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Cited by 5Renal Diseases and GlomerulopathiesLipid metabolism and disordersChronic Kidney Disease and Diabetes

A novel apolipoprotein E mutation, ApoE Ganzhou (Arg43Cys), in a Chinese son and his father with lipoprotein glomerulopathy: two case reports

Open access
Wang, Runxiu, Zhao, Chengbo, Chen, Wen, Liu, Zhiping, Xie, Fuhua·2022·Journal of Medical Case Reports
DOI 10.1186/s13256-022-03302-0PMC PMC8864814
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Abstract

Background: Lipoprotein glomerulopathy is a rare and newly recognized glomerular disease that can lead to kidney failure. Its pathological features include the presence of lipoprotein embolus in the loop cavity of glomerular capillaries. It is believed that apolipoprotein E gene mutation is the initiator of the disease. Since the discovery of lipoprotein glomerulopathy, 16 different apolipoprotein E mutations have been reported worldwide, but most of these cases are sporadic. Here we report two cases of lipoprotein glomerulopathy, a Chinese son and his father, with a novel apolipoprotein E mutation, ApoE Ganzhou (Arg43Cys). Case presentation: Case 1, a 33-year-old Chinese man, was hospitalized on 3 March 2014 owing to edema and weakness of facial and lower limbs for 1 month. Laboratory data showed urine protein 3+, hematuria 2+, serum creatinine 203 μmol/L, uric acid 670 μmol/L, total cholesterol 12.91 mmol/L, triglyceride 5.61 mmol/L, high-density lipoprotein 1.3 mmol/L, low-density lipoprotein 7.24 mmol/L, apolipoprotein B 2.48 g/L, and lipid protein (a) 571 mg/L. Renal tissue examined by immunofluorescence and electron microscopy indicated lipoprotein glomerulopathy. Case 2, 55-year-old father of case 1, was hospitalized on 12 January 2016 owing to edema of his lower extremities for 6 months. Laboratory data showed urine protein 2+, hematuria 2+, serum creatinine 95 μmol/L, uric acid 440 μmol/L, total cholesterol 4.97 mmol/L, triglyceride 1.91 mmol/L, high-density lipoprotein 1.18 mmol/L, low-density lipoprotein 3.12 mmol/L, apolipoprotein B 2.48 g/L, and lipid protein (a) 196 mg/L. Renal tissue examined by immunofluorescence and electron microscopy indicated lipoprotein glomerulopathy. Apolipoprotein E mutation test showed that they had the same gene mutation, a novel type of apolipoprotein E mutation. Based on their clinical presentation and examination findings, they were diagnosed with lipoprotein glomerulopathy. Case 1 was treated with prednisone and dual plasma replacement, followed by simvastatin, nifedipine, triptolide, and angiotensin II receptor blocker drug therapy. After 1 month, the edema symptoms of the patient were alleviated, and urinary protein, serum creatinine, and uric acid were quantitatively reduced. Case 2 was treated with Tripterygium wilfordii and angiotensin II receptor blocker drugs for 3 weeks, and his edema symptoms were alleviated, and urinary protein, serum creatinine, and uric acid were quantitatively reduced. Conclusions: The apolipoprotein E mutation in the two cases we reported was a familial aggregation phenomenon, and the mutation is a novel type, which we named ApoE Ganzhou (Arg43Cys). The location of the gene mutation is close to the most common mutation type of lipoprotein glomerulopathy, ApoE Kyoto (Arg25Cys), so we speculate that its pathogenic role might be the similar to that of ApoE Kyoto (Arg25Cys).

AI snapshot

Written from the paper’s full text.

TL;DR

This case report describes a Chinese father and son with lipoprotein glomerulopathy carrying a novel heterozygous apolipoprotein E mutation, g.127C>T (Arg43Cys), named ApoE Ganzhou. The mutation segregated paternally and was predicted damaging; the son progressed to end-stage renal disease while the father remained stable over 4 years.

