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Kidney Week

Abstract: PO1883

Enfortumab Vedotin-Induced Diabetic Ketoacidosis and AKI: A Case Report

Session Information

Category: Onco-Nephrology

  • 1500 Onco-Nephrology


  • Iftikhar, Hassaan, Washington University in St Louis, St Louis, Missouri, United States
  • Vijayan, Anitha, Washington University in St Louis, St Louis, Missouri, United States
  • Khoury, Charbel C., Washington University in St Louis, St Louis, Missouri, United States

Enfortumab vedotin is a novel antineoplastic agent in the management of advanced urolthelial cancers. While hyperglycemia has been reported, diabetic ketoacidosis and AKI are rare.

Case Description

A 69-year-old male with history of metastatic urothelial cancer (treated with carboplatin/gemcitabine and Nivolumab) and CKD who presented to hospital one week after receiving Enfortumab with Diabetic Ketoacidosis (DKA) and AKI with Cr of 3.6mg/dL (Baseline 1.8mg/dL). Urine microscopy revealed granular casts consistent with tubular injury. Patient remained hyperglycemic despite titrating dose of IV regular insulin and subsequently developed shock, toxic epidermal necrolysis, and worsening renal failure with anuria requiring continuous renal replacement therapy. Despite maximal support, patient passed away.


Enfortumab vedotin comprises antinectin-4 antibody and a microtubule-disrupting agent monomethyl auristatin E (MMAE). The drug binds to Nectin-4, expressed on tumor cells, with high affinity, which induces the internalization of MMAE and leads to subsequent cell apoptosis through impaired cell division. Dermatologic toxicity occurs from drug binding to Nectin-4 expressed on normal skin cells. AKI was reported in 1% of patients of the phase 2 trial but not in the phase 3 trial. Nectin-4 protein is expressed and can be stained in renal tubular epithelial cells. While DKA may have contributed to our patient’s tubular injury, direct tubular toxicity may be possible and requires further research. Physicians prescribing Enfortumab vedotin should be aware of this potential side effect.