Kidneys: key modulators of high-density lipoprotein levels and function

Haichun Yang1, Agnes B Fogo, Valentina Kon

  • 1aDepartments of Pediatrics, Microbiology, and Immunology bDepartments of Medicine, Microbiology, and Immunology cDepartments of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.

Insights

The kidneys significantly impact high-density lipoprotein (HDL) metabolism, affecting its levels and function. Changes in HDL may indicate kidney damage, offering new diagnostic insights.

Area of Science:

  • Nephrology
  • Cardiovascular Metabolism
  • Lipid Biochemistry

Background:

  • High-density lipoprotein (HDL) plays a crucial role in reverse cholesterol transport.
  • Kidney function is increasingly recognized to influence systemic lipid profiles.
  • Understanding the kidney's role in HDL metabolism is vital for cardiovascular and renal health.

Purpose of the Study:

  • To review current knowledge on the kidney's role in high-density lipoprotein (HDL) metabolism.
  • To examine how renal processes affect HDL particle levels, composition, and functionality.
  • To explore the potential of HDL changes as biomarkers for kidney damage.

Main Methods:

  • Literature review of studies investigating kidney-HDL interactions.
  • Analysis of data on HDL component filtration, reabsorption, and degradation in renal tubules.
  • Examination of evidence linking renal injury to alterations in plasma and urinary HDL.

Main Results:

  • HDL components, including apolipoproteins and enzymes, cross the glomerular barrier.
  • Proximal tubules process HDL components through degradation, modification, or salvage.
  • Renal injury impacts intrarenal HDL processing, altering HDL in circulation and urine.

Conclusions:

  • The kidneys play a critical role in modulating HDL levels, composition, and function.
  • Alterations in intrarenal HDL metabolism can serve as indicators of kidney damage.
  • Kidney-specific HDL changes may contribute to or reflect kidney disease pathophysiology.
Abstract

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