Key findings

  • Both patients had the same novel heterozygous ApoE mutation: nucleotide 127 in the ApoE-encoding region changed from cytosine to thymine (g.127C>T), causing amino acid 43 to change from arginine to cysteine (Arg43Cys); the mother had no mutation, and the pattern was reported as autosomal dominant.
  • Case 1 (son) laboratory values included urine protein 3+, hematuria 2+, serum creatinine 203 μmol/L, uric acid 670 μmol/L, total cholesterol 12.91 mmol/L, triglyceride 5.61 mmol/L, HDL 1.3 mmol/L, LDL 7.24 mmol/L, apolipoprotein B 2.48 g/L, and lipoprotein(a) 571 mg/L.
  • Case 2 (father) laboratory values included urine protein 2+, hematuria 2+, serum creatinine 95 μmol/L, uric acid 440 μmol/L, total cholesterol 4.97 mmol/L, triglyceride 1.91 mmol/L, HDL 1.18 mmol/L, LDL 3.12 mmol/L, apolipoprotein B 2.48 g/L, and lipoprotein(a) 196 mg/L.
  • In silico prediction with SIFT and PolyPhen gave scores of 0.008 and 0.999, respectively, indicating the mutation was harmful to ApoE protein function; GnomAD frequencies were reported as 0.00005445 in East Asia and 0.00004654 in Europe (Finland).
  • Case 1 developed end-stage renal disease 4 years after discharge and underwent maintenance hemodialysis; Case 2 was followed for 4 years with stable renal function.

Methods

  • Design: two case reports of a Chinese son and his father with lipoprotein glomerulopathy, plus family history and pedigree assessment.
  • Data/sample: renal biopsy specimens examined by light microscopy, immunofluorescence, and electron microscopy; laboratory tests; ApoE gene sequencing from kidney genomic DNA of both patients and the mother.
  • Main analysis: descriptive clinical and histopathological comparison, mutation identification, family segregation, database frequency lookup, and SIFT/PolyPhen prediction of pathogenicity.

Limitations

  • The paper states that the proband’s sister and daughter refused genetic testing, so the authors cannot rule out that they carry the mutant gene.
  • The paper states that ApoE gene mutation testing was not performed for Case 1 at initial diagnosis; testing was done about 2 years later when his father was diagnosed.
  • Evident from the text: only two related cases are reported, no functional experimental validation of the mutation is presented, and treatment responses are not from a controlled study; the abstract and case presentation also give discrepant ages for both patients (Case 1: 33 vs 29 years; Case 2: 55 vs 51 years).

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

Integrity signals

Registry

Crossref · 10.1186/s13256-022-03302-0

Cites

34 of 34 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

4 of 16 cited sources checked · 2 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Other reported ApoE mutations located outside the LDL-receptor binding site may change the spatial conformation and stability of ApoE protein.

    “Other mutations locate outside of LRBS, such as ApoE5 (Glu3Lys) [20], ApoE Kyoto (Arg25Cys) [21], ApoE Tsukuba (Arg114 Cys) [22], ApoE Las Vegas (Ala152Asp) [14], ApoE1 (Del 156-173) [23], ApoE Osak/Kurashiki (Arg158 Pro) [24], ApoE Toranomon (Gln187Glu) [25], ApoE Toyonaka (Ser 197Cys) [26], and ApoE Hong Kong (Asp230Tyr) [27]. These mutations may change the spatial conformation and stability of”
    Quote in the paperNot a substantial claim2 of 3 sources checked
    • cites [20] Takasaki S, Matsunaga A, Joh K, Saito T. A case of lipoprotein glomerulopathy with a rare apolipoprotein E isoform combined with neurofibromatosis type I. CEN Case Rep. 2018;7:127–31. source
    • cites [21] Batal I, Fakhoury G, Groopman E, D’Agati VD, Morris H. Unusual case of lipoprotein glomerulopathy first diagnosed in a protocol kidney allograft biopsy. Kidney Int Rep. 2019;4:350–4. source
    • cites [22] Hagiwara M, Yamagata K, Matsunaga T, Arakawa Y, Usui J, Shimizu Y, Aita K, Nagata M, Koyama A, Zhang B, et al. A novel apolipoprotein E mutation, ApoE Tsukuba (Arg 114 Cys), in lipoprotein glomerulopathy. Nephrol Dial Transplant. 2008;23:381–4. source
  • Findingown data

    The ApoE Ganzhou (Arg43Cys) mutation was found in the GnomAD database most commonly in East Asia and Europe (Finland), with frequencies of 0.00005445 and 0.00004654, respectively.

    “We searched the GnomAD database for this DNA sequence variant, and found that this mutation was most common in East Asia and Europe (Finland), with frequencies of 0.00005445 and 0.00004654, respectively.”
    Quote in the paperNot a substantial claim
  • Findingown data

    The ApoE Ganzhou (Arg43Cys) mutation is a novel ApoE mutation.

    “This is a novel mutation in ApoE gene, and we named it ApoE Ganzhou (Arg43Cys).”
    • Also stated in: § Conclusions · plain
      “The apolipoprotein E mutation in the two cases we reported was a familial aggregation phenomenon, and the mutation is a novel type, which we named ApoE Ganzhou (Arg43Cys).”
    Quote in the paperSubstantial claim
  • Findingnone given

    The ApoE mutation in the two reported cases was a familial aggregation phenomenon.

