Capmatinib-Induced Pseudo–Acute Kidney Injury: A Case Report

We present a case of pseudo–acute kidney injury (AKI) following capmatinib therapy in an 84-year-old man with combined non–small cell (adenocarcinoma) and small cell lung cancer with MET exon 14–skipping mutation. His past medical history was significant for chronic kidney disease stage 3 with a baseline serum creatinine (Scr) of 1.6 mg/dL rising to 2.44 mg/dL (estimated glomerular filtration rate [GFR] 24 mL/min/1.73 m²) while on capmatinib. Scr improved to 1.84 mg/dL with the cessation of capmatinib but rose again to 2.22 mg/dL upon resumption of therapy. Further investigation with cystatin C and renal iothalamate clearance showed that despite fluctuation in Scr levels, there was not much variation in GFR calculated using these methods. Urinalysis and urinary protein-creatinine ratio were unremarkable. Treatment with capmatinib was continued at reduced dose and a third instance of rise in Scr was observed, followed by a spontaneous return to baseline. Thus, MET inhibitor therapy can result in an asymptomatic rise in Scr, and it must be distinguished from AKI with more accurate non–creatinine-based methods to evaluate GFR. This could spare such patients from invasive diagnostic tests, such as a kidney biopsy, and premature cessation of prognostically important cancer therapies.