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

Abstract

Purpose of review: The review will examine advances in our understanding of the role kidneys play in high-density lipoprotein (HDL) metabolism and the effect on levels, composition, and function of HDL particles.

Recent findings: Components of the HDL particles can cross the glomerular filtration barrier. Some of these components, including apolipoproteins and enzymes involved in lipid metabolism, are taken up by the proximal tubule and degraded, modified, salvaged/returned to the circulation, or lost in the urine. Injury of the glomerular capillaries or tubules can affect these intrarenal processes and modify HDL. Changes in the plasma and urine levels of HDL may be novel markers of kidney damage or mechanism(s) of kidney disease.

Summary: The kidneys have a significant role in the metabolism of individual HDL components, which in turn modulate HDL levels, composition, and functionality of HDL particles. These intrarenal effects may be useful markers of kidney damage and have consequences on kidney-related perturbations in HDL.

Figure 1

Renal handling of HDL components. ApoA-I, pre β-HDL and LCAT can be filtered by the glomerular capillaries and taken up by proximal tubular epithelial cells through the cubilin-megalin-amnionless complex or other transporters. ApoA-I can undergo endocytosis and degradation, or direct transcytosis, or transcytosis after modification. The salvaged ApoA-I enters the interstitium, and finally is delivered back to the circulation.