    “The apolipoprotein E mutation in the two cases we reported was a familial aggregation phenomenon, and the mutation is a novel type, which we named ApoE Ganzhou (Arg43Cys).”
    Quote in the paperSubstantial claim
  • Findingnone given

    The location of the ApoE Ganzhou (Arg43Cys) mutation is close to the most common LPG mutation type, ApoE Kyoto (Arg25Cys).

    “Also, the location of the gene mutation is close to the most common mutation type of LPG, ApoE Kyoto (Arg25Cys), so we speculate that its pathogenic role might be the similar to that of ApoE Kyoto (Arg25Cys).”
    Quote in the paperSubstantial claim
  • Classified as probably not a substantial claim. 6
  • May combine two claims. 12
  • The quote only partly states this claim. 1

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

    Premisecitation

    Lipoprotein glomerulopathy has a wide age distribution, occurring in patients aged 4-69 years, with recent cases also reported in newborns and people in their seventies.

    “LPG has a wide range of age distribution, and occurs in all patients aged 4–69 years old. However, recent cases have also been reported in newborn baby and people in their seventies [28].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [28] Shimizu M, Ohno T, Kimoto H, Hosono S, Nozawa M. A newborn infant with lipoprotein glomerulopathy associated with congenital nephrotic syndrome. Pediatr Int. 2001;43:78–80. source

      The Abstract and Conclusions report a neonatal case of lipoprotein glomerulopathy, supporting the newborn portion of the claim. Our copy does not give a 4–69-year age range or report cases in people in their seventies (searched for the age range and older patients). (LLM, conf=0.87)

      Experimental — accuracy not yet measured

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

    Premisecitation

    Most reported lipoprotein glomerulopathy cases were sporadic, and some were familial.

    “In previous literature reports, most cases were sporadic, and some cases were familial [7, 8, 15, 29–33].”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [7] Xie W, Xie Y, Lin Z, Xu X, Zhang Y. A novel apolipoprotein E mutation caused by a five amino acid deletion in a Chinese family with lipoprotein glomerulopathy: a case report. Diagn Pathol. 2019;14:41. source

      The Background (page unavailable) says familial aggregation of lipoprotein glomerulopathy has been shown, and the Case presentation describes two affected members of one family. The paper does not say that most previously reported cases were sporadic, so it supports the familial part but not the claimed distribution of cases. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [8] Li W, Wang Y, Han Z, Luo C, Zhang C, Xiong J. Apolipoprotein e mutation and double filtration plasmapheresis therapy on a new Chinese patient with lipoprotein glomerulopathy. Kidney Blood Press Res. 2014;39:330–9. source
    • cites [15] Rovin BH, Roncone D, McKinley A, Nadasdy T, Korbet SM, Schwartz MM. APOE Kyoto mutation in European Americans with lipoprotein glomerulopathy. N Engl J Med. 2007;357:2522–4. source

  • May combine two claims. The quote only partly states this claim.

    Findingown data

    SIFT and PolyPhen predicted that the ApoE Ganzhou (Arg43Cys) mutation is harmful to the function of ApoE protein, with scores of 0.008 and 0.999, respectively.

    “SIFT and PolyPhen were used to predict the effect of the mutation, and the predicted scores were 0.008 and 0.999, respectively, indicating that the mutation was harmful to the function of ApoE protein.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Case 1 developed end-stage renal disease 4 years after discharge and underwent maintenance hemodialysis.

    “Case 1 developed end-stage renal disease (ESRD) 4 years after discharge and underwent maintenance hemodialysis until now.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Case 2 was followed up for 4 years and his renal function is stable.

    “Case 2 was followed up for 4 years and his renal function is stable at present.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Both patients had the same ApoE mutation, a heterozygous C-to-T transition at nucleotide 127 (g.127C>T) causing a missense mutation of amino acid 43 from arginine to cysteine (Arg43Cys).

    “The results showed that nucleotide 127 of the ApoE-gene-encoding region was mutated from cytosine to thymine (g.127C>T), which resulted in a missense mutation of amino acid 43 from arginine to cysteine (Fig. 2). His father had the same ApoE mutation, while his mother had no mutation.”
    • Also stated in: § Case 2 · plain
      “ApoE gene sequencing revealed that he had the same mutation, ApoE Ganzhou (Arg43Cys), as his son (Case 1) (Fig. 2).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Case 1 had earlier onset, presented with nephrotic syndrome, poor response to hormone and immunosuppressive therapy, rapid disease progression (entering end-stage renal disease in 3 years), and concurrent renal replacement therapy.

