CoChat
Sign Up
Cited by 2Renal Diseases and GlomerulopathiesLipid metabolism and disordersChronic Kidney Disease and Diabetes

A boy and his mother with lipoprotein glomerulopathy: Two case reports and literature review

Open access
Zhang, Shuya, Fan, Lulu, Li, Ziwei, Liu, Tiantian, Jing, Xiaoping, Guo, Qingyin·2025·Medicine
DOI 10.1097/md.0000000000041628PMC PMC11857006
Open this paper in CoChat — free account

Abstract

Rationale: Lipoprotein glomerulopathy (LPG) is a rare genetic kidney disorder. Here, we report a boy and his mother with LPG. Patient concerns: A 6-year-old boy was admitted to our hospital with a history of 6 months of experiencing foamy urine without apparent cause. Diagnoses: Urinalysis revealed 3+ protein and 2+ occult blood. A 24-hour urinary protein quantification measured 1110 mg. Other laboratory tests revealed that the level of serum albumin was 43.6 g/L, triglycerides 4.31 mmol/L were elevated, and high-density lipoprotein cholesterol 0.71 mmol/L were reduced, whereas total cholesterol and low-density lipoprotein cholesterol levels were normal. Renal biopsy revealed glomerular capillary loop expansion with lipoprotein thrombi on light microscopy, variable-sized vacuoles within the capillary loops on electron microscopy, positive Oil Red O staining, and positive immunofluorescence staining for ApoE. The mother of the patient had a history of uremia 5 years ago. Genetic testing confirmed a deletion of 9 nucleotides (CAAGCTGCG) in exon 4 of the ApoE gene at positions c.480–488 of the boy and his mother, resulting in a deletion of 3 amino acids (Lys143–Arg145del) in the ApoE amino acid sequence at positions 143–145, which was same variant as ApoE Tokyo/Maebashi. Interventions: The boy showed significant improvement after treatment with fenofibrate and telmisartan, with urine protein turning negative after 1 week and blood lipid levels returning to normal after 4 weeks. Outcomes: During 1 year follow-up period, the results of urine routine examination and blood lipid profile remained within normal ranges. Lessons: LPG is a rare and easily misdiagnosed kidney disease with no clinical characteristics. Early diagnosis by kidney biopsy and whole gene test is conducive to early detection and diagnosis, reducing missed diagnosis and misdiagnosis, and improving the long-term prognosis of patients.

AI snapshot

Written from the paper’s full text.

TL;DR

This case report describes a 6-year-old boy with lipoprotein glomerulopathy (LPG) and his mother, both carrying an APOE exon 4 deletion (c.480–488, Lys143–Arg145del) identical to ApoE Tokyo/Maebashi. The boy improved with fenofibrate and telmisartan, with urine protein turning negative after 1 week and blood lipids normalizing after 4 weeks, remaining normal at 1-year follow-up.

Key findings

  • The boy presented with 6 months of foamy urine; urinalysis showed 3+ protein and 2+ occult blood, 24-hour urinary protein was 1110 mg, serum albumin was 43.6 g/L, triglycerides were elevated at 4.31 mmol/L, and HDL-C was reduced at 0.71 mmol/L, while total cholesterol and LDL-C were normal. Admission labs showed hemoglobin 96 g/L, 24-hour urinary protein 1429.2 mg, serum albumin 30.7 g/L, total cholesterol 6.54 mmol/L, triglycerides 2.76 mmol/L, and LDL-C 4.45 mmol/L.
  • Renal biopsy showed 17 glomeruli with increased volume, extensive capillary dilation, and lightly stained vacuolated thrombus-like material; electron microscopy showed vacuolar degeneration and lipid-like vacuoles; ApoE and Oil Red O staining were positive, while immunofluorescence for IgM, IgG, IgA, C3, C4, and C1q was negative.
  • Genetic testing found an APOE exon 4 deletion of 9 nucleotides (CAAGCTGCG) at c.480–488, causing deletion of 3 amino acids (Lys143–Arg145del), the same variant as ApoE Tokyo/Maebashi; the mother and aunt carried the same mutation, the father was wild-type, the mother had uremia 5 years earlier and was on hemodialysis, and the aunt had no abnormalities on routine blood, urine, and liver/kidney tests.
  • After treatment with fenofibrate 200 mg once daily and telmisartan 40 mg twice daily, urinary protein and occult blood were negative at 1 week, 24-hour urinary protein was 158.98 mg, and at 1 month 24-hour urine protein was 30 mg with serum albumin 44.6 g/L and normal blood lipids; at 1 year, routine urinary testing, 24-hour urinary protein, and blood lipids were normal. Prior treatment with Tripterygium wilfordii glycosides, telmisartan, and piperazine ferulate produced no improvement in blood lipids or urinary protein.

