Peristenotic Collateral Circulation in Atherosclerotic Renovascular Disease

Abstract

<jats:p>The significance of peristenotic collateral circulation (PCC) development around a stenotic renal artery is unknown. We tested the hypothesis that PCC is linked to loss of kidney function and recovery potential in patients with atherosclerotic renovascular disease (ARVD). Thirty-four patients with ARVD were assigned to medical-therapy with or without revascularization based on clinical indications. The PCC was visualized using multidetector computed tomography and defined relative to segmental arteries in patients with essential hypertension. PCC number before and 3 months after treatment was correlated with various renal parameters. Thirty-four stenotic kidneys from 30 patients were analyzed. PCC number correlated inversely with kidney volume. ARVD–stenotic kidneys with baseline PCC (collateral ARVD [C-ARVD], n=13) associated with elevated 24-hour urine protein and stenotic kidney vein level of tumor necrosis factor-α, lower single-kidney volume and blood flow, and greater hypoxia than in stenotic kidneys with no PCC (no collateral ARVD [NC-ARVD], n=17). Revascularization (but not medical-therapy alone) improved stenotic kidney function and reduced inflammation in both NC-ARVD and C-ARVD. In C-ARVD, revascularization also increased stenotic kidney volume, blood flow, and oxygenation to levels comparable to NC-ARVD, and induced PCC regression. However, revascularization improved systolic blood pressure, plasma renin activity, and filtration fraction only in NC-ARVD. Therefore, patients with C-ARVD have greater kidney dysfunction, atrophy, hypoxia, and inflammation compared with patients with NC-ARVD, suggesting that PCC does not effectively protect the stenotic kidney in ARVD. Renal artery revascularization improved in C-ARVD stenotic kidney function, but not hypertension or renin-angiotensin system activation. These observations may help direct management of patients with ARVD.</jats:p>

Revascularization for Renovascular Disease: A Scientific Statement From the American Heart Association

“…75 It is likely that some preservation of volume is related to collateral vessels that can develop to replace a minimum level of perfusion. 76…”

With a Little Help From My Friends: the Role of the Renal Collateral Circulation in Atherosclerotic Renovascular Disease

“…In a recent study in 34 patients with ARVD, we found that patients with a collateral circulation in fact had greater kidney dysfunction, atrophy, hypoxia, and inflammation than patients without, and a poorer blood pressure–response to revascularization. 16 Similarly, in RAS pigs the extent of collateral circulation is inversely associated with distal cortical volume and perfusion. 28 Nonetheless, the collateral circulation may sustain the poststenotic kidney viability until revascularization is feasible.…”

“…We have recently observed an association between increased severity of ARVD with development of collateral circulation in the stenotic human kidney, 16 but the underlying mechanism is incompletely understood. 17 According to established paradigms, development of collaterals occurs through sprouting and nonsprouting formation of arteries from existing vessels (angiogenesis) 18 or through expansion of preexisting collateral vessels (arteriogenesis).…”

“…70 However, in humans, there was no difference in the blood pressure of patients with and without collaterals, and the effect of revascularization on blood pressure was lower in patients with identifiable collaterals. 16…”

“…26,27 Microvascular collaterals found in most tissues are typically <150 μm in diameter and tortuous, often with an unorganized pattern. 16,28,29 These vessels are capable of increasing their diameter 10-to 20-fold without necessarily losing wall thickness in response to increased blood flow and thereby increased tangential vascular shear stress caused by occlusion of adjacent major arteries. [30][31][32][33] This impact of shear stress upon arteriogenesis is augmented by reversal of flow in arterioles.…”