Abstract: FR-PO0461
Chronic Active Tubulointerstitial Nephritis as an Extraintestinal Manifestation of Treatment-Naïve Inflammatory Bowel Disease
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
- Shah, Riddhi, Prime Olympia Fields, Olympia Fields, Illinois, United States
- Deswal, Aradhika, Prime Olympia Fields, Olympia Fields, Illinois, United States
- Sarguroh, Tauseef A., Kidney Care Center, Olympia Fields, Illinois, United States
Introduction
Tubulointerstitial nephritis (TIN) is a rare but recognized extraintestinal manifestation of inflammatory bowel disease (IBD). Renal involvement may occur independent of nephrotoxic therapy and present as acute kidney injury (AKI). We present a case of biopsy-proven chronic active TIN in newly diagnosed treatment-naïve IBD.
Case Description
A 24-year-old male with no significant past medical history presented with AKI (creatinine 2.5 mg/dL, BUN 35 mg/dL). Over six months, he reported 3–4 episodes of loose stools daily with intermittent hematochezia alternating with constipation. Infectious stool studies were negative, while fecal calprotectin was elevated. Colonoscopy with biopsy demonstrated moderately active pancolitis and terminal ileitis consistent with newly diagnosed inflammatory bowel disease. AKI was thought to be secondary to volume depletion but failed to improve with intravenous fluid resuscitation. Kidney biopsy demonstrated chronic active tubulointerstitial nephritis with severe interstitial fibrosis and tubular atrophy involving approximately 70% of the cortex, diffuse lymphohistiocytic interstitial inflammation, and lymphocytic tubulitis. Immunofluorescence and electron microscopy were negative for immune-complex deposits. The patient had no prior exposure to 5-aminosalicylic acid (5-ASA) therapy or
other nephrotoxins before presentation. Following corticosteroid therapy, creatinine improved from 2.5 mg/dL to 1.5 mg/dL.
Discussion
TIN is an uncommon but important renal manifestation of IBD and may occur independently of medical therapy. Although 5-ASA exposure is a recognized cause of TIN, this patient was treatment-naïve at presentation, supporting immune-mediated renal involvement related to underlying IBD itself from systemic immune dysregulation, cytokine activation, and immune-mediated tubular injury. This case highlights the importance of early kidney biopsy for diagnosis and management. Severe chronicity on biopsy in a young patient further emphasizes the importance of prompt recognition and renal monitoring in patients with IBD.