Methods

  • Design: two case reports with a literature review of LPG.
  • Data/sample: a 6-year-old boy with LPG and his mother; family genetic testing included the proband, parents, and aunt; renal biopsy was performed in the boy; clinical and laboratory follow-up continued for 1 year.
  • Main analysis: descriptive reporting of clinical, laboratory, histopathological, immunofluorescence, electron microscopy, and ApoE genotyping findings, with a pedigree chart and review of published LPG data.

Limitations

  • The paper states that the pathogenic mechanisms of LPG have not been fully elucidated, the long-term efficacy of treatments remains unclear, and effective treatment must target the genetic level, which is future research. It also notes that immune adsorption and plasma exchange are not widely used due to operational difficulty, high cost, and infection risk, and that the grandparents refused genetic testing while some relatives did not undergo testing for economic reasons and were marked undetermined.
  • Evident from the text: the treatment conclusion rests on a single pediatric case with no control group, and the follow-up is limited to 1 year. The mother’s renal disease is described clinically without a reported renal biopsy or genetic details beyond carrying the same APOE mutation.

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

Integrity signals

Registry

Crossref · 10.1097/md.0000000000041628

Cites

37 of 37 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

7 of 33 cited sources checked · 3 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    The other ApoE mutations are located outside the LDLR binding region, such as ApoE Kyoto (Arg25Cys), ApoE Tsukuba (Arg114Cys), ApoE Kanto (Asp151dup), ApoE Las Vegas (Ala152Asp), ApoE Chengdu (Leu155Pro), ApoE1 (del 156-173) and ApoE Osaka/Kurashiki (Arg158Pro).

    “The other mutations are located outside the LDLR binding region, such as ApoE Kyoto (Arg25Cys),[16] ApoE Tsukuba (Arg114Cys),[23] ApoE Kanto (Asp151dup),[24] ApoE Las Vegas (Ala152Asp),[25] ApoE Chengdu (Leu155Pro),[26] ApoE1 (del 156-173)[27] and ApoE Osaka/Kurashiki (Arg158Pro).[28]”
    Quote in the paperNot a substantial claim1 of 3 sources checked
    • cites [16] Matsunaga A Sasaki J Komatsu T. A novel apolipoprotein E mutation, E2 (Arg25Cys), in lipoprotein glomerulopathy. Kidney Int. 1999; 56: 421– 7. 10432380 source
    • cites [23] Hagiwara M Yamagata K Matsunaga T. A novel apolipoprotein E mutation, ApoE Tsukuba (Arg 114 Cys), in lipoprotein glomerulopathy. Nephrol Dial Transplant. 2008; 23: 381– 4. 17967799 source
    • cites [24] Yokochi A Matsunaga A Kanemoto K Tominaga N Uda S Saito T. Lipoprotein glomerulopathy with a novel apolipoprotein E variant, APOE Kanto (Asp 151dup). CEN Case Rep. 2024. doi: 10.1007/s13730-024-00920-z. PMC11958863 39141311 source

      The Material and methods and Result sections identify APOE Kanto as Asp151dup, supporting the part of the sentence attached to this citation. The Introduction discusses mutations around the LDL receptor-binding region but does not establish that Asp151dup lies outside it. The other named variants have separate citations and are not assessed here. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
  • Premisecitation

    The substitution of proline with other amino acids is an important mutation, as it may lead to a decrease in α-helical content, exposure of hydrophobic surfaces, thermodynamic instability, and aggregation of ApoE, resulting in LPG.

