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Pathophysiological differences between multifocal fibromuscular dysplasia and atherosclerotic renal artery stenosis

Daan J L van Twist1, Alfons J H M Houben, Michiel W de Haan

  • 1aDepartment 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.

Journal of Hypertension
|January 7, 2017
PubMed
Abstract

Insights

Fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS) cause hypertension differently. FMD patients have higher renal blood flow and lower renin secretion compared to ARAS patients, challenging current theories.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Hypertension Research

Background:

  • Fibromuscular dysplasia (FMD) and atherosclerotic renal artery stenosis (ARAS) are leading causes of renovascular hypertension.
  • Current understanding suggests FMD-induced hypertension mimics ARAS mechanisms, involving reduced renal blood flow and increased renin secretion.
  • Discrepancies in blood pressure response to revascularization between FMD and ARAS patients necessitate further investigation.

Purpose of the Study:

  • To investigate the distinct pathophysiological mechanisms underlying hypertension in FMD versus ARAS.
  • To compare renal blood flow, renin secretion, and their relationship with blood pressure in patients with FMD and ARAS.

Main Methods:

  • Renal blood flow was measured using the Xenon washout method.
  • Renin secretion per kidney and blood pressure were assessed in 64 patients with multifocal FMD and 110 patients with ARAS.
  • Measurements were taken off medication and prior to revascularization.

Main Results:

  • Renal blood flow was significantly higher in FMD patients compared to ARAS patients.
  • Renin secretion lateralization to the affected kidney was observed in unilateral ARAS but not in unilateral FMD.
  • Systemic renin levels and local renin secretion were lower in FMD, with an inverse relationship between blood pressure and renin secretion compared to ARAS.

Conclusions:

  • The findings challenge the hypothesis that FMD causes hypertension through the same pathophysiological mechanisms as ARAS.
  • Distinct mechanisms may be involved in FMD-induced hypertension, warranting different therapeutic considerations.

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