Abstract: SA-PO0207
Long-Term Kidney Outcomes of Gemcitabine-Induced Thrombotic Microangiopathy in Patients with Cancer: A Case Series
Session Information
- Onconephrology: MGRS, HSCT, Electrolytes, RCC, and More
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Bertan, Sara H, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
- Shukla, Parnika, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
- Kelly, Adam, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
- Gudsoorkar, Prakash Shashikant, University of Cincinnati, Cincinnati, Ohio, United States
- Gupta, Shruti, Brigham and Women's Hospital, Boston, Massachusetts, United States
- Hanna, Paul, Medical College of Wisconsin, Milwaukee, Wisconsin, United States
Background
Gemcitabine-induced thrombotic microangiopathy (Gem-TMA) is a rare but serious complication of gemcitabine, a chemotherapeutic commonly used in the treatment of multiple malignancies. Thought to involve complement activation, Gem-TMA has been reported to respond to terminal complement (C5) inhibition. We evaluated long term renal effects in affected patients.
Methods
Using data from the TriNetX Research Network, we identified adult patients with cancer exposed to gemcitabine within 30 days of TMA diagnosis (using ICD 9 and 10 codes), subsequently treated with C5 inhibitors (eculizumab or ravulizumab). Patients with allogenic stem cell transplant, kidney transplant, or dialysis dependence were excluded. We analyzed renal outcomes (sCr, eGFR, and BP trends) and markers of TMA activity (LDH and platelet count) over six months following C5 inhibitor initiation.
Results
Among 24 patients with Gem-TMA (mean age 58.7 ± 12.2 years; 33% male), baseline hypertension was prevalent (71%), and kidney dysfunction was common (mean sCr 2.6 ± 1.5 mg/dL). The most frequently reported cancer was pancreatic cancer (50%). At the time of TMA diagnosis, the mean systolic BP was 154.6 ± 20.3 mmHg, and mean diastolic BP was 82.8 ± 11.3 mmHg. LDH and platelet counts were markedly abnormal, with mean values of 633.1 IU/L and 124.8 × 109/L, respectively. Following C5 inhibitor therapy, average trends in eGFR, sCr, BP, LDH, and platelet count demonstrated clinical improvement (Figure 1). The median interval from the last dose of gemcitabine to C5 inhibitor initiation was 36 days (IQR 28.5 - 46.5), and from TMA diagnosis to therapy initiation was 15.5 days (IQR 3.5 - 25.5). Patients received C5 inhibition for a median duration of 36.5 days (IQR 14.5 - 130).
Conclusion
C5 inhibition was associated with improved kidney function, stabilized blood pressure trend, and resolution of hematologic abnormalities over six months; these findings support its role as a mechanism-targeted therapy in the management of Gem-TMA.
Figure 1. Recovery Trends