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Cited by 24Renal Diseases and GlomerulopathiesLipid metabolism and disordersChronic Kidney Disease and Diabetes

The Novel Apolipoprotein E Mutation ApoE Chengdu (c.518T＞C, p.L173P) in a Chinese Patient with Lipoprotein Glomerulopathy

Open access
Wu, Hongyan, Yang, Yuan, Hu, Zhangxue·2018·Journal of Atherosclerosis and Thrombosis
DOI 10.5551/jat.41996PMC PMC6099066
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Abstract

AIMS: Lipoprotein glomerulopathy (LPG) is a rare inherited renal disease. Several apolipoprotein E (apoE) mutations have been reported to be related to LPG. Herein, we report a case of a LPG patient with a novel apoE mutation. METHODS: A 45-year-old Chinese female was diagnosed as LPG by renal biopsy. APOE gene was sequenced. Clinical and genetic studies were conducted. RESULTS: The patient presented with nephrotic syndrome and hypertension. A fasting lipid panel showed mild hyperlipidemia and elevated serum apoE (5.6 mg/dL). Renal biopsy revealed typical LPG lesions with whorled, mesh-like material in dilated glomerular capillary lumens that stained positive for Sudan Ⅲ and apoE. apoE gene analysis revealed a T-to-C point mutation at amino acid 173 that caused a substitution of a proline residue for a leucine residue, which has not been reported previously. We named this mutation apoE Chengdu (c.518T＞C, p.L173P). Two of five of the family members carried this mutation, including the patient's brother who was receiving hemodialysis, and her sister, whose urine protein levels were normal. All mutation carriers were heterozygotes with the apoE genotype ε3/ε3. This mutation was not found among 200 of the local people. Fenofibrate treatment for one year induced clinical improvement. CONCLUSIONS: ApoE Chengdu (p.L173P) is a novel mutation causing LPG. This case supports the hypothesis that the substitution of proline in or near the LDL receptor-binding area contributes to the development of LPG. The detailed mechanism of action of this variant remains to be elucidated.

AI snapshot

Written from the paper’s full text.

TL;DR

This case report identifies a novel APOE mutation, apoE Chengdu (c.518T>C, p.L173P), in a Chinese patient with lipoprotein glomerulopathy (LPG). The mutation was heterozygous, absent from 200 local elderly controls, and the proband improved clinically with fenofibrate treatment.

Key findings

  • The proband had nephrotic syndrome, hypertension, mild hyperlipidemia, and elevated serum apoE (5.6 mg/dL); renal biopsy showed typical LPG lesions with whorled, mesh-like material in dilated glomerular capillary lumens that stained positive for Sudan III and apoE.
  • APOE sequencing found a novel T-to-C point mutation at codon 173 causing p.L173P; all carriers were heterozygous and had the apoE genotype ε3/ε3, and the variant was not found among 200 local elderly people.
  • Two of five family members carried the mutation: one brother was on hemodialysis with possible LPG, and one sister was an asymptomatic carrier; the pedigree suggested autosomal dominant inheritance with incomplete penetrance.
  • After one year of fenofibrate treatment, the proband’s urine protein/creatinine ratio decreased to 0.58 g/g, triglycerides decreased to 55 mg/dL, apoE decreased to 4.3 mg/dL, and serum albumin normalized.

Methods

  • Case report and family/genetic study: the proband, five family members, and 200 local elderly controls were evaluated; APOE coding regions were sequenced, and genotype was confirmed by HhaI RFLP analysis.
  • Clinicopathological examination included routine laboratory tests, lipid profile and serum apoE measurement, renal biopsy with light microscopy, immunofluorescence, and electron microscopy.
  • The proband was treated with fenofibrate and hyzaar, with clinical and laboratory follow-up over one year.

Limitations

  • The paper states that the detailed mechanism of action of this variant remains to be elucidated.
  • Evident from the text: this is a single-case/family report without functional studies of the mutant protein, and one mutation-carrying brother with uremia did not undergo renal biopsy, so his LPG diagnosis is presumptive.
  • Evident from the text: the control survey included 200 local elderly people, and the report does not establish long-term outcomes beyond the proband’s one-year fenofibrate follow-up.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.5551/jat.41996

Cites

24 of 24 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

4 of 28 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Many cases have showed that intensive lipid-lowering treatment including fibrate for under 100 mg/dL of serum triglyceride could significantly reduce proteinuria and achieve clinical remission.

