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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.
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Shunt nephritis is an uncommon complication of ventriculoatrial (VA) shunts that typically manifests years after implantation. This report describes an atypical case of shunt nephritis caused by Cutibacterium acnes VA‑shunt infection occurring 24 years post-placement and presenting with unique lupus-like immunopathological findings. This highlights the importance of timely surgical and medical interventions, even in cases with prolonged latency.
A woman with hydrocephalus received a ventriculoperitoneal shunt in infancy and a VA shunt at age 7 after peritonitis. At age 26, she developed fever with blood and cerebrospinal fluid cultures positive for C. acnes, consistent with VA‑shunt infection. Urinalysis at that time was unremarkable, and antibiotic therapy yielded a temporary improvement. Recurrent intermittent fever was managed conservatively. Five years later, she presented with nephrotic syndrome, gross hematuria, and leg edema. Laboratory findings on admission (day 0) revealed nephrotic-range proteinuria and hypocomplementemia, prompting a kidney biopsy on day 9 and a microbiological investigation on day 14.
The urine protein-to-creatinine ratio was 11.6 g/gCr, with numerous red blood cells (RBCs) per high-power field (HPF) in the urine sediment. Serum albumin was 2.5 g/dL, and serum creatinine was normal (0.46 mg/dL). Complement levels were markedly decreased (C3, 32 mg/dL; C4, 3.3 mg/dL; and CH50 ≤12 U/mL). Proteinase 3–Antineutrophil Cytoplasmic Antibody (PR3-ANCA) was positive (39.1 U/mL), whereas anti-nuclear antibody, anti-double stranded DNA antibody, and other autoantibodies were negative. CRP levels were elevated (1.0 mg/dL). Drainage from the right lateral ventricle yielded C. acnes, a slow-growing anaerobe implicated in chronic shunt infections.
The biopsied specimen revealed a membranoproliferative glomerulonephritis pattern of injury, characterized by mesangial matrix expansion, endocapillary and mesangial hypercellularity, and double-contoured glomerular basement membranes. Immunofluorescence revealed co-dominant C1q, C3, and C4 deposition, suggesting classical complement pathway activation with lupus-like features. Electron microscopy confirmed subendothelial and mesangial electron-dense deposits.
After stepwise shunt removal on days 13 and 28 together with antibiotic therapy, urinary findings improved markedly (UPCR, 0.95 g/gCr; 5–9 RBCs/HPF on day 43). Although complete remission has not yet been achieved, urinary abnormalities continued to improve, indicating a favorable response.
This case demonstrates that shunt nephritis can develop decades after VA shunt placement, even without overt bacteremia. Identification of C. acnes and prompt shunt removal with antibiotic therapy were associated with renal improvement. The prolonged latency, the atypical lupus-like immunopathological findings, and PR3‑ANCA positivity broaden the understanding of infection-related glomerulonephritis and underscore the clinical and educational significance of this case. Clinicians should remain vigilant for ongoing renal surveillance in patients with cerebrospinal fluid shunts, as prompt recognition and removal of infected devices are essential for improving patient outcomes.
