Abstract: TH-PO0717
Acute Interstitial Nephritis During Phase 1 Therapy for Advanced Prostate Cancer: Red Flags in Red Urine, a Case of Chemotherapy-Induced AKI
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
- Voors, William, University of Utah Health, Salt Lake City, Utah, United States
- Barry, Marc, University of Utah Health, Salt Lake City, Utah, United States
- Gilligan, Sarah, University of Utah Health, Salt Lake City, Utah, United States
- Ramkumar, Nirupama, University of Utah Health, Salt Lake City, Utah, United States
Introduction
Chemotherapy-induced renal dysfunction encompasses a wide range of disease from pre-renal AKI from nausea and vomiting to direct nephrotoxicity. It is important to monitor for warning signs of renal involvement as new agents are being used.
Case Description
A 65-year-old male with a history of metastatic prostate cancer treated with radical prostatectomy and radiation in 2010 complicated by radiation cystitis and intermittent hematuria, hypertension and hyperlipidemia presented to the clinic for rising serum creatinine over 6 months. He was enrolled in a clinical trial for 12 months which studied used of actinium labeled antibody targeting human kallikrein-2 (hK2) and then switched to docetaxel for 3 months and cabazitaxel for 3 months before being seen Nephrology. He was also hospitalized for passing blood clots several times and underwent bladder embolization 2 months prior to being seen in the Nephrology clinic. Serum creatinine had increased from baseline of 1.1-1.2 mg/dl to 4 mg/dl during the most recent hospitalization and continued to worsen to 8.0 mg/dl over 6 months. After ruling out obstructive disease and other causes for AKI, a kidney biopsy was performed demonstrating chronic active thrombotic microangiopathy (TMA), acute tubular injury with cytologic atypia and patchy interstitial chronic inflammation suggestive of chemotherapy induced kidney toxicity. Although patient had anemia and borderline thrombocytopenia, no systemic evidence of hemolysis was noted. Of note, serum creatinine started to increase 2 months after discontinuation of the hK2 therapy due to progression of disease. Patient was also not on any chemotherapy agents for 2 months when he was seen in the kidney clinic. Steroids were considered, however, given the severity and extent of kidney injury, this was not pursued. Dialysis options were discussed and patient elected to pursue hospice and passed away 6 weeks later.
Discussion
Drugs most commonly implicated in chemotherapy related chronic TMA are anti-VEGF agents, tyrosine kinase inhibitors and gemcitabine. To our knowledge, actinium labeled antibody targeting hK2 and cabazitxel have not been linked with TMA. Docetaxel has a rare association with TMA and concomitant radiation cystitis could have contributed to the rapid progression of kidney dysfunction in our patient.