title: Pathophysiological differences between multifocal fibromuscular dysplasia and atherosclerotic renal artery stenosis.
abstract: Fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS) are the most common causes of renovascular hypertension. So far, FMD is believed to cause hypertension via similar mechanisms as in ARAS, that is, a decrease in renal blood flow, which subsequently leads to increased renin secretion. However, given the differences in the blood pressure (BP)-lowering effect of revascularization between patients with ARAS and FMD, we questioned whether this is true.
  
  
  
  We measured renal blood flow (Xenon washout method) and renin secretion per kidney and their relationship to BP in a cohort of 64 patients with multifocal FMD and 110 patients with ARAS (off medication, prior to revascularization).
  
  
  
  We found that renal blood flow is significantly higher in FMD as compared with ARAS. In patients with unilateral ARAS, renin secretion was increased in the affected kidney as compared with the unaffected kidney. This lateralization in renin secretion, however, was not found in unilateral FMD. After correction for differences in baseline characteristics, we found that systemic renin levels and local renin secretion was lower in FMD as compared with ARAS. Moreover, the relationship between BP and renin secretion in FMD was inverse to that in ARAS.
  
  
  
  These findings argue against the hypothesis that FMD induces hypertension via similar pathophysiological mechanism as in ARAS.
authors.affiliation: aDepartment of Internal Medicine bCardiovascular Research Institute Maastricht (CARIM) cDepartment of Radiology, Maastricht University Medical Center (MUMC+), Maastricht dDepartment of Internal Medicine, Zuyderland Medical Center, Sittard, The Netherlands.
authors.forename: Daan J L
authors.initials: DJ
authors.lastname: van Twist
authors.forename: Alfons J H M
authors.initials: AJ
authors.lastname: Houben
authors.forename: Michiel W
authors.initials: MW
authors.lastname: de Haan
authors.forename: Peter W
authors.initials: PW
authors.lastname: de Leeuw
authors.forename: Abraham A
authors.initials: AA
authors.lastname: Kroon
mesh_terms: D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000150:complications; D001794:Blood Pressure; D005260:Female; D005352:Fibromuscular Dysplasia / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D006978:Hypertension, Renovascular / Q000209:etiology / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D012078:Renal Artery Obstruction / Q000209:etiology / Q000503:physiopathology*; D012079:Renal Circulation; D012083:Renin / Q000097:blood / Q000378:metabolism*
chemical_list: D012083:Renin