ArticleJournal of the American Society of Nephrology : JASN2013
Nephrotic syndrome caused by immune-mediated acquired LCAT deficiency.
Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- A Case of Acquired LCAT Deficiency with the Discrepancy between Spontaneous Resolution of Proteinuria and Continually Low HDL Cholesterol Levels.Journal of atherosclerosis and thrombosis · 2026Article
- Short-Term Treatment for Immune-Mediated Acquired Lecithin-Cholesterol Acyltransferase Deficiency Restores the High-Density Lipoprotein Function: A Case Report.Journal of atherosclerosis and thrombosis · 2025Article
- Uncommon Factors Leading to Nephrotic Syndrome.Biomedicines · 2025Review
- A Rare Case of Autoimmune-Mediated Lecithin:Cholesterol Acyltransferase Insufficiency Manifesting as the Acute Onset of Extremely Hypo-High-Density Lipoprotein-Cholesterolemia and Spontaneous Improvement: A Case Report with a Review of the Literature.Journal of atherosclerosis and thrombosis · 2025Review
- Two Cases of Acquired High-Density Lipoprotein Deficiency with Immunoglobulin G4-Related Lecithin-Cholesterol Acyltransferase Autoantibody.Journal of atherosclerosis and thrombosis · 2023Article
- A rare case of nephrotic syndrome and Tangier disease.CEN case reports · 2023Article
- A rare case of renal involvement in Lecithin-Cholesterol Acyltransferase (LCAT) deficiency: lessons for the clinical nephrologist.Journal of nephrology · 2023Article
- Integrated lipidomics and network pharmacology analysis to reveal the mechanisms of berberine in the treatment of hyperlipidemia.Journal of translational medicine · 2022Article
- LCAT deficiency and pregnancy: Case report.Obstetric medicine · 2021Article
- Use of Lipid-Modifying Agents for the Treatment of Glomerular Diseases.Journal of personalized medicine · 2021Review
- Current Status of Familial LCAT Deficiency in Japan.Journal of atherosclerosis and thrombosis · 2021Review
- Novel Missense LCAT Gene Mutation Associated with an Atypical Phenotype of Familial LCAT Deficiency in Two Portuguese Brothers.JIMD reports · 2018Article
- A case of acquired lecithin:cholesterol acyltransferase deficiency with sarcoidosis that remitted spontaneously.CEN case reports · 2016Article
- Systemic and renal lipids in kidney disease development and progression.American journal of physiology. Renal physiology · 2016Review
- Podocyte injury-driven lipid peroxidation accelerates the infiltration of glomerular foam cells in focal segmental glomerulosclerosis.The American journal of pathology · 2015Article
- Foam cells and the pathogenesis of kidney disease.Current opinion in nephrology and hypertension · 2015Review
- Immunopathogenesis of membranous nephropathy: an update.Seminars in immunopathology · 2014Review
- Characteristic kidney pathology, gene abnormality and treatments in LCAT deficiency.Clinical and experimental nephrology · 2014Review
- The kidney and lipids: preface.Clinical and experimental nephrology · 2014Article
- Pathology of glomerular lipidosis.Clinical and experimental nephrology · 2014Review
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lecithin-cholesterol acyltransferase (LCAT) is an enzyme involved in maintaining cholesterol homeostasis. In familial LCAT deficiency (FLD), abnormal lipid deposition causes renal injury and nephrotic syndrome, frequently progressing to ESRD. Here, we describe a 63-year-old Japanese woman with no family history of renal disease who presented with nephrotic syndrome. The laboratory data revealed an extremely low level of serum HDL and undetectable serum LCAT activity. Renal biopsy showed glomerular lipid deposition with prominent accumulation of foam cells, similar to the histologic findings of FLD. In addition, she had subepithelial electron-dense deposits compatible with membranous nephropathy, which are not typical of FLD. A mixing test and coimmunoprecipitation study demonstrated the presence of an inhibitory anti-LCAT antibody in the patient's serum. Immunohistochemistry and immunofluorescence detected LCAT along parts of the glomerular capillary walls, suggesting that LCAT was an antigen responsible for the membranous nephropathy. Treatment with steroids resulted in complete remission of the nephrotic syndrome, normalization of serum LCAT activity and HDL level, and disappearance of foam cell accumulation in renal tissue. In summary, inhibitory anti-LCAT antibody can lead to glomerular lesions similar to those observed in FLD.
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