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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
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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.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) typically presents as pauci-immune necrotizing crescentic glomerulonephritis with hematuria and proteinuria. Tubulointerstitial inflammation is usually secondary to glomerular injury. Cases where tubulointerstitial nephritis (TIN) predominates despite minimal glomerular involvement and absence of urinary abnormalities are extremely rare. Such presentations may delay diagnosis and accelerate renal dysfunction. We report a TIN-dominant case of AAV without urinary abnormalities.
An 80-year-old woman with hypertension, deep vein thrombosis, and Parkinson’s disease was referred for anemia and elevated inflammatory markers. Laboratory results showed hemoglobin 6.6 g/dL, leukocytes 13.6 ×10³/µL, creatinine 1.3 mg/dL (eGFR 30 mL/min/1.73 m²), and IgG 2085 mg/dL. MPO-ANCA was positive at 48.5 IU/mL, while PR3-ANCA and ANA were negative. Urinalysis revealed no hematuria or proteinuria, but urinary β2-microglobulin was markedly elevated to 707 µg/L, suggesting tubular injury. A renal biopsy was performed.
Renal biopsy revealed limited glomerular involvement: of 25 glomeruli, two showed crescents and three were globally sclerotic, with only minimal necrosis and mesangial proliferation. The predominant findings were dense interstitial lymphoplasmacytic infiltration, tubulitis with basement membrane disruption, and vascular changes compatible with prior fibrinoid vasculitis. Immunofluorescence demonstrated pauci-immune staining. IgG4-related disease was excluded with an IgG4/IgG ratio of 25% and absence of storiform fibrosis. Electron microscopy confirmed features consistent with ANCA nephritis. Overall, renal dysfunction was attributed mainly to tubulointerstitial lesions and peritubular capillaritis rather than glomerular injury.
The patient was treated with prednisolone 25 mg and rituximab, resulting in improvement of anemia, normalization of inflammatory markers, and stabilization of renal function.
This case illustrates a rare presentation of AAV manifesting predominantly as TIN without urinary abnormalities. In patients with progressive renal dysfunction but unremarkable urinalysis, elevated urinary β2-microglobulin should prompt biopsy for diagnosis. Early recognition and timely immunosuppressive therapy may improve renal and systemic outcomes. Moreover, this case suggests that in AAV, not only glomerular lesions but also tubulointerstitial inflammation and peritubular capillaritis can independently drive renal impairment, making it an important clinical example.
This abstract was also submitted to The 55th Western Regional Meeting of the Japanese Society of Nephrology, and re-submission is permitted by the organizers of the original meeting.
