TY - JOUR
T1 - Estimated glomerular filtration rate changes in patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors
AU - Yilmaz, Musa
AU - Lahoti, Amit
AU - O'Brien, Susan
AU - Nogueras-González, Graciela M.
AU - Burger, Jan
AU - Ferrajoli, Alessandra
AU - Borthakur, Gautam
AU - Ravandi, Farhad
AU - Pierce, Sherry
AU - Jabbour, Elias
AU - Kantarjian, Hagop
AU - Cortes, Jorge E.
N1 - Publisher Copyright:
© 2015 American Cancer Society.
PY - 2015/11/1
Y1 - 2015/11/1
N2 - BACKGROUND Chronic use of tyrosine kinase inhibitors (TKIs) may lead to previously unrecognized adverse events. This study evaluated the incidence of acute kidney injury (AKI) and chronic kidney disease (CKD) in chronic-phase (CP) chronic myeloid leukemia (CML) patients treated with imatinib, dasatinib, and nilotinib. METHODS Four hundred sixty-eight newly diagnosed CP CML patients treated with TKIs were analyzed. The molecular and cytogenetic response data, creatinine, and glomerular filtration rate (GFR) were followed from the start of therapy to the last follow-up (median, 52 months). GFR was estimated with the Modification of Diet in Renal Disease equation. RESULTS Nineteen patients (4%) had TKI-associated AKI. Imatinib was associated with a higher incidence of AKI in comparison with dasatinib and nilotinib (P = .014). Fifty-eight patients (14%) developed CKD while they were receiving a TKI; 49 of these patients (84%) did so while they were being treated with imatinib (P < .001). Besides imatinib, age, a history of hypertension, and diabetes mellitus were also associated with the development of CKD. In patients with no CKD at the baseline, imatinib was shown to reduce GFR over time. Interestingly, imatinib did not cause a significant decline in the GFRs of patients with a history of CKD. Imatinib, dasatinib, and nilotinib increased the mean GFR after 3 months of treatment, and nilotinib led with the most significant increase (P < .001). AKI or CKD had no significant impact on overall cytogenetic and molecular response rates or survival. CONCLUSIONS The administration of TKIs may be safe in the setting of CKD in CP CML patients, but close monitoring is still warranted. Cancer 2015;121:3894-3904.
AB - BACKGROUND Chronic use of tyrosine kinase inhibitors (TKIs) may lead to previously unrecognized adverse events. This study evaluated the incidence of acute kidney injury (AKI) and chronic kidney disease (CKD) in chronic-phase (CP) chronic myeloid leukemia (CML) patients treated with imatinib, dasatinib, and nilotinib. METHODS Four hundred sixty-eight newly diagnosed CP CML patients treated with TKIs were analyzed. The molecular and cytogenetic response data, creatinine, and glomerular filtration rate (GFR) were followed from the start of therapy to the last follow-up (median, 52 months). GFR was estimated with the Modification of Diet in Renal Disease equation. RESULTS Nineteen patients (4%) had TKI-associated AKI. Imatinib was associated with a higher incidence of AKI in comparison with dasatinib and nilotinib (P = .014). Fifty-eight patients (14%) developed CKD while they were receiving a TKI; 49 of these patients (84%) did so while they were being treated with imatinib (P < .001). Besides imatinib, age, a history of hypertension, and diabetes mellitus were also associated with the development of CKD. In patients with no CKD at the baseline, imatinib was shown to reduce GFR over time. Interestingly, imatinib did not cause a significant decline in the GFRs of patients with a history of CKD. Imatinib, dasatinib, and nilotinib increased the mean GFR after 3 months of treatment, and nilotinib led with the most significant increase (P < .001). AKI or CKD had no significant impact on overall cytogenetic and molecular response rates or survival. CONCLUSIONS The administration of TKIs may be safe in the setting of CKD in CP CML patients, but close monitoring is still warranted. Cancer 2015;121:3894-3904.
KW - chronic myeloid leukemia (CML)
KW - dasatinib
KW - glomerular filtration rate changes
KW - imatinib
KW - kidney injury
KW - nilotinib
KW - outcome
KW - tyrosine kinase inhibitor
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U2 - 10.1002/cncr.29587
DO - 10.1002/cncr.29587
M3 - Article
C2 - 26217876
AN - SCOPUS:84945490814
SN - 0008-543X
VL - 121
SP - 3894
EP - 3904
JO - Cancer
JF - Cancer
IS - 21
ER -