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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.
Membranoproliferative glomerulonephritis (MPGN) is a pattern of glomerular injury characterized by capillary wall remodeling and mesangial proliferation. Its etiology can be primary or secondary to conditions like chronic infections and immune complex deposition. Abernethy malformation, or congenital extrahepatic portosystemic shunt (CEPS), is a rare vascular anomaly where portal blood bypasses the liver directly into the systemic circulation. The Morgan-Superina classification distinguishes Type I (complete absence of intrahepatic portal veins, requiring liver transplantation) from Type II (hypoplastic portal vein with a side-to-side shunt).
The association between these two entities is exceedingly rare. We present a novel case of a pediatric patient diagnosed with both MPGN and Abernethy malformation (Type Ib). Critically, to our knowledge, this is the first reported case of this combination where the patient underwent liver transplantation alone (without kidney transplantation) and subsequently demonstrated significant improvement in renal parameters, including a marked reduction in proteinuria.This case provides pivotal evidence for a pathophysiological link between glomerular pathology and portosystemic shunting, suggesting that correcting the underlying vascular malformation can directly ameliorate renal disease.
We present a case report of a 13-year-old boy admitted with severe anemia, pneumonia, and nephrotic-range proteinuria. Diagnostic workup included laboratory tests (hematology, serum chemistry, immunology, urinalysis), imaging studies (chest CT, abdominal CT, MRI, ultrasound, angiography), and a renal biopsy to confirm the diagnosis. The patient was treated medically for MPGN and subsequently underwent liver transplantation for the type Ib Abernethy malformation. His renal parameters were systematically monitored before and after the transplantation.
The patient was diagnosed with Abernethy malformation type Ib, confirmed by imaging showing a portocaval shunt, and MPGN, confirmed by renal biopsy. Pretransplantation, he had massive proteinuria (14.18 g/24h or 305 mg/kg) and low serum complement levels. Following liver transplantation, his renal condition improved significantly: proteinuria decreased substantially to 1.2 g/24h (26 mg/kg), complement levels normalized, and his severe anemia resolved. The patient achieved partial remission of his nephrotic syndrome without requiring a kidney transplant.
This case demonstrates a rare but important association between Abernethy malformation and MPGN. The observed improvement in glomerular disease after liver transplantation strongly suggests a pathophysiological link, likely involving impaired hepatic clearance of gut-derived pathogens, immune complexes, and complement components, compounded by potential renal hemodynamic changes. This highlights the critical role of correcting the underlying portosystemic shunt in managing such complex multisystem diseases and provides evidence for a hemodynamic and immunologic mechanism connecting congenital vascular anomalies to glomerular pathology.
