Imatinib treatment duration is related to decreased estimated glomerular filtration rate in chronic myeloid leukemia patients

Marcolino, Milena Soriano; Boersma, Eric; Clementino, Nelma Cristina D.; Macedo, Antônio Vaz de; Marx-Neto, A.D.; Silva, M.H.C.R.; Gelder, Teun van; Akkerhuis, K. Martijn; Ribeiro, Antônio Luiz Pinho

doi:10.1093/annonc/mdq715

Cited by 72 publications

(54 citation statements)

References 37 publications

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“…Older age and lower estimated glomerular filtration rate at the initiation of imatinib were found to be associated with later development of chronic kidney disease. 19 This confirms an earlier report by Marcolino et al 20 Since nilotinib has been reported beneficial for renal function, a switch to nilotinib may be considered in patients with these characteristics. Pricing has been a topic of serious concern in CML treatment for some time.…”

supporting

confidence: 85%

Research in the heart of hematology: chronic myeloid leukemia 2017

Hehlmann

2017

Haematologica

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supporting

confidence: 85%

Research in the heart of hematology: chronic myeloid leukemia 2017

Hehlmann

2017

Haematologica

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“…Neurological side effects are rare and must be distinguished from other causes of neurological disorders. TKI-associated acute kidney injury is rare, but long-term decrease in the glomerular filtration rate (GFR) has been described in imatinib-treated patients [70]. However, GFR was estimated using a prediction equation and not directly measured; thus, an inhibitory effect of imatinib on active tubular secretion of creatinine without any renal dysfunction cannot be ruled out.…”

Section: Other Side Effectsmentioning

confidence: 99%

Management of adverse events associated with tyrosine kinase inhibitors in chronic myeloid leukemia

Réa

2015

Ann Hematol

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Tyrosine kinase inhibitors (TKIs) targeting the breakpoint cluster region-Abelson 1 (BCR-ABL1) oncoprotein represent an outstanding progress in chronic myeloid leukemia (CML), and long-term survival has become a reality. However, the majority of patients need to be treated during their entire life span; thus, outcome does not solely depend on treatment efficacy but also on how well therapy is tolerated. TKIs have an overall favorable safety profile in clinical practice. Although many patients may encounter adverse events, these usually occur early after treatment initiation, are mild to moderate in intensity and resolve spontaneously, or are easily controlled with adequate supportive care. Whenever treatment interruption is necessary, re-exposition to the same TKI or switch to an alternative TKI is successful in the majority of the cases. However, long-term safety issues have not been fully elucidated at present, especially for new-generation TKIs. Recent evidence has emerged that these new agents may sometimes impinge on vital organs such as the heart and lung in an irreversible fashion especially when comorbidities are present; thus, decision regarding of which TKI should be used must take into account disease-related, TKI-related, and patient-related variables. The purpose of this article is to provide an up-to-date review of common adverse events associated with TKIs and how these events may be optimally managed.

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“…In a longitudinal study of 105 patients with CML who received imatinib therapy, acute kidney injury was seen in 7 % of patients, while 12 % developed chronic renal failure [49]. Interestingly, the duration of imatinib therapy was associated with a drop in the glomerular filtration rate, with a decrease of 2.77 ml/min/ 1.73 m 2 per year of imatinib use.…”

Section: Acute Kidney Injurymentioning

confidence: 99%

“…Prevention of imatinib-induced nephrotoxicity also entails the avoidance of administration of concomitant nephrotoxic drugs, prevention of dehydration, and avoidance of loop diuretics [49].…”

Section: Acute Kidney Injurymentioning

confidence: 99%

Renal Toxicities of Targeted Therapies

et al. 2015

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With the incorporation of targeted therapies in routine cancer therapy, it is imperative that the array of toxicities associated with these agents be well-recognized and managed, especially since these toxicities are distinct from those seen with conventional cytotoxic agents. This review will focus on these renal toxicities from commonly used targeted agents. This review discusses the mechanisms of these side effects and management strategies. Anti-vascular endothelial growth factor (VEGF) agents including the monoclonal antibody bevacizumab, aflibercept (VEGF trap), and anti-VEGF receptor (VEGFR) tyrosine kinase inhibitors (TKIs) all cause hypertension, whereas some of them result in proteinuria. Monoclonal antibodies against the human epidermal growth factor receptor (HER) family of receptors, such as cetuximab and panitumumab, cause electrolyte imbalances including hypomagnesemia and hypokalemia due to the direct nephrotoxic effect of the drug on renal tubules. Cetuximab may also result in renal tubular acidosis. The TKIs, imatinib and dasatinib, can result in acute or chronic renal failure. Rituximab, an anti-CD20 monoclonal antibody, can cause acute renal failure following initiation of therapy because of the onset of acute tumor lysis syndrome. Everolimus, a mammalian target of rapamycin (mTOR) inhibitor, can result in proteinuria. Discerning the renal adverse effects resulting from these agents is essential for safe treatment strategies, particularly in those with pre-existing renal disease.

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Imatinib treatment duration is related to decreased estimated glomerular filtration rate in chronic myeloid leukemia patients

Abstract: The introduction of imatinib therapy in nonclinical trial CML patients is associated with potentially irreversible acute renal injury, and the long-term treatment may cause a clinically relevant decrease in the estimated GFR.

Cited by 72 publications

References 37 publications

Research in the heart of hematology: chronic myeloid leukemia 2017

Research in the heart of hematology: chronic myeloid leukemia 2017

Management of adverse events associated with tyrosine kinase inhibitors in chronic myeloid leukemia

Renal Toxicities of Targeted Therapies

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