Lipoprotein glomerulopathy with a novel apolipoprotein E variant, APOE Kanto (Asp 151dup)
Open accessAbstract
A 33-year-old Japanese man was admitted for possible kidney disease because of massive proteinuria. Laboratory findings were characterized by marked urinary protein of 4.7 g/day and high-serum triglyceride levels of 266 mg/dL. Renal biopsy revealed segmental proliferation in the mesangium and lipoprotein thrombi in the glomerular capillary. These results suggested that the diagnosis was lipoprotein glomerulopathy (LPG), although serum apolipoprotein E (apo E) levels were within normal ranges. The APOE phenotype was identified as E2/3 by isoelectric focusing polyacrylamide gel electrophoresis. Direct DNA sequencing analyses for apo E identified a duplication of amino acid 151, aspartic acid, and the gene mutation was named APOE Kanto. APOE gene mutations due to amino acid duplication are rare, and this is the first report showing that amino acid duplication among apo E gene mutations is involved in LPG. It is also noteworthy that the patient developed end-stage kidney disease after over than 10 years despite fibrate treatment.
AI snapshot
Written from the paper’s full text.
TL;DR
A 33-year-old Japanese man with lipoprotein glomerulopathy (LPG) was found to have a novel APOE variant, APOE Kanto (Asp151dup), caused by a heterozygous duplication of aspartic acid at codon 151. He progressed to end-stage kidney disease over more than 10 years despite fibrate treatment.
Key findings
- The patient presented with massive proteinuria (4.7 g/day), serum triglyceride 266 mg/dL, total cholesterol 229 mg/dL, LDL-cholesterol 123 mg/dL, HDL-cholesterol 50 mg/dL, and a normal serum apo E level of 4.3 mg/dL.
- Renal biopsy showed LPG-compatible findings: of 19 glomeruli, 4 had global sclerosis and 7 had segmental mesangial-cell proliferation and matrix increase with lipoprotein thrombi; immunofluorescence was negative, and electron microscopy showed lamellar thrombus-like substances with vacuoles.
- APOE phenotyping showed apo E2/E3, and DNA sequencing identified a heterozygous duplication, c.508_510dupGAT, leading to Asp151dup (p.Asp169dup), named APOE Kanto; no other mutations were found in APOE exons 3 and 4.
- The authors state this is the first report of LPG with an APOE mutation due to duplicated amino acid residues; the patient’s proteinuria decreased from about 3 g/gCr to around 1.0 g/gCr after 3 years, but eGFR fell from 50 to 25 mL/min/1.73 m² over 13 years, and ESKD developed after fibrate was discontinued when serum creatinine reached 2.5 mg/dL.
Methods
- Single case report with clinical, laboratory, renal biopsy, and long-term follow-up data.
- Serum APOE phenotype analyzed by isoelectric focusing polyacrylamide gel electrophoresis; APOE exons 3 and 4 were PCR-amplified, cloned, and 12 clones were sequenced.
- An amplification refractory mutation system (ARMS) was used to confirm the c.508_510dupGAT mutation.
Limitations
- The authors state it is difficult to discuss whether the double amino acid duplication alone can cause the etiological mechanism of LPG, and that accumulation of more cases with amino acid duplication in APOE is required.
- Evident from the text: this is a single case report without functional assays (e.g., receptor-binding or thermodynamic studies), so causality and mechanism for APOE Kanto remain unproven.
- Evident from the text: the comparison with other LPG cases is limited to a small number of Japanese cases with normal apo E levels, and no systematic case–control or genotype–phenotype analysis is presented.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
3 of 17 cited sources checked · 3 supported · 0 flagged
- Premisecitation
Until now, out of 45 cases diagnosed as LPG in Japan, there is only one with APOE Tsukuba and two with APOE Osaka/Kurashiki in which the ranges of apo E are normal.
“Until now, out of 45 cases diagnosed as LPG in Japan, there is only one with APOE Tsukuba [7] and two with APOE Osaka/Kurashiki [8,9] in which the ranges of apo E are normal.”
Quote in the paperSubstantial claim2 of 3 sources checked- cites [7] Hagiwara M, Yamagata K, Matsunaga T, et al. A novel apolipoprotein E mutation, ApoE Tsukuba (Arg 114 Cys), in lipoprotein glomerulopathy. Nephrol Dial Transplant. 2008;23:381–4. source
- cites [8] Mitani A, Ishigami M, Watase K, Minakata T, Yamamura T. A novel apolipoprotein E mutation, ApoE Osaka (Arg158 Pro), in a dyslipidemic patient with lipoprotein glomerulopathy. J Atheroscler Thromb. 2011;18:531–5. source
- cites [9] Tokura T, Itano S, Kobayashi S, et al. A Novel mutation apoE2 Kurashiki (R158P) in a patient with lipoprotein glomerulopathy. J Atheroscler Thromb. 2011;18:536–41. source
- Findingnone given
Hypertriglyceridemia quickly improved after treatment.