    “Many cases in our previous work and others have showed that intensive lipid-lowering treatment including fibrate for under 100 mg/dL of serum triglyceride could significantly reduce proteinuria and achieve clinical remission1, 13, 17, 21–23).”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [1] 1) Hu Z, Huang S, Wu Y, Liu Y, Liu X, Su D, Tao Y, Fu P, Zhang X, Peng Z, Zhang S and Yang Y: Hereditary features, treatment, and prognosis of the lipoprotein glomerulopathy in patients with the APOE Kyoto mutation. Kidney Int, 2014; 85: 416-424 source
    • cites [13] 13) Tokura T, Itano S, Kobayashi S, Kuwabara A, Fujimoto S, Horike H, Satoh M, Komai N, Tomita N, Matsunaga A, Saito T, Sasaki T and Kashihara N: A novel mutation ApoE2 Kurashiki (R158P) in a patient with lipoprotein glomerulopathy. J Atheroscler Thromb, 2011; 18: 536-541 source

      The Results report that one patient with lipoprotein glomerulopathy received bezafibrate and had complete remission on urinalysis after six months; the Discussion likewise reports remission after fibrate therapy. This supports the treatment-and-remission part of the claim, but the paper does not establish an under-100 mg/dL triglyceride target or show that many cases achieved this outcome. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [17] 17) Hagiwara M, Yamagata K, Matsunaga T, Arakawa Y, Usui J, Shimizu Y, Aita K, Nagata M, Koyama A, Zhang B, Mastunaga A, Saku K and Saito T: A novel apolipoprotein E mutation, ApoE Tsukuba (Arg 114 Cys), in lipoprotein glomerulopathy. Nephrol Dial Transplant, 2008; 23: 381-384 source
  • Findingown data

    All mutation carriers were heterozygotes with the apoE genotype ε3/ε3.

    “All mutation carriers were heterozygotes with the apoE genotype ε3/ε3.”
    Quote in the paperNot a substantial claim
  • Findingnone given

    In this study, carriers of mutated apoE showed normally or mildly elevated serum apoE levels.

    “In this study, carriers of mutated apoE showed normally or mildly elevated serum apoE levels.”
    Quote in the paperSubstantial claim
  • Findingown data

    The apoE Chengdu mutation has not been reported previously.

    “which has not been reported previously”
    • Also stated in: § DNA Sequence Analysis, APOE Genotype, and Pedigree Study · plain
      “Search in the Exome Sequencing Project, 1000 Genomes Project, and Exome Aggregation Consortium revealed that this mutation was a novel apoE variant.”
    Quote in the paperSubstantial claim
    • Rests on an assumption: The Exome Sequencing Project, 1000 Genomes Project, and Exome Aggregation Consortium databases are adequate to establish that the apoE Chengdu mutation is novel.
  • Findingown data

    APOE gene analysis revealed a T-to-C point mutation at amino acid 173 causing substitution of a proline residue for a leucine residue.

    “apoE gene analysis revealed a T-to-C point mutation at amino acid 173 that caused a substitution of a proline residue for a leucine residue”
    • Also stated in: § DNA Sequence Analysis, APOE Genotype, and Pedigree Study · plain
      “The APOE gene analysis of the patient (II-4) revealed a T-to-C nucleotide substitution at codon 173 of the apoE gene that caused the substitution of a leucine residue with a proline residue”
    Quote in the paperSubstantial claim
  • May combine two claims. 10
  • Classified as probably not a substantial claim. 5

  • May combine two claims.

    Premisecitation

    LPG patients with normal serum apoE levels have been reported previously, although these levels in LPG are usually two or three times higher than the normal range.

    “Actually, LPG patients with normal serum apoE levels have been reported previously13, 14, 17), although these levels in LPG are usually two or three times higher than the normal range.”
    Quote in the paperSubstantial claim2 of 3 sources checked
    • cites [13] 13) Tokura T, Itano S, Kobayashi S, Kuwabara A, Fujimoto S, Horike H, Satoh M, Komai N, Tomita N, Matsunaga A, Saito T, Sasaki T and Kashihara N: A novel mutation ApoE2 Kurashiki (R158P) in a patient with lipoprotein glomerulopathy. J Atheroscler Thromb, 2011; 18: 536-541 source
    • cites [14] 14) Mitani A, Ishigami M, Watase K, Minakata T and Yamamura T: A novel apolipoprotein E mutation, ApoE Osaka (Arg158 Pro), in a dyslipidemic patient with lipoprotein glomerulopathy. J Atheroscler Thromb, 2011; 18: 531-535 source
    • cites [17] 17) Hagiwara M, Yamagata K, Matsunaga T, Arakawa Y, Usui J, Shimizu Y, Aita K, Nagata M, Koyama A, Zhang B, Mastunaga A, Saku K and Saito T: A novel apolipoprotein E mutation, ApoE Tsukuba (Arg 114 Cys), in lipoprotein glomerulopathy. Nephrol Dial Transplant, 2008; 23: 381-384 source

