Key result
MRE detects ~19% greater renal medullary stiffness in RAS versus healthy kidneys, worsening in ARAS.
Why the study?
Does 3-dimensional MRE detect in vivo renal medullary fibrosis secondary to renal artery stenosis in a swine model?
Does 3-dimensional MRE detect in vivo renal medullary fibrosis secondary to renal artery stenosis in a swine model?
Absolute Event Rate: 12.7% vs 10.7%
p-value: p=0.004
Noninvasive 3-dimensional MRE can detect increased renal medullary stiffness in vivo, which correlates with histological fibrosis in a swine model of renal artery stenosis.
Supports noninvasive MRE for renal fibrosis detection in swine RAS; leaves open human translation and clinical adoption.
OBJECTIVES: Magnetic resonance elastography (MRE) can noninvasively sample tissue stiffness in vivo. Renal fibrosis secondary to renal artery stenosis (RAS), which is aggravated in atherosclerotic RAS (ARAS), may increase its stiffness. An increase in cortical stiffness in vivo can be masked by intrinsic hemodynamic determinants, whereas renal medullary stiffness is less dependent on renal hemodynamics. Therefore, this study tested the hypothesis that MRE-determined medullary stiffness would correspond to the histological degree of medullary fibrosis in stenotic kidneys in RAS and detect its exacerbation in ARAS. MATERIALS AND METHODS: Seventeen pigs were studied 10 weeks after induction of unilateral RAS (n = 6), ARAS (n = 5), or sham (n = 6). Stiffness of the cortex and the medulla was determined through 3-dimensional MRE, and renal perfusion and function were determined using multidetector computed tomography. Kidney fibrosis was subsequently assessed ex vivo using the Masson trichrome staining. RESULTS: Renal stenotic cortex and medulla were significantly more fibrotic in RAS and ARAS compared with healthy kidney. However, MRE detected increased stiffness in RAS compared with the healthy kidney (12.7 ± 0.41 kPa vs 10.7 ± 0.18 kPa; P = 0.004) only in the medulla, which was further increased in ARAS (16.6 ± 1.3 kPa; P = 0.017 vs RAS). Magnetic resonance elastography-derived medullary, but not cortical, stiffness significantly correlated with histological degree of fibrosis, although cortical and medullary fibroses were correlated. Renal blood flow and function were similarly decreased in RAS and ARAS compared with the healthy kidney. CONCLUSIONS: Noninvasive 3-dimensional MRE detects increased renal medullary stiffness in RAS and ARAS in vivo, which correlates with its fibrosis ex vivo and may also reflect cortical fibrosis. Hence, MRE-derived medullary stiffness can be potentially useful in detecting renal fibrosis and track disease progression.
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Korsmo et al. (2012) studied Renal artery stenosis (RAS) and atherosclerotic RAS (ARAS) (n=17). Magnetic resonance elastography (MRE) vs. Healthy kidney (sham) was evaluated on Renal medullary stiffness (p=0.004). Magnetic resonance elastography detected increased renal medullary stiffness in RAS compared with healthy kidneys (12.7 vs 10.7 kPa; P=0.004), which was further increased in ARAS (16.6 kPa; P=0.017).
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