Abstract
Atherosclerotic renal artery stenosis has a range of manifestations depending on the severity of vascular occlusion. The aim of this study was to examine whether exceeding the limits of adaptation to reduced blood flow ultimately leads to tissue hypoxia, as determined by blood oxygen level dependent MRI. We compared 3 groups of hypertensive patients, 24 with essential hypertension, 13 with "moderate" (Doppler velocities 200-384 cm/s), and 17 with "severe" atherosclerotic renal artery stenosis (ARAS; velocities >384 cm/s and loss of functional renal tissue). Cortical and medullary blood flows and volumes were determined by multidetector computed tomography. Poststenotic kidney size and blood flow were reduced with ARAS, and tissue perfusion fell in the most severe lesions. Tissue medullary deoxyhemoglobin, as reflected by R2 * values, was higher as compared with the cortex for all of the groups and did not differ between subjects with renal artery lesions and essential hypertension. By contrast, cortical R2 * levels were elevated for severe ARAS (21.6±9.4 per second) as compared with either essential hypertension (17.8±2.3 per second; P<0.01) or moderate ARAS (15.7±2.1 per second; P<0.01). Changes in medullary R2 * after furosemide administration tended to be blunted in severe ARAS as compared with unaffected (contralateral) kidneys. These results demonstrate that severe vascular occlusion overwhelms the capacity of the kidney to adapt to reduced blood flow, manifest as overt cortical hypoxia as measured by blood oxygen level-dependent MRI. The level of cortical hypoxia is out of proportion to the medulla and may provide a marker to identify irreversible parenchymal injury.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1066-1072 |
| Number of pages | 7 |
| Journal | Hypertension |
| Volume | 58 |
| Issue number | 6 |
| DOIs | |
| State | Published - Dec 2011 |
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Keywords
- Hypertension
- Hypoxia
- MRI
- Renal artery stenosis
- Renal physiology
ASJC Scopus subject areas
- Internal Medicine
Cite this
Blood oxygen level-dependent magnetic resonance imaging identifies cortical hypoxia in severe renovascular disease. / Gloviczki, Monika L.; Glockner, James; Crane, John A.; McKusick, Michael A.; Misra, Sanjay; Grande, Joseph Peter; Lerman, Lilach O; Textor, Stephen C.
In: Hypertension, Vol. 58, No. 6, 12.2011, p. 1066-1072.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Blood oxygen level-dependent magnetic resonance imaging identifies cortical hypoxia in severe renovascular disease
AU - Gloviczki, Monika L.
AU - Glockner, James
AU - Crane, John A.
AU - McKusick, Michael A.
AU - Misra, Sanjay
AU - Grande, Joseph Peter
AU - Lerman, Lilach O
AU - Textor, Stephen C
PY - 2011/12
Y1 - 2011/12
N2 - Atherosclerotic renal artery stenosis has a range of manifestations depending on the severity of vascular occlusion. The aim of this study was to examine whether exceeding the limits of adaptation to reduced blood flow ultimately leads to tissue hypoxia, as determined by blood oxygen level dependent MRI. We compared 3 groups of hypertensive patients, 24 with essential hypertension, 13 with "moderate" (Doppler velocities 200-384 cm/s), and 17 with "severe" atherosclerotic renal artery stenosis (ARAS; velocities >384 cm/s and loss of functional renal tissue). Cortical and medullary blood flows and volumes were determined by multidetector computed tomography. Poststenotic kidney size and blood flow were reduced with ARAS, and tissue perfusion fell in the most severe lesions. Tissue medullary deoxyhemoglobin, as reflected by R2 * values, was higher as compared with the cortex for all of the groups and did not differ between subjects with renal artery lesions and essential hypertension. By contrast, cortical R2 * levels were elevated for severe ARAS (21.6±9.4 per second) as compared with either essential hypertension (17.8±2.3 per second; P<0.01) or moderate ARAS (15.7±2.1 per second; P<0.01). Changes in medullary R2 * after furosemide administration tended to be blunted in severe ARAS as compared with unaffected (contralateral) kidneys. These results demonstrate that severe vascular occlusion overwhelms the capacity of the kidney to adapt to reduced blood flow, manifest as overt cortical hypoxia as measured by blood oxygen level-dependent MRI. The level of cortical hypoxia is out of proportion to the medulla and may provide a marker to identify irreversible parenchymal injury.
AB - Atherosclerotic renal artery stenosis has a range of manifestations depending on the severity of vascular occlusion. The aim of this study was to examine whether exceeding the limits of adaptation to reduced blood flow ultimately leads to tissue hypoxia, as determined by blood oxygen level dependent MRI. We compared 3 groups of hypertensive patients, 24 with essential hypertension, 13 with "moderate" (Doppler velocities 200-384 cm/s), and 17 with "severe" atherosclerotic renal artery stenosis (ARAS; velocities >384 cm/s and loss of functional renal tissue). Cortical and medullary blood flows and volumes were determined by multidetector computed tomography. Poststenotic kidney size and blood flow were reduced with ARAS, and tissue perfusion fell in the most severe lesions. Tissue medullary deoxyhemoglobin, as reflected by R2 * values, was higher as compared with the cortex for all of the groups and did not differ between subjects with renal artery lesions and essential hypertension. By contrast, cortical R2 * levels were elevated for severe ARAS (21.6±9.4 per second) as compared with either essential hypertension (17.8±2.3 per second; P<0.01) or moderate ARAS (15.7±2.1 per second; P<0.01). Changes in medullary R2 * after furosemide administration tended to be blunted in severe ARAS as compared with unaffected (contralateral) kidneys. These results demonstrate that severe vascular occlusion overwhelms the capacity of the kidney to adapt to reduced blood flow, manifest as overt cortical hypoxia as measured by blood oxygen level-dependent MRI. The level of cortical hypoxia is out of proportion to the medulla and may provide a marker to identify irreversible parenchymal injury.
KW - Hypertension
KW - Hypoxia
KW - MRI
KW - Renal artery stenosis
KW - Renal physiology
UR - http://www.scopus.com/inward/record.url?scp=83155192129&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=83155192129&partnerID=8YFLogxK
U2 - 10.1161/HYPERTENSIONAHA.111.171405
DO - 10.1161/HYPERTENSIONAHA.111.171405
M3 - Article
C2 - 22042812
AN - SCOPUS:83155192129
VL - 58
SP - 1066
EP - 1072
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 6
ER -