  • May combine two claims.

    Premisecitation

    These structural changes led to defective binding capacity for the LDL receptor and enhanced protein and lipoprotein aggregation, which contribute to the pathogenesis of hyperlipoproteinemia and the formation of lipoprotein thrombi.

    “These changes led to a defective binding capacity for the LDL receptor and enhanced protein and lipoprotein aggregation, which contribute to the pathogenesis of hyperlipoproteinemia and the formation of lipoprotein thrombi15).”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [15] 15) Georgiadou D, Stamatakis K, Efthimiadou EK, Kordas G, Gantz D, Chroni A and Stratikos E: Thermodynamic and structural destabilization of apoE3 by hereditary mutations associated with the development of lipoprotein glomerulopathy. J Lipid Res, 2013; 54: 164-176 source

      The section “Mutations cause aggregation of apoE3 and structurally defective lipoprotein particles” reports enhanced aggregation and suggests that it may contribute to kidney deposition and lipoprotein glomerulopathy; the paper also describes lipoprotein thrombi as a feature of that disease (page numbers unavailable). It does not establish defective LDL-receptor binding by these variants or show that the structural changes cause hyperlipoproteinemia. The proposed contribution to thrombus formation is more tentative than the citing sentence implies. (LLM, conf=0.87)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Findingown data

    Two of five family members carried the apoE Chengdu mutation, including the patient's brother who was receiving hemodialysis and her sister whose urine protein levels were normal.

    “Two of five of the family members carried this mutation, including the patient's brother who was receiving hemodialysis, and her sister, whose urine protein levels were normal.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The patient presented with nephrotic syndrome and hypertension.

    “The patient presented with nephrotic syndrome and hypertension.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The patient had mild hyperlipidemia and elevated serum apoE (5.6 mg/dL).

    “A fasting lipid panel showed mild hyperlipidemia and elevated serum apoE (5.6 mg/dL).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data

    The pedigree study showed that LPG secondary to apoE Chengdu is an autosomal dominant trait with incomplete penetrance.

    “The pedigree study showed that LPG secondary to apoE Chengdu is an autosomal dominant trait with incomplete penetrance.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationcitation

    Mutated apoE exhibits enhanced binding to glomerular capillaries, which might be a part of the pathogenic mechanism of LPG.

    “These studies suggest that mutated apoE exhibits enhanced binding to glomerular capillaries, which might be a part of the pathogenic mechanism of LPG.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [20] 20) Murano T, Matsumura R, Misawa Y, Ozaki H, Miyashita Y, Yoshida S, Sueioshi M, Sugiyama T and Shirai K: Interaction of endothelial cells and triglyceride-rich lipoproteins with apolipoprotein E (Arg-->Cys) from a patient with lipoprotein glomerulopathy. Metabolism, 2002; 51: 201-205 source
    • cites [11] 11) Sam R, Wu H, Yue L, Mazzone T, Schwartz MM, Arruda JA, Dunea G and Singh AK: Lipoprotein glomerulopathy: a new apolipoprotein E mutation with enhanced glomerular binding. Am J Kidney Dis, 2006; 47: 539-548 source

  • May combine two claims.

    Interpretationreasoning

    Subject II-2 might have had LPG although he did not undergo a renal biopsy because he suffered from uremia and showed hypertriglyceridemia.

    “Subject II-2 might have had LPG although he did not undergo a renal biopsy because he suffered from uremia and showed hypertriglyceridemia.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    To date, 16 apoE variants have been reported to be related to LPG, including apoE Chengdu.

    “To date, 16 apoE variants10) have been reported to be related to LPG, including apoE Chengdu.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [10] 10) Saito T, Matsunaga A, Ito K and Nakashima H: Topics in lipoprotein glomerulopathy: an overview. Clin Exp Nephrol, 2014; 18: 214-217 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    LPG is a rare autosomal dominant renal disease with incomplete penetrance that has mainly been reported in eastern Asia.

