Abstract: TH-PO0720
From Routine to Kidney Failure: A Case of Severe Acute Tubular Necrosis After Endoscopic Retrograde Cholangiopancreatography (ERCP) Prophylaxis
Session Information
- AKI: Prevention, Diagnostics, and Management
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 101 AKI: Epidemiology, Risk Factors, and Prevention
Authors
- Graydon, Drew N., Temple University, Philadelphia, Pennsylvania, United States
- Boyle, Suzanne, Temple University, Philadelphia, Pennsylvania, United States
- Brobst, Rachel Emily, Temple University, Philadelphia, Pennsylvania, United States
Introduction
Acute tubular necrosis (ATN) is the most common cause of acute kidney injury (AKI) in hospitalized patients. It is often difficult to isolate the inciting event. We describe a case of biopsy-proven severe ATN associated with a dose of rectal indomethacin.
Case Description
A previously healthy 21-year-old man presented with left upper quadrant pain. CT, MRI and ultrasound suggested acute cholecystitis without classic physical exam features. Liver function tests were consistent with hepatocellular injury. However, HIDA failed to visualize the gallbladder and common bile duct prompting an ERCP, which demonstrated choledocholithiasis. A liver biopsy showed drug-induced liver injury and mild cholestatic injury.
Forty-eight hours after ERCP, the creatinine more than tripled (0.8 mg/dl to 2.9 mg/dl) and peaked at 9.0 mg/dl within one week. Renal ultrasound was normal. Urine microscopy had granular casts, white blood cells, and tubular epithelial cells. There was no hypotension. Review for nephrotoxins revealed intravenous contrast (48 hours before creatinine rise) and a dose of rectal indomethacin (100 mg) before ERCP for pancreatitis prophylaxis.
Due to persistent AKI, kidney biopsy was performed. There was moderate-to-severe acute tubular injury with granular casts and rare WBC cast. Glomeruli were normal. There were no bilirubin casts, no significant interstitial inflammation, and IF and EM were negative.
Discussion
We describe unexpectedly severe ATN given the identified insults, which included intravenous (IV) contrast and a single dose of rectal indomethacin—both 48 hours prior to the creatinine rise. There are several lessons here. One is that nephrologists should know rectal indomethacin is routinely given as prophylaxis for ERCP-induced pancreatitis. Indomethacin undergoes hepatic metabolism, which is slowed in liver injury, potentiating nephrotoxicity. It is also albumin-bound, so hypoalbuminemia can increase free drug levels. Lastly, acute liver injury can increase vasodilators like nitric oxide, which activate the renin-angiotensin system, making the kidney more susceptible to injury with non-steroidal anti-inflammatory agents. Although indomethacin is routinely used for prophylaxis with minimal reported incidence of AKI, our patient had evidence of hepatocellular injury, which is atypical with biliary obstruction. It is possible that this heightened AKI risk.