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Review
. 2015 May;22(3):224-31.
doi: 10.1053/j.ackd.2014.10.004.

Atherosclerotic renal artery stenosis: current status

Soon Hyo Kwon  1 , Lilach O Lerman  2
Affiliations
Review

Atherosclerotic renal artery stenosis: current status

Soon Hyo Kwon et al. Adv Chronic Kidney Dis. 2015 May.

Abstract

Atherosclerotic renal artery stenosis (ARAS) remains a major cause of secondary hypertension and kidney failure. Randomized prospective trials show that medical treatment should constitute the main therapeutic approach in ARAS. Regardless of intensive treatment and adequate blood pressure control, however, renal and extrarenal complications are not uncommon. Yet, the precise mechanisms, accurate detection, and optimal treatment in ARAS remain elusive. Strategies oriented to early detection and targeting these pathogenic pathways might prevent development of clinical end points. Here, we review the results of recent clinical trials, current understanding of the pathogenic mechanisms, novel imaging techniques to assess kidney damage in ARAS, and treatment options.

Keywords: Atherosclerosis; Hypertension; Inflammation; Ischemia; Renal artery obstruction.

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Conflict of interest statement

Conflict of interest: The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Schematic of interactive mechanisms responsible for kidney injury in atherosclerotic renal artery stenosis (ARAS). A critical renovascular occlusion activates the renin-angiotensin-aldosterone system (RAAS), elicits hypoxia, and increases oxidative stress. Together with atherosclerosis this process induces parenchymal inflammation, fibrosis, microvascular loss, and kidney dysfunction.
Figure 2
Figure 2
Representative 3D micro-computed tomography images from a normal (left) and a stenotic swine kidney, showing a decreased number of cortical and medullary microvessels in the hypo-perfused kidney.
Figure 3
Figure 3
Blood oxygen-level-dependent (BOLD) parametric map in normal pigs (left) and in a swine model of atherosclerotic renal artery stenosis (ARAS) (right) obtained before and after injection of furosemide, which inhibits oxygen-dependent tubular transport and thereby increases kidney oxygenation. Arrows indicate the medullary regions, and crosses blood vessels. Medullary R2* was higher (more red) both at baseline and after furosemide in ARAS, suggesting greater hypoxia and blunted response to furosemide compared to normal pig kidneys.
See this image and copyright information in PMC

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