Abstract: SA-PO167
Crizotinib-Induced Pseudo-AKI: A Case Report
Session Information
- Onco-Nephrology: Clinical
November 09, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onco-Nephrology
- 1500 Onco-Nephrology
Authors
- Cosmai, Laura, San Carlo Borromeo Hospital, Milano, Italy
- Pedone, Meri, ASST Santi Paolo e Carlo Borromeo - Ospedale San Carlo Borromeo, Milan, Italy
- Gri, Nicole, I.R.C.C.S. Istituti Cllinici Scientifici Maugeri, Pavia, Italy
- Rizzo, Mimma, ICS Maugeri, Viggianello, Italy
- Foramitti, Marina, ASST Cremona, Cremona, Italy
- Porta, Camillo, University of Pavia, Pavia, Italy
- Cozzolino, Mario, Department of Health Sciences, University of Milan, Milan, Italy
Introduction
The appearance of treatment-related Acute Kidney Injury (AKI) or the worsening of a pre-existing Chronic Kidney Disease (CKD) often limit the correct administration of many potentially life prolonging Oncological treatments. Crizotinib is a multikinase inhibitor, used to treat ALK-traslocated non-small cell lung cancers (NSCLC). Chronic and acute (mainly due to competitive inhibition of creatinine at renal proximal tubule) kidney failure possibly related to Crizotinib treatment have been described
Case Description
A 59 year old male came to onconephrological evaluation with stage 5 CKD (creatinine 6.1 mg/dl, urea 76 mg/dl, no clinical signs of uremia); he had a solitary kidney after a previous right nephrectomy for urothelial carcinoma, and carried a left ureteral stent for concomitant nephrolithiasis. More importantly, he had a metastatic ALK-traslocated NSCLC previously treated with Cisplatin-based chemotherapy (CT), which lead to a first episode of AKI and then to CKD, presently treated with Crizotinib 250 mg b.i.d. with optimal disease control. Creatinine levels worsened from 1.6 mg/dl post nephrectomy, to 2.2 post CT, to 4 mg/dl after Crizotinib. The oncological treatment was thus stopped. When referred to us, a kidney sequential scintigraphy with Tc 99mDTPA was performed, which showed a glomerular clearance of 26 ml/min (vs a CKD-EPI of 9.2 ml/min and a Cockroft Gault of 13.2 ml/min). We thus postulated that CKD worsening could be due to the inhibition of creatinine tubular secretion by Crizotinib. We thus recommended to restart Crizotinib treatment at the reduced dose of 250 mg o.d., suggesting to perform more frequent urotelial stent changes. Two years after restarting Crizotinib, the patient is still on treatment, with stable oncological disease, as well as renal function
Discussion
Crizotinib may induce inhibition of creatinine tubular secretion together with creatinine increase, thus mimicking AKI on CKD. This case highlights the importance of renal scintigraphy in assessing these patients, as well as the role of Onco-Nephrologist