“Hypertriglyceridemia quickly improved”
Quote in the paperNot a substantial claim - Findingown data
The patient was a 33-year-old Japanese man admitted for possible kidney disease because of massive proteinuria.
“A 33-year-old Japanese man was admitted for possible kidney disease because of massive proteinuria.”
Quote in the paperNot a substantial claim - Findingown data
Direct DNA sequencing analyses for apo E identified a duplication of amino acid 151, aspartic acid.
“Direct DNA sequencing analyses for apo E identified a duplication of amino acid 151, aspartic acid”
- Also stated in: § Result · plain
“The heterozygous mutation, Asp151 dup, p.Asp169 dup, was detected by DNA sequencing of exons 3 and 4 of the APOE gene (Fig. 2b).”
Quote in the paperSubstantial claim - Also stated in: § Result · plain
- Findingown data
Proteinuria decreased from about 3 g/gCr to around 1.0 g/gCr after 3 years.
“Proteinuria decreased from about 3 g/ gCr to around 1.0 g/gCr after 3 years.”
Quote in the paperNot a substantial claim
- Findingnone given
The patient developed end-stage kidney disease after more than 10 years despite fibrate treatment.
“It is also noteworthy that the patient developed end-stage kidney disease after over than 10 years despite fibrate treatment.”
- Also stated in: § Discussion · plain
“In contrast, the patient in our case presented with nephrotic-range proteinuria and finally developed ESKD despite the long-term use of fibrate”
Quote in the paperNot a substantial claim - Also stated in: § Discussion · plain
- Findingown data
ApoE levels showed a decreasing trend over 3 years after diagnosis.
“ApoE levels were measured for 3 years after diagnosis and showed a decreasing trend.”
Quote in the paperNot a substantial claim - Findingown data
The APOE phenotype was identified as E2/3 by isoelectric focusing polyacrylamide gel electrophoresis.
“The APOE phenotype was identified as E2/3 by isoelectric focusing polyacrylamide gel electrophoresis.”
- Also stated in: § Result · plain
“The patient had apo E2/E3 (Fig. 2a).”
Quote in the paperSubstantial claim - Also stated in: § Result · plain
- Findingown data
The patient's serum apo E level was within normal ranges.
“although serum apolipoprotein E (apo E) levels were within normal ranges”
Quote in the paperNot a substantial claim - Findingown data
No other mutations were found in exons 3 and 4 of the APOE gene.
“No other mutations were found in exons 3 and 4 of the APOE gene.”
Quote in the paperSubstantial claim - Findingown data
eGFR reduced almost linearly from 50 to 25 mL/min/1.73m2 over 13 years.
“However, the eGFR reduced, almost linearly, from 50 to 25 mL/min/1.73m 2 over 13 years.”
Quote in the paperNot a substantial claim - Findingown data
In our case, the high-serum apo E level, which is characteristic of LPG, was not observed.
“In our case, the high-serum apo E level, which is characteristic of LPG, was not observed.”
Quote in the paperNot a substantial claim- Rests on an assumption: High serum apo E level is characteristic of LPG.
- Study design and conductown data
The Asp151dup mutation was confirmed by the presence of PCR product amplification via ARMS.
“The Asp151dup mutation was also confirmed by the presence of PCR product amplification via ARMS (Fig. 2c).”
Quote in the paperNot a substantial claim - Interpretationown data
APOE Kanto having duplication of the 151st amino acid residue, aspartic acid, was responsible for LPG.
“APOE Kanto having duplication of the 151st amino acid residue, aspartic acid, was responsible for LPG”
Quote in the paperSubstantial claim - Interpretationown data
The absence of other mutations suggested that the phenotype, apo E2, was due to the insertion of the acidic amino acid, Asp.
“The absence of other mutations, as revealed by DNA sequencing, suggested that the phenotype, apo E2, was due to the insertion of the acidic amino acid, Asp.”
Quote in the paperSubstantial claim - Premisecitation
APOE gene mutations due to amino acid duplication are rare.
“APOE gene mutations due to amino acid duplication are rare”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [2] Matsunaga A, Saito T. Apolipoprotein E mutations: a comparison between lipoprotein glomerulopathy and type III hyperlipoproteinemia. Clin Exp Nephrol. 2014;18:220–4. source
- Interpretationown data
The patient was diagnosed with lipoprotein glomerulopathy (LPG).
