Chronic furosemide administration blunts renal BOLD magnetic resonance response to an acute furosemide stimulus in patients being evaluated for renal artery revascularization

Background Blood Oxygen Level Dependent (BOLD) magnetic resonance (MR) is a novel imaging tool that is able to detect tissue oxygenation and has recently been utilized to evaluate renal function in patients with renal artery stenosis (RAS). Renal BOLD imaging is typically performed before and after a furosemide stimulus to assess kidney viability. Furosemide blocks the sodium-potassium2chloride transporter, an oxygen-dependent process, in the ascending loop of Henle located in the renal medulla. Presumably, kidneys that are able to decrease oxygen consumption and increase BOLD (T2*) signal in response to furosemide would be viable and benefit from revascularization procedures. A standard dose of 20mg of intravenous (IV) furosemide is administered to evaluate renal responsiveness (increased T2* signal intensity) and viability. However, little is known about the effect of prior exposure to furosemide on the ability of BOLD MR techniques to evaluate renal function.