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Abstract: SA-PO218

Renal-Limited Thrombotic Microangiopathy from Bleomycin-Etoposide-Cisplatin Chemotherapy in a Young Male with Testicular Cancer

Session Information

Category: Onconephrology

  • 1700 Onconephrology


  • Rizvi, Ali Waris, The Ohio State University Wexner Medical Center Department of Internal Medicine, Columbus, Ohio, United States
  • Brodsky, Sergey V., Ohio State University Wexner Medical Center, Department of Pathology, Columbus, Ohio, United States
  • Gutkoski, Tyler, The Ohio State University Wexner Medical Center Department of Internal Medicine, Columbus, Ohio, United States
  • Yau, Amy, The Ohio State University Wexner Medical Center Department of Internal Medicine, Columbus, Ohio, United States

Thrombotic microangiopathy (TMA) is a systemic illness stemming from endothelial dysfunction. However some patients present with only renal-limited. In the context of chemotherapy, TMA is typically drug induced, classically associated with therapies such as gemcitabine and mitomycin with a delayed onset or with newer therapies such as tyrosine kinase inhibitors and anti-vascular endothelial growth factor (anti-VEGF) therapies any time during therapy. TMA can also be related to malignancy alone. However TMA has rarely been described in the context of testicular cancer and its therapies.

Case Description

We present a 33 year old caucasian male with past medical history of type 1 diabetes mellitus, CKD stage 3a/A3 due to genetic focal segmental glomerulosclerosis (FSGS) mitochondrial disorder with maternal inherited diabetes and deafness (MIDD) syndrome. His baseline Cr was 1.7 mg/dL with proteinuria of 4-5 grams over 24 hours despite maximal antiproteinuric therapy. He presented to the hospital with worsening edema, 20 pound weight gain, and rise in creatinine to 3.5 mg/dL. Proteinuria had dramatically increased to 11 g in 24 hours with microscopic hematuria. He was recently diagnosed with testicular cancer just two months prior and was now status post radical orchiectomy and is on cycle 2 of bleomycin, cisplatin, and etoposide. Just two weeks prior he was admitted for shiga toxin negative diarrhea and neutropenic fever in the setting of significant pancytopenia. Renal biopsy revealed active TMA with endothelial cell swelling seen on electron microscopy with stable moderate foot process effacement with mild to moderate chronic kidney disease. Unfortunately, due to his hypervolemia, he was initiated on renal replacement therapy followed by eculizumab with hopes his renal function would recover.


Drug-induced TMA (DITMA) accounts for 10-13% of all TMA cases however its pathophysiology is unclear. Drugs which do not cause TMA when administered alone may do so when combined with other nephrotoxic agents. This is the second reported case of bleomycin-etoposide-cisplatin therapy related TMA. Understanding which chemotherapeutic combinations increase risk for TMA and how they affect the complement cascade can help prognosticate the degree of renal recovery and after treatment using complement inhibition therapy.