“These results suggested that the diagnosis was lipoprotein glomerulopathy (LPG)”
- Also stated in: § Pathologic findings · plain
“These pathologic findings corresponded to LPG.”
Quote in the paperSubstantial claim - Also stated in: § Pathologic findings · plain
- Interpretationreasoning
This is the first report showing that amino acid duplication among apo E gene mutations is involved in LPG.
“this is the first report showing that amino acid duplication among apo E gene mutations is involved in LPG.”
- Also stated in: § Discussion · plain
“This is the first report of a case of LPG with a novel APOE gene mutation due to a duplicated amino acid residue, APOE Kanto (Asp151dup, p.Asp169dup).”
Quote in the paperSubstantial claim - Also stated in: § Discussion · plain
- Premisecitation
Fibrate should be effective for LPG.
“which should be effective for LPG [10,11].”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [10] Saito T, Matsunaga A, Ito K, Nakashima H. Topics in lipoprotein glomerulopathy: an overview. Clin Exp Nephrol. 2014;18:214–7. source
- cites [11] Hu Z, Huang S, Wu Y, et al. Hereditary features, treatment, and prognosis of the lipoprotein glomerulopathy in patients with the APOE Kyoto mutation. Kidney Int. 2014;85:416–24. source
- Premisecitation
No case involving the duplication of an amino acid residue in APOE has been known to be involved in renal lesions.
“no case involving the duplication of an amino acid residue in APOE has been known to be involved in renal lesions.”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [5] Havekes L, de Wit E, Leuven JG, et al. Apolipoprotein E3-Leiden. A new variant of human apolipoprotein E associated with familial type III hyperlipoproteinemia. Hum Genet. 1986;73:157–63. source
- cites [6] Yamanouchi Y, Takano T, Hamaguchi H, Tokunaga K. A novel apolipoprotein E5 variant with a 24-bp insertion causing hyperlipidemia. J Hum Genet. 2001;46:633–9. source
- Premisecitation
The APOE mutation sites in LPG, including APOE Kanto, are ordinarily found around the LDL receptor domain.
“The APOE mutation sites in LPG, including APOE Kanto, are ordinarily found around the LDL receptor domain”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [2] Matsunaga A, Saito T. Apolipoprotein E mutations: a comparison between lipoprotein glomerulopathy and type III hyperlipoproteinemia. Clin Exp Nephrol. 2014;18:220–4. source
- Premisecitation
Missense mutations in LPG were often arginine-to-proline substitutions like APOE Sendai, resulting in structural changes in the apo E molecule.
“the missense mutations were often arginine-to-proline substitutions like APOE Sendai [2], resulting in structural changes in the apo E molecule.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [2] Matsunaga A, Saito T. Apolipoprotein E mutations: a comparison between lipoprotein glomerulopathy and type III hyperlipoproteinemia. Clin Exp Nephrol. 2014;18:220–4. source
- Classified as probably not a substantial claim. 8
- May combine two claims. 3
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSome etiology studies using APOE Sendai suggest that reduced receptor-binding activity and thermodynamic abnormalities may play important roles in the pathogenesis of LPG.
“Some etiology studies using APOE Sendai suggest that the reduced receptor-binding activity [12] and thermodynamic abnormalities [13] may play important roles in the pathogenesis of LPG.”
Quote in the paperNot a substantial claim1 of 2 sources checked- cites [12] Hoffmann MM, Scharnagl H, Panagiotou E, et al. Diminished LDL receptor and high heparin binding of apolipoprotein E2 Sendai associated with lipoprotein glomerulopathy. J Am Soc Nephrol. 2001;12:524–30. source
- cites [13] Georgiadou D, Stamatakis K, Efthimiadou EK, et al. Tharmodynamic and structural destabilization of apoE3 by hereditary mutations associated with the development of lipoprotein glomerulopathy. J Lipid Res. 2013;54:164–76. source
May combine two claims.
Findingown dataRenal biopsy revealed segmental proliferation in the mesangium and lipoprotein thrombi in the glomerular capillary.
“Renal biopsy revealed segmental proliferation in the mesangium and lipoprotein thrombi in the glomerular capillary.”
Quote in the paperSubstantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataThe patient's serum apo E level was 4.3 mg/dL.
“His serum apo E level was 4.3 mg/dL.”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataThe patient's urinary protein excretion was 4.7 g/day.
