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Abstract: FR-PO202

Role for Calcineurin Inhibitor in Tyrosine Kinase Inhibitor-induced Focal Segmental Glomerulosclerosis

Session Information

Category: Onconephrology

  • 1600 Onconephrology

Authors

  • Teruel, Benjamin R., Medical University of South Carolina, Charleston, South Carolina, United States
  • Bruner, Evelyn, Medical University of South Carolina, Charleston, South Carolina, United States
  • McMahon, Blaithin A., Medical University of South Carolina, Charleston, South Carolina, United States
Introduction

As the use and indications of anti-angiogenic therapies such as vascular endothelial growth factor (VEGF) and tyrosine kinases inhibitors (TKI’s) continues to expand, clinicians will be faced with an increase in adverse kidney events associated with these therapies. Focal segmental glomerulosclerosis (FSGS) and thrombotic microangiopathies are well recognized renal pathologies identified in patients receiving anti-angiogenic therapy. Options to treat the nephrotoxicity induced by of these agents include discontinuation or dose reduction of the anti-angiogenic therapy or a trial of corticosteroids (in the case of FSGS).

Case Description

We describe a 74-year-old Caucasian man with metastatic papillary thyroid carcinoma who developed nephrotic syndrome, hypertension, and peripheral edema following treatment with Lenvatinib, 20mg. Renal biopsy revealed focal segmental glomerulosclerosis. Partial resolution of proteinuria (>1.0g/g) was achieved via temporary discontinuation of Lenvatinib and treatment with oral prednisone. Subsequently, tumor burden increased off Lenvatinib and a collective decision was made to resume this medication at a lower dose. Unfortunately, proteinuria increased to nephrotic range (>4.0g/g) following resumption of Lenvatinib, 14mg. Over the next three months the patient went into a complete clinical remission of his nephrotic syndrome following administration of the calcineurin-inhibitor, tacrolimus and allowed ongoing concurrent use of Lenvatinib.

Discussion

There are many documented cases of TKI-induced FSGS resistant to glucocorticoid treatment. Our case demonstrates that calcineurin inhibitors may have efficacy as a second-line treatment in these instances.