title: Renal hemodynamics and renin-angiotensin system activity in humans with multifocal renal artery fibromuscular dysplasia.
abstract: Fibromuscular dysplasia (FMD) is the second most common cause of renovascular hypertension. Nonetheless, knowledge on the renal microvasculature and renin-angiotensin system (RAS) activity in kidneys with FMD is scarce. Given the fairly good results of revascularization, we hypothesized that the renal microvasculature and RAS are relatively spared in kidneys with FMD.
  
  
  
  In 58 hypertensive patients with multifocal renal artery FMD (off medication) and 116 matched controls with essential hypertension, we measured renal blood flow (Xenon washout method) per kidney and drew blood samples from the aorta and both renal veins to determine renin secretion and glomerular filtration rate per kidney.
  
  
  
  We found that renal blood flow and glomerular filtration rate in FMD were comparable to those in controls. Although systemic renin levels were somewhat higher in FMD, renal renin secretion was not elevated. Moreover, in patients with unilateral FMD, no differences between the affected and unaffected kidney were observed with regard to renal blood flow, glomerular filtration rate, or renin secretion. In men, renin levels and renin secretion were higher as compared with women. The renal blood flow response to RAS modulation (by intrarenal infusion of angiotensin II, angiotensin-(1-7), an angiotensin II type 1 receptor blocker, or a nitric oxide synthase blocker) was also comparable between FMD and controls.
  
  
  
  Renal blood flow, glomerular filtration, and the response to vasoactive substances in kidneys with multifocal FMD are comparable to patients with essential hypertension, suggesting that microvascular function is relatively spared. Renin secretion was not increased and the response to RAS modulation was not affected in kidneys with FMD.
authors.affiliation: aDepartment of Internal Medicine and Cardiovascular Research Institute Maastricht (CARIM) bDepartment of Radiology, Maastricht University Medical Centre (MUMC+), Maastricht cDepartment of Internal Medicine, Zuyderland Medical Centre, Sittard-Geleen, The Netherlands.
authors.forename: Daan J L
authors.initials: DJ
authors.lastname: van Twist
authors.forename: Alphons 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; D000803:Angiotensin I / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D016022:Case-Control Studies; D004791:Enzyme Inhibitors / Q000494:pharmacology; D000075222:Essential Hypertension; D005260:Female; D005352:Fibromuscular Dysplasia / Q000150:complications / Q000503:physiopathology*; D005919:Glomerular Filtration Rate; D006801:Humans; D006973:Hypertension / Q000503:physiopathology; D006978:Hypertension, Renovascular / Q000209:etiology / Q000503:physiopathology*; D008297:Male; D055806:Microvessels; D008875:Middle Aged; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D010446:Peptide Fragments / Q000494:pharmacology; D012077:Renal Artery / Q000378:metabolism; D012079:Renal Circulation / Q000187:drug effects; D012083:Renin / Q000097:blood / Q000378:metabolism; D012084:Renin-Angiotensin System / Q000187:drug effects; D012737:Sex Factors
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D004791:Enzyme Inhibitors; D010446:Peptide Fragments; D000804:Angiotensin II; D000803:Angiotensin I; D019001:Nitric Oxide Synthase; D012083:Renin; C118790:angiotensin I (1-7)