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The renal artery ostium flow diverter: structure and potential role in atherosclerosis

Edward B Neufeld1, Zu-Xi Yu, Danielle Springer

  • 1Laboratory of Cardiac Energetics, NHLBI, NIH, Bethesda, MD 20892, United States. neufelde@mail.nih.gov

Atherosclerosis
|February 13, 2010
PubMed

Insights

A newly identified renal artery flow diverter at the caudal ostium directs blood flow and retains low-density lipoprotein (LDL), initiating renal atherosclerosis. This finding explains a previously unknown mechanism for the development of this vascular disease.

Area of Science:

  • Cardiovascular Biology
  • Renal Physiology
  • Atherosclerosis Research

Background:

  • Renal atherosclerosis initiation is primarily observed at the caudal region of the renal artery ostium.
  • The precise mechanism driving atherosclerosis initiation at this specific site remains unsubstantiated.

Purpose of the Study:

  • To identify the mechanism responsible for the initiation of renal atherosclerosis at the caudal renal artery ostium.
  • To investigate the role of a specific anatomical structure in the early stages of renal atherosclerosis.

Main Methods:

  • High-resolution ultrasound to visualize blood flow dynamics in vivo.
  • Two-photon excitation en face microscopy to examine the microstructure of the renal artery ostium.
  • Utilizing fluorescent low-density lipoprotein (LDL) to track its retention patterns.

Main Results:

  • Identification of a renal artery flow diverter on the caudal wall of the renal artery ostium.
  • Ultrasound confirmed the diverter generates flow eddies, directing aortic flow into the renal artery.
  • Microscopy revealed reduced elastic lamina, exposing LDL retention sites, and fluorescent LDL was selectively retained by the diverter.

Conclusions:

  • The renal artery flow diverter plays a crucial role in directing blood flow and selectively retaining LDL.
  • The rigid macromolecular structure of the diverter is essential for its vascular function.
  • This diverter-mediated LDL retention is proposed as a key contributor to the initiation of renal atherosclerosis.

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