Kidney Week

Abstract: FR-PO0466

When the Bacillus Escapes the Bladder: Severe Granulomatous Interstitial Nephritis After Intravesical Bacillus Calmette-Guerin Therapy

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

• Vega Batista, Franklyn, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States

Franklyn Vega Batista, MD

• Lorenzo Capps, Maria Jose, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States

Maria Jose Lorenzo Capps, MD

• Davidson, George, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States

George Davidson, MD

• Chigbu, Naomi Cc, Rutgers The State University of New Jersey, New Brunswick, New Jersey, United States

Naomi Cc Chigbu, MBChB

• El-Charabaty, Elie, RWJBarnabas Health, Livingston, New Jersey, United States

Elie El-Charabaty, MD, FASN

Introduction

Intravesical Bacillus Calmette-Guérin (BCG) is standard therapy for non–muscle-invasive bladder carcinoma. Systemic complications are uncommon, and renal involvement, particularly granulomatous interstitial nephritis, is exceedingly rare.

Case Description

A 79-year-old man with hypertension, chronic thrombocytopenia, and non–muscle-invasive bladder carcinoma on intravesical BCG was admitted with weakness and functional decline. He was hemodynamically stable. Labs showed AKI, with creatinine rising from 1.15 to 3.02 mg/dL in the setting of dehydration and recent NSAID use. Initial concern was acute tubular necrosis with possible acute interstitial nephritis. Extensive Serologic workup, including autoimmune profile and paraproteinemia, was unrevealing except for Bence Jones protein. Renal ultrasound showed no hydronephrosis. Despite NSAID discontinuation and supportive care, renal function failed to improve, prompting a kidney biopsy. Pathology demonstrated acute interstitial nephritis with necrotizing granulomatous inflammation, consistent with BCG-induced granulomatous nephritis. He did not require RRT. With no evidence of active mycobacterial infection, systemic corticosteroids were initiated, resulting in improvement in renal parametes and discharged to rehab facility.

Discussion

Granulomatous interstitial nephritis after intravesical BCG is rare and often underdiagnosed. Proposed mechanisms include hematogenous dissemination of Mycobacterium bovis after mucosal disruption and delayed-type hypersensitivity mediated by T-cell activation and macrophage-driven inflammation. Diagnosis is challenging because presentation mimics common AKI etiologies, and M. bovis is rarely isolated, making biopsy essential. Corticosteroids may be used when immune-mediated injury predominates, while antimycobacterial therapy is reserved for suspected systemic infection or refractory disease.

Non-necrotizing granulomatous inflammation