“His urinary protein excretion rate was 4.7 g/day”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
Findingown dataThe patient's serum triglyceride level was 266 mg/dL.
“a triglyceride (TG) level of 266 mg/ dL”
Quote in the paperNot a substantial claimMay combine two claims.
Findingown dataAfter fibrate discontinuation, urinary protein levels reached 6 g/day, leading to end-stage kidney disease a year later.
“the administration of fibrate was discontinued; however, urinary protein levels reached 6 g/day thereafter, leading to endstage kidney disease (ESKD) a year later”
Quote in the paperNot a substantial claimProbably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationSome in-frame deletions of amino acid residues are known to have a causative role in LPG.
“On the other hand, some in-frame deletions of amino acid residues are also known to have a causative role in LPG.”
Quote in the paperNot a substantial claimClassified as probably not a substantial claim.
PremisecitationLipoprotein glomerulopathy (LPG) is a rare disease characterized by lipoprotein thrombi in the glomerular capillaries due to heterozygous APOE gene mutations.
“Lipoprotein glomerulopathy (LPG) is a rare disease characterized by lipoprotein thrombi in the glomerular capillaries due to heterozygous APOE gene mutations [1].”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [1] 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. source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationMost APOE gene mutations causing LPG are missense mutations due to substitution of amino acid residues around the LDL receptor-binding region.
“Most of them are missense mutations due to the substitution of amino acid residues around the low-density lipoprotein (LDL) receptor-binding region.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [2] Matsunaga A, Saito T. Apolipoprotein E mutations: a comparison between lipoprotein glomerulopathy and type III hyperlipoproteinemia. Clin Exp Nephrol. 2014;18:220–4. source
Probably not a substantial claim: may not pass S3 (load-bearing).
PremisecitationThe APOE gene mutation due to duplicated amino acid residues was included among APOE gene mutations causing LPG.
“In addition , the APOE gene mutation due to duplicated amino acid residues was included there [2].”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [2] Matsunaga A, Saito T. Apolipoprotein E mutations: a comparison between lipoprotein glomerulopathy and type III hyperlipoproteinemia. Clin Exp Nephrol. 2014;18:220–4. source
May combine two claims.
PremisecitationAPOE Leiden and APOE5 have been reported to be associated with elevated triglycerides.
“APOE Leiden (a partial duplication of 21 nucleotides coding for seven amino acids) associated with type III hyperlipoproteinemia [5] and APOE5 (Val 135_Arg142dup) heterozygote [6] have been reported to be associated with elevated triglycerides”
Quote in the paperNot a substantial claim0 of 2 sources checked- cites [5] Havekes L, de Wit E, Leuven JG, et al. Apolipoprotein E3-Leiden. A new variant of human apolipoprotein E associated with familial type III hyperlipoproteinemia. Hum Genet. 1986;73:157–63. source
- cites [6] Yamanouchi Y, Takano T, Hamaguchi H, Tokunaga K. A novel apolipoprotein E5 variant with a 24-bp insertion causing hyperlipidemia. J Hum Genet. 2001;46:633–9. source
The paper relies on this without support.
High serum apo E level is characteristic of LPG.
“the high-serum apo E level, which is characteristic of LPG, was not observed.”
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?
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]”
From A boy and his mother with lipoprotein glomerulopathy: Two case reports and literature review (2025) · cites this paper as [24]
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 measuredFive 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 [80]
Cites
Havekes, L., de Wit, E., Leuven, J. G., Klasen, E., Utermann, W., Weber, W., & Beisiegel, U. (1986) · Human Genetics · doi:10.1007/bf00291607 · Cited by 99 · see citing works
Impact of Lipoprotein Glomerulopathy on the Relationship Between Lipids and Renal Diseases
Saito, T., Matsunaga, A., & Oikawa, S. (2006) · American Journal of Kidney Diseases · doi:10.1053/j.ajkd.2005.10.017 · Cited by 96 · see citing works
