Abstract: SA-PO144
Capmatinib-Associated AKI: A Case Series
Session Information
- Onconephrology: Clinical and Research Advances - II
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Sandoval, Leticia Assad Maia, Mayo Clinic Research Rochester, Rochester, Minnesota, United States
- Radhakrishnan, Yeshwanter, Mayo Clinic Research Rochester, Rochester, Minnesota, United States
- Potter, Ashley, Mayo Clinic Research Rochester, Rochester, Minnesota, United States
- Mansfield, Aaron, Mayo Clinic Research Rochester, Rochester, Minnesota, United States
- Herrmann, Sandra, Mayo Clinic Research Rochester, Rochester, Minnesota, United States
Background
Capmatinib is a MET inhibitor used in non-small cell lung cancers that harbor MET exon 14 skipping mutations. It can cause serum creatinine (SCr) elevation without evidence of a kidney injury (AKI), termed pseudo-AKI, and likely due to inhibition of renal transporters multidrug and toxic extrusion protein 1 and 2-K (MATE1 and MATE2-K). We present 13 patients who developed AKI with capmatinib therapy.
Methods
We performed a retrospective multi-center observational study of all patients who received capmatinib at Mayo Clinic campus between 05/2020 and 10/2021. We analyzed demographics, comorbidities, laboratory values, and outcomes of those who developed AKI.
Results
Among 38 patients on capmatinib, 13 (34%) had an elevation of SCr and were diagnosed with AKI based on KDIGO criteria (table 1). Patients had a median age of 78 years ± SD 10.28% were male, with a mean baseline SCr of 1.05 ± SD 0.42 mg/dL. Seven patients presented with dyspnea, fatigue, and lower extremity edema without acid-base or electrolyte disturbances. Patients who had available urinalysis had no active sediment. Cystatin C and Iothalamate Glomerular Filtration Rate (GFR) clearance during AKI did not show variation from baseline, although SCr was elevated, raising the possibility of pseudo-AKI (figure 1). All patients had SCr reduction within three months. None of these patients required kidney replacement therapy.
Conclusion
In our experience, one-third of patients at our institution had elevations in SCr while on capmatinib. Pseudo-AKI is possible, as two patients did not have variations in cystatin C or Iothalamate-based GFRs during AKI. Pseudo-AKI may result in inappropriate dose-adjustments. Estimating GFR with cystatin C and iothalamate should be considered in these patients instead of relying on SCr.