    “From the medical history, the son (case 1) had earlier onset, presenting as nephrotic syndrome, poor response to hormone and immunosuppressive therapy, rapid disease progression (entering end-stage renal disease in 3 years), and concurrent renal replacement therapy.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Case 2 had late onset and relatively mild disease.

    “However, the onset time of the father (case 2) was late, and the disease was relatively mild.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data

    The proband's sister and daughter are currently asymptomatic but cannot be ruled out as carriers of the mutant gene because they refused genetic testing.

    “Although the proband’s sister and daughter are currently asymptomatic, we cannot rule out that they carry the mutant gene because they have refused to undergo genetic testing.”
    Quote in the paperNot a substantial claim

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

    Premisecitation

    Since the discovery of lipoprotein glomerulopathy, 16 different apolipoprotein E mutations have been reported worldwide.

    “So far, 16 different types of gene mutations have been reported worldwide (Fig. 5B).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [3] Saito T, Matsunaga A, Fukunaga M, Nagahama K, Hara S, Muso E. Apolipoprotein E-related glomerular disorders. Kidney Int. 2020;97:279–88. source

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

    Premisecitation

    ApoE contains an LDL-receptor binding site (amino acids 136-150), a hinge site (amino acids 192-215), and a lipid binding region (amino acids 244-272).

    “ApoE contains several primary domains, including LDL-receptor binding site (LRBS, amino acids 136–150), hinge site (HR, amino acids 192–215), and lipid binding region (LBR, amino acids 244 to 272) [3].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [3] Saito T, Matsunaga A, Fukunaga M, Nagahama K, Hara S, Muso E. Apolipoprotein E-related glomerular disorders. Kidney Int. 2020;97:279–88. source

  • May combine two claims.

    Premisecitation

    Apolipoprotein E gene mutation is the initiator or a cause of lipoprotein glomerulopathy.

    “It is believed that apolipoprotein E gene mutation is the initiator of the disease.”
    • Also stated in: § Discussion and conclusions · plain
      “but ApoE gene mutation was recognized as one of causes of the disease.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [3] Saito T, Matsunaga A, Fukunaga M, Nagahama K, Hara S, Muso E. Apolipoprotein E-related glomerular disorders. Kidney Int. 2020;97:279–88. source

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

    Premisecitation

    Immunofluorescence microscopy in lipoprotein glomerulopathy shows positive staining of ApoE and ApoB in lumen thrombotic substances.

    “Immunofluorescence microscopy shows positive staining of ApoE and ApoB in lumen thrombotic substances.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [2] Saito T, Sato H, Kudo K, Oikawa S, Shibata T, Hara Y, Yoshinaga K, Sakaguchi H. Lipoprotein glomerulopathy: glomerular lipoprotein thrombi in a patient with hyperlipoproteinemia. Am J Kidney Dis. 1989;13:148–53. source

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

    Premisecitation

    Under light microscopy, the capillary lumen in lipoprotein glomerulopathy is typically highly dilated and filled with lightly stained reticular material.

    “Under light microscopy, the capillary lumen is typically highly dilated and filled with lightly stained reticular material.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [2] Saito T, Sato H, Kudo K, Oikawa S, Shibata T, Hara Y, Yoshinaga K, Sakaguchi H. Lipoprotein glomerulopathy: glomerular lipoprotein thrombi in a patient with hyperlipoproteinemia. Am J Kidney Dis. 1989;13:148–53. source

  • May combine two claims.

    Premisecitation

    Nearly half of reported ApoE mutations in lipoprotein glomerulopathy occurred in the LDL-receptor binding site, and these mutations might result in reduced binding capacity of ApoE protein to the LDL receptor.

