Kidney Week

Abstract: SA-PO0346

Oxaliplatin-Induced AKI

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

Authors

• Dekmak, Batoul, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Batoul Dekmak, MD

• Kallakury, Bhaskar, MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Bhaskar Kallakury, MD

• Aron, Abraham W., MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Abraham W. Aron, MD

• Greenberg, Keiko I., MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Keiko I. Greenberg, MD

• Choi, Michael J., MedStar Georgetown University Hospital, Washington, District of Columbia, United States

Michael J. Choi, MD

Introduction

Oxaliplatin is a platinum-based chemotherapeutic agent widely used in FOLFOX regimens for colorectal cancer. While generally considered less nephrotoxic than cisplatin, rare but severe cases of acute kidney injury (AKI) have been documented. We report a case of oxaliplatin-induced AKI with concurrent hemolytic anemia in a patient with pre-existing chronic kidney disease (CKD) following his ninth FOLFOX cycle.

Case Description

A 50 yo male with CKD G3 (baseline creatinine 1.5 mg/dL), hypertension, and metastatic colorectal cancer presented on cycle 9, day 3 of FOLFOX. He had chills during infusion managed with antihistamines and steroids. Within 24 hours he developed jaundice, dark urine followed by anuria. Creatinine was 9.15 mg/dL. Urinalysis showed glycosuria, proteinuria, hematuria, and pyuria. Hemoglobin 9.3 g/dL, platelets 38,000/μL, LDH 1,625 units/L, haptoglobin <10 mg/dL, and DAT positive. Peripheral smear showed few schistocytes and no spherocytes. Renal biopsy demonstrated ATN with focal acute interstitial nephritis for which prednisone 80 mg/d was initiated. The patient was started on hemodialysis and oxaliplatin permanently discontinued. One month after discharge, creatinine was 2.38 mg/dl with early signs of renal recovery and hemodialysis weaned to twice weekly.

Discussion

Unlike cisplatin, whose nephrotoxicity is mediated through proximal tubular cell necrosis, oxaliplatin renal toxicity is rare. Two mechanisms may be operative here. The infusion reaction and hemolysis suggest immune-mediated injury, whereby oxaliplatin-dependent anti-RBC antibodies drive intravascular hemolysis and pigment-induced tubular injury. Direct dose-dependent tubular toxicity, as seen with cisplatin, cannot be excluded given cumulative exposure and underlying CKD. Both pathways lead to acute tubular injury — the predominant biopsy finding. The focal interstitial nephritis likely reflects a T-cell mediated hypersensitivity response, a recognized but rare oxaliplatin toxicity. Oxaliplatin nephrotoxicity can be severe and irreversible, though prompt recognition and discontinuation may allow partial renal recovery. This challenges the perceived safety of oxaliplatin in CKD, suggesting closer monitoring and a lower threshold for discontinuation are warranted.