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We appreciate the interest of Dr Tanemoto [1] in our study on the pathophysiological differences between multifocal fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS) [2]. Although we agree with Dr Tanemoto that the mechanisms leading to hypertension in multifocal FMD remain to be elucidated, we do not agree with his view that the absence of lateralization in renin secretion in patients with unilateral multifocal FMD is the result of compensatory systemic hypertension that maintains blood flow in the affected kidney.

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