Role of apolipoprotein E variants in lipoprotein glomerulopathy and other renal lipidoses

T. Saito, Y. Ishigaki, S. Oikawa, T. T. Yamamoto

Research output: Contribution to journalReview articlepeer-review

17 Citations (Scopus)


Lipoprotein glomerulopathy (LPG) is a new renal lipidosis entity, characterized by peculiar histology and abnormal lipoprotein profiles mimicking type III hyperlipoproteinemia. Recently, it has been clarified that LPG is associated with novel apolipoprotein E (apoE) mutations. In particular, ApoE-Sendai, which substitutes arginine 145 with proline, is observed in most Japanese patients with LPG, although isoelectric focusing polyacrylamide gel electrophoresis has shown that it is consistent with the apoE2 isoform. To confirm the etiological role of these apoE mutations, we established an animal model of LPG. The model was created by the introduction of recombinant adenovirus containing human apoE-Sendai into apoE knockout mice. Both clinical and experimental findings indicate that LPG is caused not only by hyperlipoproteinemia but also by an in situ interaction between apoE variants and glomerular elements. In addition, several studies suggest that the apoE2 mutation is responsible for the development of diabetic nephropathy and IgA nephropathy, as well as renal lipidosis with type III hyperlipoproteinemia. In this review, we present the clinical and histological features of LPG and its pathogenesis, and discuss the role of apoE abnormalities, especially apoE-Sendai and apoE2, in LPG and other renal lipidoses.

Original languageEnglish
Pages (from-to)201-208
Number of pages8
JournalClinical and experimental nephrology
Issue number4
Publication statusPublished - 2001 Dec 1


  • Apolipoprotein E
  • Diabetic nephropathy
  • Lipoprotein glomerulopathy
  • Type III hyperlipoproteinemia

ASJC Scopus subject areas

  • Physiology
  • Nephrology
  • Physiology (medical)


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