    “Nearly half of mutations occurred in the LDL-receptor binding site (LRBS), such as ApoE Sendai (Arg145Pro) [2], ApoE Chicago (Arg147Cys) [16], ApoE Guangzhou (Arg150Pro)[17], ApoE Modena (Arg 150Cys) [11], ApoE Okayama (Arg150Gly) [18], ApoE Tokyo (Del 141-143) [19], and ApoE Maebasi (Del 142-144). These mutations might result in reduced binding capacity of ApoE protein to LDL receptor.”
    Quote in the paperNot a substantial claim0 of 3 sources checked
    • cites [2] Saito T, Sato H, Kudo K, Oikawa S, Shibata T, Hara Y, Yoshinaga K, Sakaguchi H. Lipoprotein glomerulopathy: glomerular lipoprotein thrombi in a patient with hyperlipoproteinemia. Am J Kidney Dis. 1989;13:148–53. source
    • cites [16] Sam R, Wu H, Yue L, Mazzone T, Schwartz MM, Arruda JA, Dunea G, Singh AK. Lipoprotein glomerulopathy: a new apolipoprotein E mutation with enhanced glomerular binding. Am J Kidney Dis. 2006;47:539–48. source
    • cites [17] Luo B, Huang F, Liu Q, Li X, Chen W, Zhou SF, Yu X. Identification of apolipoprotein E Guangzhou (arginine 150 proline), a new variant associated with lipoprotein glomerulopathy. Am J Nephrol. 2008;28:347–53. source
15 of 15

  • The paper relies on this without support.

    The exact pathogenesis of lipoprotein glomerulopathy has not been fully elucidated.

    “However, the exact pathogenesis of the disease has not been fully elucidated.”
    “The exact pathogenesis of LPG has not been fully elucidated, but ApoE gene mutation was recognized as one of causes of the disease.”
1 of 1

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?

  • APOE Ganzhou (Arg43Cys) is correctly described as APOE (p.Arg43Cys), which is the same variant as APOE Kyoto (Arg25Cys).

    “As for incorrectly reported variants, APOE Ganzhou (Arg43Cys)91) is correctly described as APOE (p.Arg43Cys), which is the same variant as APOE Kyoto (Arg25Cys)87).”

    From Impact of Apolipoprotein E Variants: A Review of Naturally Occurring Variants and Clinical Features (2025) · cites this paper as [91]

    The Case presentation (Case 1) identifies ApoE Ganzhou as an arginine-to-cysteine substitution at position 43. But the Abstract conclusion and Discussion treat ApoE Kyoto (Arg25Cys) as a separate mutation located close to Ganzhou, not the same variant. The paper supports the Arg43Cys identification but contradicts the claimed equivalence. (LLM, conf=0.89)

    Checked by a reasoning model — may be wrong.

    Experimental — accuracy not yet measured

  • Approximately 14 different ApoE gene variants have been identified in association with LPG.

    “To date, approximately 14 different ApoE gene variants have been identified in association with LPG.[4,5]”

    From A boy and his mother with lipoprotein glomerulopathy: Two case reports and literature review (2025) · cites this paper as [4]

    The Background and Discussion and conclusions confirm that multiple ApoE mutations have been associated with LPG, but both sections give 16 previously reported mutations, not approximately 14. The Fig. 5 caption counts 17 when the newly reported mutation is included. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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.

  • Time to end-stage renal disease differs by one year

    Major

    The follow-up section says case 1 developed end-stage renal disease four years after discharge, but the discussion says he entered end-stage renal disease in three years.

  • The concluding mutation name gives the wrong amino-acid change

    Minor

    The conclusion names ApoE Ganzhou as Arg25Cys, whereas the paper repeatedly identifies it as Arg43Cys and identifies Arg25Cys as ApoE Kyoto.

  • Case 2 has two reported ages

    Minor

    The abstract describes the father as 55 years old, while his case presentation describes him as 51 years old.

  • Case 1 has two reported ages

    Minor

    The abstract describes case 1 as 33 years old, while the case presentation describes him as 29 years old.

4 of 4

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Related

Authors
Wang, R., Zhao, C., Chen, W., Liu, Z., & Xie, F.
Affiliations
Gannan Medical University (CN)
Corresponding author
  • Liu, Zhiping
  • Xie, Fuhua
ORCID
Venue
Journal of Medical Case Reports
Publisher
Springer Science and Business Media LLC
Published
2022-02-23
Volume
16
Issue
1
Pages
78-78
ISSN
1752-1947 (ISSN-L)
DOI
10.1186/s13256-022-03302-0
PMC
PMC8864814
OpenAlex
W4213444412
Semantic Scholar
a8b8787bf24626059c74d2404ccd70d11ab26e89
Cited by
5
References
34
Citations by year
2025: 2 · 2024: 2 · 2022: 1
FWCI
0.79
Type
journal article
Language
en
Open access
Licence
Locations
  • Journal of Medical Case Reports (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Youth Science Foundation of Jiangxi Province (GJJ170866)
  • BC Renal Agency (20165348)
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, glomerular capillaries, proteinuria, hyperuricemia, hyperlipidemia, protein A, renal failure, Chinese patients
MeSH terms
Adult, Apolipoproteins E, China, Humans, Kidney Diseases, Male, Middle Aged, Mutation

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