What is critical renal artery stenosis?: Implications for treatment

Abstract

Renovascular disease due to progressive atherosclerotic renal artery stenosis is being diagnosed with increasing frequency in the elderly. At what degree of renal artery stenosis should intervention be recommended is not clear. To answer this question, unilateral or bilateral activation of the renin-angiotensin system or its absence were detected by captopril-stimulated renal vein renin measurements in 49 hypertensive patients, aged 63 years, with normal or near-normal renal function (serum creatinine concentration < or =2.0 mg/dL), and the information was matched against radiographic measurements of the extent of renal artery stenosis. With few exceptions, unilateral or bilateral hypersecretion of renin was associated with 80% or greater reduction of renal artery lumen diameter. In contrast, normal secretion or suppression of renin production in a kidney contralateral to an ischemic one was associated with either normal caliber renal artery or renal artery stenosis less than 80%. These findings suggest that renal artery stenosis less than 80% should be monitored rather than treated because improvement of renal function and amelioration of hypertension are not expected unless the renin-angiotensin system has been activated in the affected kidney. Renoprotection by early intervention is uncertain because progression of renal artery stenosis is unpredictable. Normal captopril-stimulated renal vein renin measurements in hypertensive patients obviate the need for further work-up or interventional therapy of renovascular disease.

Renovascular Hypertension and Ischemic Nephropathy

“…Studies using balloon occlusion in humans indicate that this process requires development of a gradient across the lesion such that distal pressures fall at least by 10-20% below aortic pressure 18. Such pressure differences correspond to translesional peak systolic gradients of 15-25 mm and develop only when the cross-sectional area of occlusion approaches 70-80% as illustrated in FIGURE 1 19. An important corollary of this observation is that vascular lesions that fail to generate such a gradient are unlikely to participate in renovascular hypertension and do not benefit from measures to open the vessel.…”

Timing and Selection for Renal Revascularization in an Era of Negative Trials: What to Do?

“…(FIGURE 2). Renal vein renin sampling confirms that clinically detectable lateralization of renin production appear to require 80% stenosis (13). Hence, even lesions that are estimated at 60–70% lumen obstruction by a clinical test, such as duplex ultrasonography, may be non-functional.…”

The Cardiovascular Outcomes in Renal Atherosclerotic Lesions Study and the Future of Renal Artery Stenting

“…In dog studies, a reduction in renal blood flow and an increase in blood pressure was not observed until renal artery constriction exceeded 75% . In humans, renin secretion, as assessed by captopril‐stimulated renal vein renin secretion, was observed to be stimulated only in patients with >80% stenosis . Loss of tissue perfusion and cortical oxygenation was reported with a mean stenosis of 77% .…”