    “The substitution of proline with other amino acids is an important mutation, such as ApoE Sendai, ApoE Chicago, ApoE Chengdu, ApoE Guangzhou, and ApoE Osaka/Kurashiki, as it may lead to a decrease in α-helical content, exposure of hydrophobic surfaces, thermodynamic instability, and aggregation of ApoE, resulting in LPG.[29]”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [29] Georgiadou D Stamatakis K Efthimiadou EK. Thermodynamic and structural destabilization of apoE3 by hereditary mutations associated with the development of lipoprotein glomerulopathy. J Lipid Res. 2013; 54: 164– 76. 23110818 PMC3520522 source

      The paper’s introductory passage and ‘Mutations cause N-terminus misfolding’ section describe arginine being replaced by proline, not proline being replaced by other amino acids. The ‘Secondary structure’ and ‘A causal link between apoE3 variants and LPG’ sections support the reported loss of helicity, destabilization, aggregation, and possible link to LPG, but the study examines Sendai, Chicago, and Osaka/Kurashiki—not Chengdu or Guangzhou. Page numbers were not available in our copy. (LLM, conf=0.89)

      Experimental — accuracy not yet measured
  • Findingown data

    The proband's father, grandparents, aunt, and aunt's daughters have not exhibited symptoms of LPG to date.

    “The proband’s father, grandparents, aunt, and aunt’s daughters have not exhibited symptoms of LPG to date”
    Quote in the paperNot a substantial claim
  • Findingnone given

    The boy's mother rapidly progressed to end-stage renal disease after a renal injury.

    “In contrast, the patient’s mother had rapidly progressed to end-stage renal disease after a renal injury.”
    Quote in the paperNot a substantial claim
  • Findingown data

    The aunt's routine blood, urine, and liver and kidney function tests showed no abnormalities.

    “However, the aunt’s routine blood, urine, and liver and kidney function tests showed no abnormalities.”
    Quote in the paperNot a substantial claim
  • Classified as probably not a substantial claim. 6
  • May combine two claims. 20

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

    Premisecitation

    The age of onset of LPG varies widely, ranging from 4 to 72 years, with approximately equal sex distribution and familial clustering.

    “The age of onset varies widely, ranging from 4 to 72 years, with approximately equal sex distribution and familial clustering.[1,3]”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [1] Li MS Li Y Liu Y Zhou XJ Zhang H. An updated review and meta analysis of lipoprotein glomerulopathy. Front Med (Lausanne). 2022; 9: 905007. 35602473 PMC9120586 source

      The Epidemiology section reports 137 males and 137 females and describes familial clustering. It shows a wide range of onset ages, but does not give 4–72 years as the onset range; its 7–72-year range refers to age at diagnosis, not onset (page unavailable). (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [3] Saito T Matsunaga A Oikawa S. Impact of lipoprotein glomerulopathy on the relationship between lipids and renal diseases. Am J Kidney Dis. 2006; 47: 199– 211. 16431249 source

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

    Premisecitation

    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]”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [4] Wang R Zhao C Chen W Liu Z Xie F. A novel apolipoprotein E mutation, ApoE Ganzhou (Arg43Cys), in a Chinese son and his father with lipoprotein glomerulopathy: two case reports. J Med Case Rep. 2022; 16: 78. 35193676 PMC8864814 source

      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
    • cites [5] 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. 31092271 PMC6521367 source

  • May combine two claims.

    Premisecitation

    Lipoprotein glomerulopathy (LPG) is a rare autosomal dominant inherited kidney disease with incomplete penetrance.

    “Lipoprotein glomerulopathy (LPG), is a rare autosomal dominant inherited kidney disease with incomplete penetrance.”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [1] Li MS Li Y Liu Y Zhou XJ Zhang H. An updated review and meta analysis of lipoprotein glomerulopathy. Front Med (Lausanne). 2022; 9: 905007. 35602473 PMC9120586 source

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

    Premisecitation

    Another report indicates that plasma exchange using heparin-induced extracorporeal lipoprotein precipitation system can effectively treat LPG, significantly reducing cholesterol and triglycerides, because the system can activate LPL and hepatic triglyceride lipase through heparin, making TRL easier to clear.

    “Another report indicates that plasma exchange using heparin-induced extracorporeal lipoprotein precipitation system can effectively treat LPG, significantly reducing cholesterol and triglycerides. This is because the heparin-induced extracorporeal lipoprotein precipitation system can activate LPL and hepatic triglyceride lipase through heparin, making TRL (such as VLDL and intermediate-density lip”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [21] Russi G Furci L Leonelli M. Lipoprotein glomerulopathy treated with LDL-apheresis (Heparin-induced Extracorporeal Lipoprotein Precipitation system): a case report. J Med Case Rep. 2009; 3: 9311. 20062740 PMC2803834 source

  • May combine two claims.

