While atherosclerotic Renal Artery Stenosis (ARAS) is a common cause of secondary hypertension and poses a threat to kidney viability, the degree to which reduced blood flow to cortical or medullary segments leads to a reduction in tissue oxygenation and/or increased overall oxygen consumption is not well understood. These studies have been limited due to the lack of an adequate method to assess tissue oxygenation in humans. BOLD (blood oxygen-level-dependent) magnetic resonance imaging detects local levels of tissue deoxyhemoglobin without requiring contrast. The normal kidney circulation consistently develops tissue oxygen gradients, leaving some areas within the deep sections of medulla relatively hypoxic, reflected by corresponding differences in cortical and medullary R2∗values. Moderate reductions in renal blood flow that occur with ARAS do not invariably lead to renal hypoxia, likely due to both a surplus of oxygenated blood and a parallel decrease in GFR and tubular reabsorption of sodium that leads to decrease in Oxygen consumption. However, at some point, vascular occlusion threatens the viability of the kidney and can lead to loss of kidney function. In this chapter we will review the implementation of BOLD MRI in the diagnosis and management of renovascular disease.
- BOLD MRI
- Renal artery stenosis
- Renal hypoxia and renovascular imaging
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