Evidence map›Paper›PMID 29740794›Full record

ArticleCEN case reports2018

Focal segmental glomerulosclerosis with heterozygous apolipoprotein E5 (Glu3Lys).

Masaru Sasaki, Tetsuhiko Yasuno, Kenji Ito, Akira Matsunaga, Satoshi Hisano, Yasuhiro Abe, Katsuhisa Miyake, Kosuke Masutani, Hitoshi Nakashima, Takao Saito

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in CEN case reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Apolipoprotein E and Atherosclerosis.Current atherosclerosis reports · 2021
    Review
  4. Review
  5. Mechanisms of Scarring in Focal Segmental Glomerulosclerosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Masaru SasakiDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Tetsuhiko YasunoDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan. yasuno9584@fukuoka-u.ac.jp.
Kenji ItoDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Akira MatsunagaDepartment of Laboratory Medicine, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Satoshi HisanoDepartment of Pathology, Faculty of Medicine, Fukuoka University, Fukuoka, Japan.
Yasuhiro AbeDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Katsuhisa MiyakeDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Kosuke MasutaniDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Hitoshi NakashimaDivision of Nephrology and Rheumatology, Department of Internal Medicine, Faculty of Medicine, Fukuoka University, 7-45-1 Nanakuma, Jonan-ku, Fukuoka, 814-0180, Japan.
Takao SaitoSanko Clinic, Fukuoka, Japan.
Fukuoka University · JPOno Clinic · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apolipoprotein (apo) E5 is a rare apoE isoform. The apoE5 (Glu3Lys) variant, which is caused by the substitution of lysine with glutamic acid at codon 3, has a relative frequency of 0.1% in Japan. Previous studies have reported that apoE5 (Glu3Lys) is associated with hyperlipidemia and cardiovascular diseases, but this isoform has higher LDL receptor-binding activity than that of normal apoE3. Nephropathy associated with apoE5 (Glu3Lys) alone has not yet been reported. We present a case of a 51-year-old man with nephrotic syndrome. On renal biopsy, three glomeruli showed segmental sclerosis with hypertrophy of podocytes and intracapillary marked infiltration of intraglomerular foam cells. These findings were compatible with focal segmental glomerulosclerosis (FSGS). The patient had mild diabetes mellitus and monoclonal gammopathy of undetermined significance, but there were no specific findings of nephrolopathy related to these diseases. Various factors are involved in the pathogenesis of FSGS, including dyslipidemia and apoE activity. Our findings suggest that abnormal lipid metabolism by ApoE5 (Glu3Lys) is involved in the onset of FSGS.

Indexed as

Angiotensin Receptor AntagonistsApolipoproteins EAsian PeopleFoam CellsGlomerulosclerosis, Focal SegmentalHeterozygoteHumansHydroxymethylglutaryl-CoA Reductase InhibitorsHypertrophyKidneyKidney GlomerulusMaleMiddle AgedMonoclonal Gammopathy of Undetermined SignificanceNephrotic SyndromePhenotypeAngiotensin Receptor Antagonistsapolipoprotein E5Apolipoproteins EHydroxymethylglutaryl-CoA Reductase InhibitorsApoE isoformFoam cellsHyperlipidemiaPodocyte injuryVariant

Identifiers

PMID29740794
PMCPMC6181881
OpenAlexW2800327863

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.