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Related Experiment Video

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Apolipoprotein E-related glomerular disorders.

Takao Saito1, Akira Matsunaga2, Megumu Fukunaga3

  • 1Sanko Clinic, Fukuoka, Japan; Faculty of Medicine, Fukuoka University, Fukuoka, Japan.

Kidney International
|December 26, 2019
PubMed
Summary

Apolipoprotein E (apoE) mutations cause distinct glomerular disorders like apoE2 homozygote glomerulopathy and lipoprotein glomerulopathy (LPG). Macrophages play a key role in foam cell formation in apoE2 homozygote glomerulopathy and lipoprotein accumulation in LPG.

Keywords:
apolipoprotein E Toyonakaapolipoprotein E2 homozygote glomerulopathyapolipoprotein E5apolipoprotein mutationslipoprotein glomerulopathymacrophage

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Area of Science:

  • Nephrology
  • Genetics
  • Molecular Biology

Background:

  • Apolipoprotein E (apoE) mutations are linked to specific glomerular diseases.
  • Two main conditions, apoE2 homozygote glomerulopathy and lipoprotein glomerulopathy (LPG), have been identified.
  • These disorders involve distinct histological features and underlying molecular mechanisms.

Purpose of the Study:

  • To elucidate the mechanisms by which various apolipoprotein E (apoE) mutations lead to glomerular disorders.
  • To differentiate the pathological pathways of apoE2 homozygote glomerulopathy and lipoprotein glomerulopathy (LPG).
  • To explore the role of macrophages and lipoprotein aggregation in the pathogenesis of these kidney diseases.

Main Methods:

  • Histological examination of kidney biopsies.
  • Tandem mass spectrometry for apoE accumulation analysis.
  • Review of recent studies on apoE mutation-induced glomerulopathies.

Main Results:

  • ApoE2 homozygote glomerulopathy shows glomerulosclerosis with foam cells and occasional lipoprotein thrombi.
  • ApoE Toyonaka mutation combined with apoE2/2 can lead to membranous nephropathy-like features due to lipid-free apoE accumulation.
  • Lipoprotein glomerulopathy (LPG) is characterized by lamellated lipoprotein thrombi without foam cells, linked to apoE aggregation and potential apoE5 involvement.

Conclusions:

  • Diverse apoE mutations contribute to distinct glomerular pathologies through varied mechanisms.
  • Macrophages are crucial in foam cell formation in apoE2 homozygote glomerulopathy.
  • Lipoprotein accumulation and thrombi in LPG may result from apoE dysfunction and aggregation.