Abstract: FR-PO004
Tumor Lysis Syndrome with Venetoclax
Session Information
- Fellows/Residents Case Reports: AKI and Drug-Related Interactions
November 03, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Parikh, Nishita, Hofstra Northwell School of Medicine, Great neck, New York, United States
- Barrientos, Jacqueline, CLL Research and Treatment Center, Lake Success, New York, United States
- Barnett, Richard L., Hofstra Northwell School of Medicine, Great neck, New York, United States
- Katsetos, John F, CLL Research and Treatment Center, Lake Success, New York, United States
- Merzkani, Massini, Hofstra Northwell School of Medicine, Great Neck, New York, United States
- Mathew, Anna, Hofstra Northwell School of Medicine, Great neck, New York, United States
- Jhaveri, Kenar D., Hofstra Northwell School of Medicine, Great neck, New York, United States
Background
Venetoclax is a BCL2 inhibitor approved for CLL treatment. A low dose of this drug has led to fatal cases of tumor lysis syndrome (TLS) in the initial trials.
Methods
A 64 year old female with CLL was admitted for worsening lymphadenopathy. After failing all therapy, she was planned to start on venetoclax( BCL2 inhibitor). Given her admission serum creatinine(Scr) of 1.9mg/dl, uric acid level of 8.1mg/dl, and serum phosphorus was 4.8mg/dl, she was started on crystalloid fluid resusitation and received one dose of rasburicase(0.2mg/kg). Pt. Scr improved to 1.3mg/dl. Given high tumor burden, nephrology was consulted early for TLS prevention. The patient was initiated at 20mg dose of venetoclax and TLS labs were monitored every four hours. Three hours after the initial dose, the patient had a sudden rise in the LDH to 1158u/dl, Scr was 1.6mg/dl and serum phosphorus was 7.6 g/dL, despite urine output of 100 cc of urine per hour. An early transfer to intensive care unit and initiation of continuous renal replacement therapy (CRRT) allowed for ongoing dosing of venetoclax with controlled clearance of phosphate, potassium and uric acid. She received a modified dosing of this drug and ultimately was given 50mg of the dose before CRRT was discontinued. LDH was followed serially as a marker for ongoing TLS. Following resolution of TLS lab markers, CRRT was stopped, the patient received 100mg of venetoclax, with stable renal function and no abnormal TLS markers. Figure below summarizes the lab data supporting early successful prevention of fatal TLS reported with this agent.
Conclusion
This case illustrates that early involvement of nephrology in high risk TLS associated with venetoclax can improve patient outcomes. Early initiation of CRRT even without significant renal injury along with modified dose escalation can prevent fatal TLS outcomes as described in the initial trials of this agent. Nephrologists need to be aware of this toxicity with this agent as it becomes commonly used.