Abstract: FR-PO0456
Atypical ANCA-Associated Vasculitis Presenting as Dialysis-Dependent AKI Mimicking Acute Tubular Necrosis
Session Information
- AKI: Case Reports - TMA, Vasculitis, Immune-Mediated Injury, and Systemic Disease
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Singh, Amrinder, Virginia Commonwealth University, Richmond, Virginia, United States
- Patrick, Kennerly Clinton, Virginia Commonwealth University, Richmond, Virginia, United States
- Sriperumbuduri, Sriram, Virginia Commonwealth University, Richmond, Virginia, United States
Introduction
ANCA-associated vasculitis (AAV) typically presents with pauci-immune crescentic glomerulonephritis. Atypical presentations without significant glomerular involvement may mimic acute tubular necrosis (ATN), delaying diagnosis.
Case Description
A 68-year-old man with hypertension and pre-diabetes presented with months of fatigue, malaise, and 30-lb weight loss. Baseline creatinine was 1.1 mg/dL, rising to 3.97 mg/dL on admission and peaking at 8.45 mg/dL.
Urinalysis showed proteinuria with muddy brown casts. CT imaging revealed bilateral striated nephrograms. Initial impression favored ATN due to poor oral intake and possible contrast exposure.
Marked inflammation was noted (ESR 119 mm/hr, CRP 21.7 mg/dL, ferritin ~3000 ng/mL). Serologic workup revealed p-ANCA positivity (1:80) with elevated MPO antibodies; ANA, anti-GBM, and myeloma studies were negative.
Kidney biopsy demonstrated small vessel necrotizing vasculitis with fibrinoid necrosis and relative glomerular sparing, without crescents or immune deposits.
The patient developed uremia requiring hemodialysis. He was treated with pulse-dose steroids followed by prednisone and rituximab. He remained dialysis-dependent at discharge.
Discussion
This case highlights an atypical AAV presentation with predominant vascular injury and minimal glomerular involvement, mimicking ATN clinically and on urine microscopy. Muddy brown casts and plausible ischemic insults initially obscured the diagnosis.
Systemic inflammation and weight loss were key clues prompting further evaluation. Early kidney biopsy enabled diagnosis and treatment. Delayed recognition may result in irreversible kidney injury. In conclusion, AAV may present as AKI resembling ATN when glomerular involvement is minimal. Recognition of systemic inflammatory features and timely biopsy are critical.