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Worsening membranous nephropathy in a patient with GIST treated with sunitinib
  1. Shahrzad Zonoozi1,
  2. Matthew Palmer2,
  3. Teitelbaum Ursina3 and
  4. Abdallah Geara3
  1. 1Pennsylvania Hospital, University of Pennsylvania Health System, Philadelphia, Pennsylvania, USA
  2. 2Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
  3. 3Department of Medicine and Abramson Cancer Center, University of Pennsylvania, Philadelphia, Pennsylvania, USA
  1. Correspondence to Dr Abdallah Geara; abdallah.geara{at}pennmedicine.upenn.edu

Abstract

Tyrosine kinase inhibitors (TKI) are anticancer agents widely used for a variety of malignancies including gastrointestinal stromal tumours (GIST). Although generally well-tolerated, TKIs have been associated with a number of adverse events including hypertension, proteinuria and nephrotic syndrome. We present the case of a 70-year-old patient with metastatic GIST on long-standing sunitinib who developed hypertension, oedema and hypoalbuminemia with a rising serum creatinine and was found to have nephrotic syndrome. Workup revealed elevated antiphospholipase A2 receptor (PLA2R) antibody IgG titres and a kidney biopsy confirmed PLA2R-positive membranous nephropathy without findings of thrombotic microangiopathy. Cessation of sunitinib led to reduction in anti-PLA2R antibody IgG titres while resumption, due to concern for cancer progression, led to worsening symptoms. Treatment with rituximab led to undetectable anti-PLA2R IgG titres. We highlight the importance of maintaining a systematic approach for evaluating nephrotic syndrome and provide a case showing that TKIs can exacerbate underlying nephrotic syndrome.

  • nephrotic syndrome
  • proteinurea

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Footnotes

  • Contributors SZ, MD reviewed the clinical case, wrote the first draft of the manuscript and contributed in the final editing MP, MD, PhD read the kidney biopsy, contributed to the discussion of the management and wrote and edited the manuscript TU, MD treated the patient, wrote and edited the manuscript AG, MD treated the patient, wrote and edited the manuscript

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.