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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Background:Lipoprotein glomerulopathy (LPG) is a rare inherited renal disease caused by mutations in the apolipoprotein E (APOE) gene, characterized by lipoprotein thrombi in glomerular capillaries and progressive renal dysfunction. No standard therapy has been established.
Case Presentation:A 51-year-old man was admitted to our hospital for cerebral thrombosis at age 44. His father had end-stage renal disease on dialysis, and he was from Miyagi Prefecture, Japan. Laboratory data showed severe proteinuria and renal dysfunction: urinary protein (UP) 6.15 g/gCr, serum creatinine (Cr) 2.43 mg/dL, and estimated glomerular filtration rate (eGFR) 25 mL/min/1.73 m². Renal biopsy performed on day 23 revealed LPG. The patient was transferred to a rehabilitation hospital and returned to our hospital on day 200, when UP was 1.95 g/gCr, Cr 2.57 mg/dL, and eGFR 23.3 mL/min/1.73 m². As renal dysfunction was progressing, pharmacologic therapy was initiated on day 200 before genetic confirmation. APOE genotyping later identified the APOE Sendai mutation.
Results:Pemafibrate was started at a low dose (0.1 mg every other day), increased to 0.1 mg daily along with an angiotensin II receptor blocker (ARB). On day 361, rhabdomyolysis developed, and the dose of pematibrate was reduced to the initial dose. Thereafter, Cr remained around 2.0 mg/dL, with persistent mild proteinuria (0.5–1.0 g/gCr). Three years later, UP increased to 4.7 g/gCr, and Cr rose to 2.5 mg/dL after four years. With full informed consent, pemafibrate was increased to 0.2 mg/day. Since proteinuria persisted, additional ARB, eicosapentaenoic acid (EPA), an SGLT2 inhibitor, and ezetimibe were introduced. Renal function stabilized, maintaining eGFR around 25 mL/min/1.73 m² for eight years.
Discussion:LPG is a rare disease, with approximately 50–60% of patients progressing to end-stage renal failure within 10 years of onset. Few patients maintain renal function long-term. Although bezafibrate has been reported to be effective in some cases, in this case, renal function had already declined at diagnosis, and bezafibrate was contraindicated. Continuous administration of low-dose pemafibrate, combined with EPA, ARB, and particularly SGLT2 inhibitors, appeared to contribute to long-term stabilization.
Conclusion:This is a rare case of LPG with APOE Sendai mutation in which renal function was preserved for eight years under pemafibrate-based therapy. Pemafibrate may represent a safe and effective treatment option for patients with LPG and renal impairment.