    Findingnone given

    The boy showed significant improvement after treatment with fenofibrate and telmisartan, with urine protein turning negative after 1 week and blood lipid levels returning to normal after 4 weeks.

    “The boy showed significant improvement after treatment with fenofibrate and telmisartan, with urine protein turning negative after 1 week and blood lipid levels returning to normal after 4 weeks.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    The boy's mother was diagnosed with uremia before 5 years and has been undergoing hemodialysis.

    “The patient’s mother was diagnosed with uremia before 5 years and has been undergoing hemodialysis.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The proband's mother and aunt, but not the father, carried the same ApoE gene mutation.

    “The proband’s mother and aunt, but not the father, carried the same ApoE gene mutation.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Renal biopsy of the boy revealed glomerular capillary loop expansion with lipoprotein thrombi on light microscopy, variable-sized vacuoles within the capillary loops on electron microscopy, positive Oil Red O staining, and positive immunofluorescence staining for ApoE.

    “Renal biopsy revealed glomerular capillary loop expansion with lipoprotein thrombi on light microscopy, variable-sized vacuoles within the capillary loops on electron microscopy, positive Oil Red O staining, and positive immunofluorescence staining for ApoE.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingnone given

    Our patient had a relatively short disease course, presenting clinically with nephrotic syndrome accompanied by anemia.

    “Our patient had a relatively short disease course, presenting clinically with nephrotic syndrome accompanied by anemia.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Patients with LPG often exhibit abnormalities in lipid metabolism similar to type III hyperlipoproteinemia, elevated concentrations of ApoE, and varying degrees of proteinuria.

    “Patients with LPG often exhibit abnormalities in lipid metabolism (similar to type III hyperlipoproteinemia) and elevated concentrations of ApoE, as well as varying degrees of proteinuria.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [6] Matsunaga A Saito T. Apolipoprotein E mutations: a comparison between lipoprotein glomerulopathy and type III hyperlipoproteinemia. Clin Exp Nephrol. 2014; 18: 220– 4. 24570178 source

  • May combine two claims.

    Interpretationreasoning

    Although the boy's aunt carries a variation in the ApoE gene, she has not developed LPG or experienced renal dysfunction, indicating that other factors can also induce LPG.

    “Although the boy’s aunt carries a variation in the ApoE gene, she has not developed LPG or experienced renal dysfunction, indicating that other factors can also induce LPG.”
    Quote in the paperSubstantial claim

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

    Premisecitation

    ApoE3 and ApoE4 have normal binding ability to LDLR, while ApoE2 exhibits a binding defect with LDLR, leading to impaired lipid clearance and its association with type III hyperlipoproteinemia.

    “ApoE3 and ApoE4 have normal binding ability to LDLR, while ApoE2 exhibits a binding defect with LDLR, leading to impaired lipid clearance and its association with type III hyperlipoproteinemia.[14]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [14] Nguyen D Dhanasekaran P Nickel M. Molecular basis for the differences in lipid and lipoprotein binding properties of human apolipoproteins E3 and E4. Biochemistry. 2010; 49: 10881– 9. 21114327 PMC3025481 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Previous case reports found combined treatment with glucocorticoids and immunosuppressants ineffective; intensified treatment with lipid-lowering drugs including fibrates provided clinical and histological relief, with serum cholesterol, triglycerides, and ApoE decreased, and consecutive renal biopsies demonstrated complete disappearance of lipoprotein thrombi.

    “Previous case reports that found combined treatment with glucocorticoids and immunosuppressants ineffective used intensified treatment with lipid-lowering drugs (including fibrates) to provide clinical and histological relief for patients. In those cases, serum cholesterol, triglycerides, and ApoE decreased, and consecutive renal biopsies demonstrated complete disappearance of lipoprotein thrombi.”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [22] Kinomura M Sugiyama H Saito T. A novel variant apolipoprotein E Okayama in a patient with lipoprotein glomerulopathy. Nephrol Dial Transplant. 2008; 23: 751– 6. 18045818 source
    • cites [32] Ieiri N Hotta O Taguma Y. Resolution of typical lipoprotein glomerulopathy by intensive lipid-lowering therapy. Am J Kidney Dis. 2003; 41: 244– 9. 12500244 source
    • cites [33] Arai T Yamashita S Yamane M. Disappearance of intraglomerular lipoprotein thrombi and marked improvement of nephrotic syndrome by bezafibrate treatment in a patient with lipoprotein glomerulopathy. Atherosclerosis. 2003; 169: 293– 9. 12921981 source
    • cites [34] Matsunaga A Furuyama M Hashimoto T Toyoda K Ogino D Hayasaka K. Improvement of nephrotic syndrome by intensive lipid-lowering therapy in a patient with lipoprotein glomerulopathy. Clin Exp Nephrol. 2009; 13: 659– 62. 19603250 source

  • May combine two claims.