    “Lipoprotein glomerulopathy (LPG) is a rare autosomal dominant renal disease with incomplete penetrance that has mainly been reported in eastern Asia1, 2).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [1] 1) Hu Z, Huang S, Wu Y, Liu Y, Liu X, Su D, Tao Y, Fu P, Zhang X, Peng Z, Zhang S and Yang Y: Hereditary features, treatment, and prognosis of the lipoprotein glomerulopathy in patients with the APOE Kyoto mutation. Kidney Int, 2014; 85: 416-424 source
    • cites [2] 2) Saito T, Matsunaga A and Oikawa S: Impact of lipoprotein glomerulopathy on the relationship between lipids and renal diseases. Am J Kidney Dis, 2006; 47: 199-211 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Several apoE mutations have been reported to be related to LPG, including apoE Sendai and apoE Kyoto.

    “To date, several apoE mutations have been reported to be related to LPG, including apoE Sendai4) and apoE Kyoto5).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [4] 4) Oikawa S, Matsunaga A, Saito T, Sato H, Seki T, Hoshi K, Hayasaka K, Kotake H, Midorikawa H, Sekikawa A, Hara S, Abe K, Toyota T, Jingami H, Nakamura H and Sasaki J: Apolipoprotein E Sendai (arginine 145-->proline): a new variant associated with lipoprotein glomerulopathy. J Am Soc Nephrol, 1997; 8: 820-823 source
    • cites [5] 5) Matsunaga A, Sasaki J, Komatsu T, Kanatsu K, Tsuji E, Moriyama K, Koga T, Arakawa K, Oikawa S, Saito T, Kita T and Doi T: A novel apolipoprotein E mutation, E2 (Arg25Cys), in lipoprotein glomerulopathy. Kidney Int, 1999; 56: 421-427 source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Clinically, LPG often presents as moderate to severe proteinuria and hypertriglyceridemia with elevated serum apoE levels.

    “Clinically, LPG often presents as moderate to severe proteinuria and hypertriglyceridemia with elevated serum apoE levels2).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [2] 2) Saito T, Matsunaga A and Oikawa S: Impact of lipoprotein glomerulopathy on the relationship between lipids and renal diseases. Am J Kidney Dis, 2006; 47: 199-211 source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Massive lipoprotein thrombi in the lumens of dilated glomerular capillaries are the typical pathological manifestation of LPG.

    “Massive lipoprotein thrombi in the lumens of dilated glomerular capillaries are the typical pathological manifestation of LPG3).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [3] 3) Saito T, Sato H, Kudo K, Oikawa S, Shibata T, Hara Y, Yoshinaga K and Sakaguchi H: Lipoprotein glomerulopathy: glomerular lipoprotein thrombi in a patient with hyperlipoproteinemia. Am J Kidney Dis, 1989; 13: 148-153 source
13 of 13

  • The paper relies on this without support.

    The 200 local elderly people surveyed are representative of the local population for assessing the frequency of the apoE Chengdu mutation.

    “After identifying the specific mutation site, we searched the apoE Chengdu (p.L173P) mutation among 200 local elderly people.”

  • The paper relies on this without support.

    The Exome Sequencing Project, 1000 Genomes Project, and Exome Aggregation Consortium databases are adequate to establish that the apoE Chengdu mutation is novel.

    “Search in the Exome Sequencing Project, 1000 Genomes Project, and Exome Aggregation Consortium revealed that this mutation was a novel apoE variant.”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Most LPG patients have been reported to present elevated plasma apoE levels, while normalization or reduction of apoE levels following various treatments results in remission or improvement of the disease.

    “Most of the LPG patients have been reported to present elevated plasma apoE levels (5, 6, 23-25), while it has been observed that normalization or reduction of apoE levels following various treatments (e.g., lipid-lowering treatments with fenofibrate or protein A immunoadsorption) result in remission or improvement of the disease (24,25,47).”

