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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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Abstract titles should be brief and reflect the content of the abstract.
IgA nephropathy (IgAN) is the most common primary glomerulonephritis worldwide and usually follows a slow, chronic course. However, in rare cases, an extracapillary or crescentic variant may develop, leading to rapidly progressive renal failure. The coexistence of IgAN with malignancy, particularly breast cancer, is exceptionally uncommon but may suggest a paraneoplastic or immune-mediated link. Understanding such associations is clinically relevant, as early recognition of atypical glomerular presentations in oncology patients may improve outcomes.
A 52-year-old woman with a history of stage II right-sided invasive ductal carcinoma of the breast, treated in 2023 with radical mastectomy, anthracycline–taxane chemotherapy (AC-T), and radiotherapy, achieved complete oncologic remission confirmed by SPECT imaging. In January 2025, she presented with macroscopic hematuria, new-onset hypertension (150/95 mmHg), and rapidly worsening renal function. Laboratory tests revealed elevated serum creatinine (4.7 mg/dL; baseline 1.2 mg/dL), urea 211 mg/dL, estimated GFR 10 mL/min/1.73 m², and subnephrotic proteinuria (1,854 mg/24h). Urinalysis showed active sediment with 65% dysmorphic erythrocytes and red blood cell casts. Complement levels were within normal range (C3: 112 mg/dL; C4: 23 mg/dL), and autoimmune serologies were negative for ANA, ANCA, and anti-dsDNA. Viral panels for hepatitis B, C, and HIV were non-reactive. A percutaneous renal biopsy was performed for diagnostic confirmation (see Table 1 for relevant laboratory parameters).
Light microscopy demonstrated proliferative extracapillary glomerulonephritis with cellular crescents in 64% of glomeruli and rupture of Bowman's capsule. The Oxford classification was M0 E0 S1 T1 C2. Direct immunofluorescence revealed dominant mesangial deposits of IgA (3+) and fibrinogen (2+). These findings confirmed IgA crescentic nephropathy. The patient was treated with intravenous methylprednisolone (500 mg/day for 3 days), followed by oral prednisone (1 mg/kg/day) and intravenous cyclophosphamide every 15 days for 3 months according to a rapidly progressive glomerulonephritis protocol (0.5 g/m²). Despite treatment, renal function did not recover and chronic hemodialysis was required. Representative histopathological and immunofluorescence findings from renal biopsy are presented in Figures A–D, illustrating extracapillary proliferation, rupture of Bowman's capsule, and mesangial deposition of IgA and fibrinogen.
This case illustrates a rare and aggressive presentation of crescentic IgA nephropathy following remission from breast cancer. Although the pathogenetic link remains uncertain, tumor-related immune dysregulation or chemotherapy-induced mechanisms could have contributed to the glomerular injury. Clinicians should maintain a high index of suspicion for glomerular disease in cancer patients with hematuria or acute renal dysfunction, even during remission.
