artery. The activation of the renin-angiotensin system resulting in angiotensin II–mediated vasoconstriction is a central component to this process. In contrast, the nonstenotic kidney, subjected to higher perfusion pressure, responds by an increase in the excretion of sodium (“pressure natriuresis”) that will tend to lower the pressure. This decrease in systemic pressure will in turn decrease the perfusion pressure in the stenotic kidney and further stimulate the release of renin. Elevated levels of angiotensin II induce vasoconstriction and trigger the secretion of aldosterone. The latter enhances sodium reabsorption in proximal and distal tubules. Thus, renovascular hypertension is mediated initially by elevated plasma renin, although in case of sustained hypertension, plasma renin activity will tend to decrease. Renovascular hypertension fundamentally depends on the presence and magnitude of a pressure drop due to the stenosis.
Simplified scheme illustrating the pathophysiology of renovascular hypertension.
The most common cause of renal insufficiency in patients with RAS is the association ...