    Premisecitation

    Compared with the control group, the fibrates treatment group has significantly higher survival rate and kidney survival rate during the 3-year follow-up period.

    “Compared with the control group, the fibrates treatment group has significantly higher survival rate and kidney survival rate during the 3-year follow-up period.[35]”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [35] Hu Z Huang S Wu Y. Hereditary features, treatment, and prognosis of the lipoprotein glomerulopathy in patients with the APOE Kyoto mutation. Kidney Int. 2014; 85: 416– 24. 24025644 source

  • May combine two claims.

    Premisecitation

    ApoE Sendai and ApoE Kyoto are the 2 most common mutations, and they exhibit only 5% of the activity of normal proteins when binding to LDLR, leading to aggregation and clearance impairment of lipoproteins.

    “ApoE Sendai and ApoE Kyoto are the 2 most common mutations, and in terms of receptor binding ability, they exhibit only 5% of the activity of normal proteins when binding to LDLR, leading to the aggregation and clearance impairment of lipoproteins.[1]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [1] Li MS Li Y Liu Y Zhou XJ Zhang H. An updated review and meta analysis of lipoprotein glomerulopathy. Front Med (Lausanne). 2022; 9: 905007. 35602473 PMC9120586 source

      Not checked in the free run.

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

    Premisecitation

    ApoE is primarily synthesized in the liver, but can also be produced by mesangial cells in the kidney.

    “It is primarily synthesized in the liver, but can also be produced by mesangial cells in the kidney.[9]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [9] Chen G Paka L Kako Y Singhal P Duan W Pillarisetti S. A protective role for kidney apolipoprotein E. Regulation of mesangial cell proliferation and matrix expansion. J Biol Chem. 2001; 276: 49142– 7. 11579084 source

  • May combine two claims.

    Premisecitation

    Only 1 Chinese study reported no apparent ApoE gene mutations in 17 LPG patients, while other patients exhibited ApoE gene mutations, indicating that other factors may also induce LPG.

    “Currently, only 1 Chinese study reported no apparent ApoE gene mutations in 17 LPG patients, while other patients exhibited ApoE gene mutations,[30] indicating that other factors may also induce LPG.”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [30] Chen S Liu ZH Zheng JM Zhang X Li LS. A complete genomic analysis of the apolipoprotein E gene in Chinese patients with lipoprotein glomerulopathy. J Nephrol. 2007; 20: 568– 75. 17918142 source

  • Probably not a substantial claim: may not pass S3 (load-bearing), S4 (based).

    Interpretationreasoning

    The boy's anemia may be associated with lipid deposition in the bone marrow affecting hematopoiesis.

    “although his anemia suggests a possible association with lipid deposition in the bone marrow, affecting hematopoiesis.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Literature reports that there have been a total of 6 cases of LPG patients undergoing kidney transplantation worldwide, with 5 cases experiencing LPG recurrence in the transplanted kidney, and ApoE abnormalities in the recipients may induce lipoprotein thrombosis in the transplanted kidney.

    “Literature reports that there have been a total of 6 cases of LPG patients undergoing kidney transplantation worldwide, with 5 cases experiencing LPG recurrence in the transplanted kidney, and ApoE abnormalities in the recipients may induce lipoprotein thrombosis in the transplanted kidney.[8]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [8] Saito T Matsunaga A Fukunaga M Nagahama K Hara S Muso E. Apolipoprotein E-related glomerular disorders. Kidney Int. 2020; 97: 279– 88. 31874799 source

  • May combine two claims.

    Premisecitation

    Glucocorticoids, immunosuppressants, and anticoagulants have all demonstrated poor efficacy in LPG.