    From Thermodynamic destabilization and aggregation propensity as the mechanism behind the association of apoE3 mutants and lipoprotein glomerulopathy (2018) · cites this paper as [47]

    The Discussion (page unavailable) says serum apoE is usually elevated in LPG. The Clinical Course (page unavailable) reports that apoE fell into the stated normal range while the patient improved after fenofibrate treatment. The paper does not establish that lowering plasma apoE caused remission, and the passages found do not discuss protein A immunoadsorption. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • LPG-related mutations found in China include APOE-Kyoto, APOE-Tokyo/Maebashi, APOE-Guangzhou, and APOE-Chengdu.

    “LPG‐related mutations found in China include APOE‐Kyoto, APOE‐Tokyo/Maebashi, APOE‐Guangzhou, and APOE‐Chengdu (Han et al., 2010; Wu, Yang, & Hu, 2018).”

    From Clinical and genetic analysis of lipoprotein glomerulopathy patients caused by <i>APOE</i> mutations (2020) · cites this paper as Wu, Yang, & Hu, 2018

    The Introduction identifies apoE Kyoto as LPG-related and reports apoE Chengdu in a Chinese patient; the Discussion also identifies apoE Guangzhou as LPG-related. The References list an LPG-associated apoE Tokyo mutation, but the paper does not establish that Tokyo was found in China, and it does not mention Maebashi. It therefore does not support the full list as mutations found in China. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • Five variants in helix 4 that were not in the LDL receptor binding site-APOE Kanto (Asp151dupAsp), APOE Las Vegas (Ala152Asp), APOE Chengdu (Leu155Pro), APOE1 (156_173del), and APOE Osaka/Kurashiki (Arg158Pro)-were reported to cause LPG.

    “Five variants in helix 4 that were not in the LDL receptor binding site were identified (Fig.5), but were reported to cause LPG, namely, APOE Kanto (Asp151dupAsp)70, 80), APOE Las Vegas (Ala152Asp)81), APOE Chengdu (Leu155Pro)82), APOE1 (156_173del)83), and APOE Osaka/Kurashiki (Arg158Pro)84, 85).”

    From Impact of Apolipoprotein E Variants: A Review of Naturally Occurring Variants and Clinical Features (2025) · cites this paper as [82]

    The DNA Sequence Analysis section identifies apoE Chengdu in a patient with LPG, and the Discussion places it near, rather than within, the LDL receptor-binding region. However, our copy calls the variant p.L173P, not Leu155Pro, and does not identify its location as helix 4. It does not establish the claim's exact residue numbering or helix designation. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • More than 15 APOE mutations, or eighteen APOE variants, have been associated with LPG.

    “More than 15 APOE mutations have been associated with LPG”

    From Identification of a founder haplotype of <i>APOE Kyoto</i> variant in lipoprotein glomerulopathy (2025) · cites this paper as [13]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Proband's ApoA1/ApoB100 ratio is miscalculated

    Minor

    For subject II-4, the listed ApoA1 and ApoB100 values give a ratio of 2.50, not 2.34.

    Reported 2.34 · recomputed 2.5

  • Patient's age differs between abstract and case presentation

    Minor

    The abstract describes the patient as 45 years old, while the case presentation and Table 2 identify her as 48 years old.

2 of 2

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Authors
Wu, H., Yang, Y., & Hu, Z.
Affiliations
Sichuan University (CN)
Corresponding author
Hu, Zhangxue
ORCID
Venue
Journal of Atherosclerosis and Thrombosis
Publisher
Japan Atherosclerosis Society
Published
2018-08-01
Volume
25
Issue
8
Pages
733-740
ISSN
  • 1340-3478 (ISSN-L)
  • 1880-3873
DOI
10.5551/jat.41996
PMC
PMC6099066
OpenAlex
W2789272364
Semantic Scholar
0fae8829a24b8635565d2e645fa5d4d408dcc264
Cited by
24
References
24
Citations by year
2026: 1 · 2025: 4 · 2024: 2 · 2022: 5 · 2021: 6 · 2020: 1 · 2019: 4 · 2018: 1
FWCI
2.46
Type
journal article
Language
en
Open access
Licence
cc-by-nc-sa
Locations
  • Journal of Atherosclerosis and Thrombosis (publishedVersion, cc-by-nc-sa)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
  • PubMed Central (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (-HM01-)
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, novel mutations, proline substitution, LDL receptor binding, nephrotic syndrome, familial inheritance, fenofibrate, hyperlipidemia, Chinese patients
MeSH terms
Apolipoproteins E, China, Female, Genotype, Humans, Kidney Diseases, Male, Middle Aged, Mutation, Pedigree, Prognosis

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Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-10-31.

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