Abstract: SA-PO0351
Anuric AKI from Contrast-Induced Osmotic Tubulopathy
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 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
Author
- Lai, Huanchun Nana, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
Introduction
Contrast-induced nephropathy remains controversial because many post-contrast creatinine rises are confounded and labeled as contrast-associated AKI (CA-AKI), whereas true contrast-induced AKI (CI-AKI) is uncommon. However, osmotic tubulopathy may rarely cause oligo-anuric AKI when renal reserve is limited or exposure is repeated.
Case Description
An 82-year-old man with diabetes, hypertension, urinary retention with a suprapubic catheter, and CKD (baseline creatinine 1.4–1.7 mg/dL) presented with abdominal pain. CT A/P with 100 mL iohexol showed fecal impaction and a 4.1-cm bladder lesion. Within 3 days, creatinine rose from 1.6 to 6.25 mg/dL and he became anuric. Repeat noncontrast CT 3 days later showed persistent bilateral corticomedullary nephrogram, consistent with delayed contrast retention. Given severe anuric AKI out of proportion to obstruction or hemodynamics, kidney biopsy was performed. Biopsy showed chronic diabetic nephropathy with 40% global glomerulosclerosis and tubular atrophy, but also acute osmotic tubulopathy secondary to contrast. He was started briefly on hemodialysis for two sessions. Hours after biopsy, he developed flank pain; repeat noncontrast CT revealed a subcapsular/perinephric hematoma. Subsequent CTA obtained showed left renal infarction, consistent with Page-kidney physiology. Kidney function eventually recovered to creatinine 1.7 mg/dL at discharge 2 weeks later.
Discussion
This case highlights biopsy-proven CI-AKI presenting as anuric osmotic tubulopathy with persistent nephrogram and delayed contrast retention. Chaudhari et al. emphasize that CI-AKI is often confounded, but its risk is low, not zero. Abrupt anuria, contrast retention, and biopsy findings support true contrast-mediated tubular injury rather than an associative creatinine rise. Clinically indicated contrast should not be withheld, but high-risk patients with CKD, diabetes, and hemodynamic instability are at increased risk for developing true CI-AKI with major morbidity.
Acknowledgment
Rocky Mountain Regional VA Medical Center