    “Glucocorticoids, immunosuppressants, and anticoagulants have all demonstrated poor efficacy.[3,31]”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [3] Saito T Matsunaga A Oikawa S. Impact of lipoprotein glomerulopathy on the relationship between lipids and renal diseases. Am J Kidney Dis. 2006; 47: 199– 211. 16431249 source
    • cites [31] 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. 25300642 source

  • May combine two claims.

    Premisecitation

    The main characteristics of LPG include proteinuria, hematuria, or both, elevated blood lipids, and increased serum ApoE.

    “The main characteristics of LPG include proteinuria, hematuria, or both, elevated blood lipids, and increased serum ApoE.[7]”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [7] Tsimihodimos V Elisaf M. Lipoprotein glomerulopathy. Curr Opin Lipidol. 2011; 22: 262– 9. 21464714 source

  • May combine two claims.

    Premisecitation

    A study in China demonstrated the feasibility of staphylococcal protein A immunoadsorption therapy, because staphylococcal protein A can bind to the Fc of IgG, thereby clearing circulating ApoE and deposited ApoE in renal tissues, and regular treatment can significantly delay the progression of renal disease.

    “A study in China demonstrated the feasibility of staphylococcal protein A immunoadsorption therapy,[36] because staphylococcal protein A can bind to the Fc of IgG, thereby clearing circulating ApoE and deposited ApoE in renal tissues,[37] and regular treatment can significantly delay the progression of renal disease.”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [36] Xin Z Zhihong L Shijun L. Successful treatment of patients with lipoprotein glomerulopathy by protein A immunoadsorption: a pilot study. Nephrol Dial Transplant. 2009; 24: 864– 9. 18840890 source
    • cites [37] Atkins KL Burman JD Chamberlain ES. S. aureus IgG-binding proteins SpA and Sbi: host specificity and mechanisms of immune complex formation. Mol Immunol. 2008; 45: 1600– 11. 18061675 source
22 of 22

  • The paper relies on this without support.

    The mother’s uremia was caused by LPG (she had LPG).

    “The mother of the patient had a history of uremia 5 years ago.”

  • The paper relies on this without support.

    The boy’s improvement after fenofibrate and telmisartan was due to the treatment rather than natural course or other factors.

    “The boy showed significant improvement after treatment with fenofibrate and telmisartan, with urine protein turning negative after 1 week and blood lipid levels returning to normal after 4 weeks.”

  • The paper relies on this without support.

    Early diagnosis by kidney biopsy and whole gene test improves the long-term prognosis of LPG patients.

    “Early diagnosis by kidney biopsy and whole gene test is conducive to early detection and diagnosis, reducing missed diagnosis and misdiagnosis, and improving the long-term prognosis of patients.”
3 of 3

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.

  • ApoE Chicago is incorrectly included among proline substitutions

    Minor

    The paper names ApoE Chicago as an example of a proline substitution, but elsewhere specifies its substitution as Arg147Cys, which does not involve proline.

  • ApoE Sendai is assigned two different substitutions

    Minor

    The discussion first identifies ApoE Sendai as Arg145Cys, but later identifies it as Arg145Pro.

2 of 2

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Related

Authors
Zhang, S., Fan, L., Li, Z., Liu, T., Jing, X., & Guo, Q.
Affiliations
  • Henan University of Chinese Medicine (CN)
  • Shanghai Jiao Tong University (CN)
Corresponding author
Guo, Qingyin
ORCID
Venue
Medicine
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2025-02-21
Volume
104
Issue
8
Pages
e41628
ISSN
  • 0025-7974 (ISSN-L)
  • 1536-5964
DOI
10.1097/md.0000000000041628
PMC
PMC11857006
OpenAlex
W4407872797
Semantic Scholar
32cae74aea889b37aaf2fe613ad13facfc671b78
Cited by
2
References
37
Citations by year
2026: 1 · 2025: 1
FWCI
1.39
Type
journal article
Language
en
Open access
Licence
Locations
  • Medicine (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • 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, familial hypertriglyceridemia, nephrotic syndrome, proteinuria, renal biopsy, fenofibrate, telmisartan, genetic testing, pediatric kidney disease
MeSH terms
Telmisartan, Adult, Apolipoproteins E, Child, Female, Humans, Kidney Diseases, Male, Mothers

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Claims read by deepseek-v4.1-flash under definition version 3 (extract-v3) on 2026-11-01.

Classified by jev-1.13-20260917 (gold-guideline-v0.2) on 2026-11-01.

Cited sources are checked by gpt-6-sol.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review