Kidney Week

Abstract: SA-PO223

Atypical Presentation of Drug-Induced Thrombotic Microangiopathy: Time Does Not Matter

Session Information

• Onconephrology: Kidney Outcomes during Cancer Treatment and Nephropathies
  October 26, 2024 | Location: Exhibit Hall, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Onconephrology

• 1700 Onconephrology

Authors

• Veguilla Rivera, Nahomie Ivette, University of South Florida, Tampa, Florida, United States

Nahomie Ivette Veguilla Rivera, MD

• Dhamelia, Archi Kishorbhai, University of South Florida, Tampa, Florida, United States

Archi Kishorbhai Dhamelia, MBBS

• Rosaly Martinez, Jan Paul, University of South Florida, Tampa, Florida, United States

Jan Paul Rosaly Martinez, MD

• Punchayil Narayanankutty, Naveen, University of South Florida, Tampa, Florida, United States

Naveen Punchayil Narayanankutty, MD

Introduction

Thrombotic Microangiopathy (TMA) is a disorder that causes disseminated occlusive microvascular thrombosis, thrombocytopenia, and end organ damage, commonly in the kidneys and brain. In cancer patients, especially those in multi-drug chemotherapy regimens, TMA is a diagnostic challenge due to overlap with other thrombotic disorders such as TTP, aHUS, and DIC. TMA can occur as a manifestation of the cancer itself and has been reported in mucin-producing adenocarcinomas. Chemotherapy-associated TMA can occur due to immune-mediated reaction or dose-dependent toxicity. TMA secondary to VEGF inhibitors has been described; however, literature reporting TMA due to Tyrosine Kinase Inhibitors (TKI) is limited. We present a case of TMA secondary to lenvatinib and bevacizumab.

Case Description

We report a case of a 31-year-old man with history of metastatic hepatocellular adenocarcinoma who was referred to the hospital with nephrotic-range proteinuria. Prior therapy regimen included bevacizumab and more recently Lenvatinib, last dose 3 weeks prior presentation of AKI. Creatinine increased to 4 mg/dL from a baseline of 1.5 mg/dL. Coagulation panel, ADAMST13 were normal. ALP and LDH were elevated. Other bloodwork revealed new thrombocytopenia and hypoalbunemia. TTP, aHUS and DIC were ruled out. Due to unclear cause, patient underwent renal biopsy that showed Chronic thrombotic microangiopathy with FSGS. After confirmation of results, patient remained on therapy for HCC and was offered hemodialysis.

Discussion

This case highlights the importance of evaluating the etiology of TMA, particularly in patients on chemotherapy independent of the time of administration of therapy. Distinguishing the cause of AKI in this patient is clinically important for appropiate treatment and avoidance of future drug toxicity. It also shows that renal biopsy can aid in the diagnosis. Restarting the offending medication a lower dose may help to avoid recurrent TMA.