Abstract: SA-PO219
Renal-Limited Thrombotic Microangiopathy due to Anti-VEGF/Tyrosine Kinase Inhibitor (TKI) Immunotherapy for Metastatic Renal Cell Carcinoma Presenting as Nephrotic Syndrome
Session Information
- Onconephrology: Immunological Cross-Talk
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1700 Onconephrology
Authors
- Sardar, Sundus, Penn State College of Medicine, Hershey, Pennsylvania, United States
- Salameh, Omar Khaleel Mohammad, Penn State College of Medicine, Hershey, Pennsylvania, United States
- Akkari, Abdel-Rauof M., Penn State College of Medicine, Hershey, Pennsylvania, United States
- Gul Yousaf Khan, Mohammad, Penn State College of Medicine, Hershey, Pennsylvania, United States
- Trivedi, Naman, Penn State College of Medicine, Hershey, Pennsylvania, United States
- Ghahramani, Nasrollah, Penn State College of Medicine, Hershey, Pennsylvania, United States
Introduction
Vascular endothelial growth factor (VEGF) inhibition may result in proteinuria, worsening hypertension, chronic kidney injury or glomerular disease. Recently, systemic VEGF inhibition has been reported to cause nephrotic disorders and thrombotic microangiopathy (TMA). We present a unique case of renal-limited TMA presenting as nephrotic syndrome in a patient on anti-VEGF/TKI immunotherapy for metastatic renal cell carcinoma.
Case Description
A 73-year-old male with history of metastatic renal cell carcinoma, managed with combination immunotherapy with axitinib and pembrolizumab, who presented with generalized swelling, increasing weight gain up to 30 lbs, heavy proteinuria, hypoalbuminemia concerning for nephrotic syndrome. Workup showed urine protein creatinine ratio of 14. Renal biopsy revealed renal-limited thrombotic microangiopathy, most likely attributed to anti-VEGF/TKI therapy. He had no evidence of immune complex deposition on electron microscopy; however, noted to have extensive foot process effacement which accounted for heavy proteinuria. His anti-VEGF/TKI therapy was discontinued and he is maintained on losartan and dapaglifozin with improvement in urine protein creatinine ratio to 7g upon followup.
Discussion
Our case suggests that renal involvement in patients on anti-VEGF/TKI immunotherapy may manifest as nephrotic-range proteinuria and clinically nephrotic syndrome with renal-limited histological TMA and cessation of anti-VEGF/TKI therapy results in significant improvement in proteinuria with possibility of re-challenge with immunotherapy. In such cases, other differentials may include minimal change disease or collapsing focal segmental glomerulosclerosis (FSGS). Cessation of anti-VEGF/TKI therapy results in significant improvement in proteinuria with possibility of immunotherapy re-challenge in the future. In case of concerns for renal sequelae with anti-VEGF/TKI involvement, prompt referral to nephrology for further evaluation is necessitated for appropriate and timely management.