Self-citationHu, Z., Huang, S., Wu, Y., Liu, Y., Liu, X., Su, D., Tao, Y., Fu, P., Zhang, X., Peng, Z., et al. (2014) · Kidney International · doi:10.1038/ki.2013.335 · Cited by 60 · see citing works
HOFFMANN, M. M., SCHARNAGL, H., PANAGIOTOU, E., BANGHARD, W. T., WIELAND, H., & MA[Combining Diaeresis]RZ, W. (2001) · Journal of the American Society of Nephrology · doi:10.1681/asn.v123524 · Cited by 42 · see citing works
A novel variant apolipoprotein E Okayama in a patient with lipoprotein glomerulopathy
Kinomura, M., Sugiyama, H., Saito, T., Matsunaga, A., Sada, K.-E., Kanzaki, M., Takazawa, Y., Maeshima, Y., Yanai, H., & Makino, H. (2007) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfm675 · Cited by 40 · see citing works
Self-citationGeorgiadou, D., Stamatakis, K., Efthimiadou, E. K., Kordas, G., Gantz, D., Chroni, A., & Stratikos, E. (2013) · Journal of Lipid Research · doi:10.1194/jlr.m030965 · Cited by 37 · see citing works
Matsunaga, A., & Saito, T. (2014) · Clinical and Experimental Nephrology · doi:10.1007/s10157-013-0918-1 · Cited by 33 · see citing works
Self-citationTopics in lipoprotein glomerulopathy: an overview
Saito, T., Matsunaga, A., Ito, K., & Nakashima, H. (2014) · Clinical and Experimental Nephrology · doi:10.1007/s10157-013-0887-4 · Cited by 33 · see citing works
Self-citation(1995) · Clinical Genetics · Cited by 32 · see citing works
Self-citationA Novel Mutation ApoE2 Kurashiki (R158P) in a Patient with Lipoprotein Glomerulopathy
Tokura, T., Itano, S., Kobayashi, S., Kuwabara, A., Fujimoto, S., Horike, H., Satoh, M., Komai, N., Tomita, N., Matsunaga, A., et al. (2011) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.8102 · Cited by 28 · see citing works
Self-citationA novel apolipoprotein E mutation, ApoE Tsukuba (Arg 114 Cys), in lipoprotein glomerulopathy
Hagiwara, M., Yamagata, K., Matsunaga, T., Arakawa, Y., Usui, J., Shimizu, Y., Aita, K., Nagata, M., Koyama, A., Zhang, B., et al. (2007) · Nephrology Dialysis Transplantation · doi:10.1093/ndt/gfm735 · Cited by 27 · see citing works
Self-citationMitani, A., Ishigami, M., Watase, K., Minakata, T., & Yamamura, T. (2011) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.7377 · Cited by 24 · see citing works
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Self-citationA novel apolipoprotein E5 variant with a 24-bp insertion causing hyperlipidemia
Yamanouchi, Y., Takano, T., Hamaguchi, H., & Tokunaga, K. (2001) · Journal of Human Genetics · doi:10.1007/s100380170014 · Cited by 8 · see citing works
Havekes, L. M., Klasen, E. C., & Utermann, G. (1986) · Springer eBooks · doi:10.1007/978-1-4615-9474-1_26
Flagged first, then by citations
Cited by
Sorted by citations
Impact of Apolipoprotein E Variants: A Review of Naturally Occurring Variants and Clinical Features
Matsunaga, A., & Saito, T. (2025) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.65393 · Cited by 14 · see citing works
Self-citationA boy and his mother with lipoprotein glomerulopathy: Two case reports and literature review
Zhang, S., Fan, L., Li, Z., Liu, T., Jing, X., & Guo, Q. (2025) · Medicine · doi:10.1097/md.0000000000041628 · Cited by 2 · see citing works
A case of lipoprotein glomerulopathy in which complete remission was achieved by pemafibrate therapy
Tomita, C., Sato, T., Suzuki, Y., Arakawa, M., Shimizu, Y., Suzuki, Y., Yasuda, H., & Misaki, T. (2026) · CEN Case Reports · doi:10.1007/s13730-026-01148-9
- Authors
- Yokochi, A., Matsunaga, A., Kanemoto, K., Tominaga, N., Uda, S., & Saito, T.
- Affiliations
- Kanto Rosai Hospital (JP)
- Fukuoka University (JP)
- Kawasaki Municipal Tama Hospital (JP)
- Corresponding author
- Yokochi, Akio
- Venue
- CEN Case Reports
- Published
- 2024-08-14
- Volume
- 14
- Issue
- 2
- Pages
- 162-166
- ISSN
- 2192-4449 (ISSN-L)
- PMC
- PMC11958863
- OpenAlex
- W4401575851
- Cited by
- 3
- References
- 14
- Citations by year
- 2026: 1 · 2025: 2
- FWCI
- 0.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- CEN Case Reports (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- 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, proteinuria, hypertriglyceridemia, mesangial cell proliferation, end-stage renal disease, fibrate therapy
- MeSH terms
- Adult, Apolipoproteins E, Biopsy, Humans, Kidney Diseases, Kidney Failure, Chronic, Kidney Glomerulus, Male, Mutation, Proteinuria, Apolipoprotein E2
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