Cited by 7Renal Diseases and GlomerulopathiesLipid metabolism and disordersChronic Kidney Disease and Diabetes

Macrophage Infiltration into the Glomeruli in Lipoprotein Glomerulopathy

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Takasaki, Satoshi, Maeda, Kunihiko, Joh, Kensuke, Yamakage, Shu, Fukase, Sachiko, Takahashi, Toshiyuki, Suzuki, Masayuki, Matsunaga, Akira +1 more·2015·Case Reports in Nephrology and Dialysis

Abstract

Lipoprotein glomerulopathy (LPG) is characterized by histopathological features showing intra-glomerular lipoprotein thrombi and type III hyperlipoproteinemia (HLP), with heterozygote mutation of apolipoprotein (apo) E gene. On the other hand, as another renal lipidosis with type III HLP, apoE2 homozygote-related glomerulopathy (apoE2-GN) showing foamy macrophages has been reported. The case of a 25-year-old man who had LPG by clinical behavior and gene analysis, but demonstrated atypical histopathological features with a substantial amount of foamy macrophage infiltration in the glomeruli, is presented. The combination of alleles for apoE Tokyo/Maebashi and classical apoE2 (Arg158Cys) was inferred to be the leading cause of the unique renal pathology with lipoprotein thrombi and foamy macrophages. In addition, foamy macrophages infiltrated some part of the apoE-positive region within the glomerulus, but did not exist in lipoprotein thrombi despite apoE positivity, suggesting that properties of apoE are crucial in the development of LPG rather than macrophage function. This case provides important information related to the pathogenesis of LPG and apoE2-GN.

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Crossref · 10.1159/000441715

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  • The APOE Tokyo/Maebashi mutation is found at the LDL receptor binding site of apoE.

    “The APOE Tokyo/Maebashi mutation is found at the LDL receptor binding site of apoE,13 which is where most mutations associated with LPG occur.35”

    From Lipoprotein Glomerulopathy, First Case Report from Canada (2022) · cites this paper as [13]

    The Case Report section (Phenotype, Genotype, and DNA Sequence Analysis of apoE; page unavailable) identifies Tokyo/Maebashi as a deletion at codons 141–143. Neither that section nor the Discussion identifies those codons as the LDL receptor-binding site, so the specific site claim is not established by our copy. (LLM, conf=0.78)

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Research works printed but not linked: 12

  1. [2]Saito T Matsunaga A Ito K Nakashima H Topics in lipoprotein glomerulopathy: an overview Clin Exp Nephrol 2014 18 214 217 24149835
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  6. [8]Kanamaru Y Nakao A Shirato I Okumura K Ogawa H Tomino Y Ra C Chronic graft-versus-host autoimmune disease in Fc receptor γ chain-deficient mice results in lipoprotein glomerulopathy J Am Soc Nephrol 2002 13 1527 1533 12039982
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Authors
Takasaki, S., Maeda, K., Joh, K., Yamakage, S., Fukase, S., Takahashi, T., Suzuki, M., Matsunaga, A., & Saito, T.
Affiliations
  • Yamagata Saisei Hospital (JP)
  • Yamagata Prefectural University of Health Sciences (JP)
  • Tohoku University (JP)
  • Yamagata Prefectural Central Hospital (JP)
  • Fukuoka University (JP)
Corresponding author
Takasaki, Satoshi
Venue
Case Reports in Nephrology and Dialysis
Publisher
S. Karger AG
Published
2015-12-15
Volume
5
Issue
3
Pages
204-212
ISSN
2296-9705 (ISSN-L)
OpenAlex
W2231013303
Cited by
7
References
3
Citations by year
2024: 1 · 2022: 3 · 2019: 1 · 2018: 1 · 2016: 1
FWCI
0.58
Type
journal article
Language
en
Open access
Locations
  • Case Reports in Nephrology and Dialysis (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Keywords
lipoprotein glomerulopathy, apolipoprotein E, foam cells, macrophage infiltration, type III hyperlipoproteinemia, glomerular pathology, APOE genotype, pathogenesis

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