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BMJ Case Rep ; 14(8)2021 Aug 11.
Article in English | MEDLINE | ID: mdl-34380680

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.


Subject(s)
Gastrointestinal Stromal Tumors , Glomerulonephritis, Membranous , Nephrotic Syndrome , Aged , Autoantibodies , Gastrointestinal Stromal Tumors/drug therapy , Glomerulonephritis, Membranous/chemically induced , Glomerulonephritis, Membranous/drug therapy , Humans , Nephrotic Syndrome/chemically induced , Nephrotic Syndrome/drug therapy , Sunitinib
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