Sunitinib and sorafenib in metastatic renal cell carcinoma patients with renal insufficiency

Khan, Gazala; Golshayan, Ali Reza; Elson, Paul; Wood, Laura S.; García, Jorge A.; Bukowski, Ronald M.; Rini, Brian I.

doi:10.1093/annonc/mdp603

Cited by 51 publications

(45 citation statements)

References 22 publications

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“…Among patients receiving sunitinib in other malignancies, the incidence of creatinine elevation, whatever the grade, ranges from 12.4 to 65.6% [28,31,32] . However, renal function was deteriorated in 57% of patients with pre-existing renal impairment at the start of therapy with tyrosine kinase inhibitors [33] . Laboratory abnormalities including elevated serum creatinine levels, whatever the grade, during everolimus treatment have been reported in 50-77% of patients in some series [34,35] , while grade 3/4 occurred in less than 1%.…”

Section: Discussionmentioning

confidence: 99%

Not All Patients with a Pancreatic Neuroendocrine Tumour Will Benefit from All Approved or Recommended Therapeutic Options: A Real-Life Retrospective Study

Berdelou¹,

Boige

Arfi-Rouche

et al. 2016

Neuroendocrinology

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Background: At least nine therapeutic options are recommended or approved for pancreatic neuroendocrine tumour (pNET). The primary endpoint of this study was to determine the number of therapeutic lines given before death. Secondary endpoints were to determine toxic events as a function of number of therapeutic lines and of time. Methods: Patients with pNET treated between 1998 and 2010 at our centre were characterised. All therapeutic lines were recorded as well as tumour- or toxic-related deaths. Persistent treatment-related toxicity (PTRT) was defined as: chronic kidney disease, anaemia, thrombocytopenia, neutropenia, severe liver failure, cardiac failure and recurrent sepsis, precluding at least one other therapeutic option or second cancers. Results: Ninety-two patients were analysed. The median follow-up was 7 years. The 1-, 2- and 5-year overall survival rates were 90, 81 and 51%, respectively. After 3 and 5 therapeutic lines, 23 and 50% of patients had died, respectively. After 3 and 5 lines, the frequency of toxic events was 8 and 24%, respectively. Overall, 17 toxic events were observed including 6 treatment-related deaths and 11 PTRT. After 1, 2 and 5 years of treatment, the frequency of toxic events was 6, 9 and 16%, respectively. Conclusion: Tumour- and toxic-related deaths as well as PTRT may preclude access to all therapeutic options in patients with pNET. Optimised risk benefit sequence should be investigated.

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Section: Discussionmentioning

confidence: 99%

Not All Patients with a Pancreatic Neuroendocrine Tumour Will Benefit from All Approved or Recommended Therapeutic Options: A Real-Life Retrospective Study

Berdelou¹,

Boige

Arfi-Rouche

et al. 2016

Neuroendocrinology

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“…So it is possible that these various kinase inhibitors exhibit differential effects on creatinine, metformin, and cisplatin clearance. Interestingly, similar to vandetanib, gefitinib and sunitinib are known to be potent inhibitors of both MATE1 and MATE2K in vitro and increase plasma creatinine levels in cancer patients (Khan et al, 2010;Petrylak et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Assessment of Vandetanib as an Inhibitor of Various Human Renal Transporters: Inhibition of Multidrug and Toxin Extrusion as a Possible Mechanism Leading to Decreased Cisplatin and Creatinine Clearance

et al. 2013

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Vandetanib was evaluated as an inhibitor of human organic anion transporter 1 (OAT1), OAT3, organic cation transporter 2 (OCT2), and multidrug and toxin extrusion (MATE1 and MATE2K) transfected (individually) into human embryonic kidney 293 cells (HEK293). Although no inhibition of OAT1 and OAT3 was observed, inhibition of OCT2-mediated uptake of 1-methyl-4-phenylpyridinium (MPP + ) and metformin was evident (IC 50 of 73.4 6 14.8 and 8.8 61.9 mM, respectively).

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“…Khan et al [26] reported a group of patients who developed renal insufficiency due to treatment with MTKI. This was a retrospective review of all patients treated with more than 3 months of MTKI at their institution.…”

Section: Discussionmentioning

confidence: 99%

Nephrotoxicities Associated with the Use of Tyrosine Kinase Inhibitors: A Single-Center Experience and Review of the Literature

et al. 2010

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Background: Sunitinib is an oral multitargeted tyrosine kinase receptor inhibitor (MTKI) used for the treatment of renal cell carcinoma. These small-molecule agents inhibit signaling through receptor tyrosine kinases such as vascular endothelial growth factor receptor, platelet-derived growth factor receptor and cytokine stem cell factor receptor, among others. Although the development of these novel molecular-targeted agents represents a substantial advance in the treatment of metastatic cancer, the spectrum of their adverse effects may be broader than initially predicted. Method: We performed a retrospective chart review of patients who had received sunitinib and developed renal insufficiency. Results: We describe 4 patients with renal cell carcinoma and 1 patient with transitional cell carcinoma treated with sunitinib who experienced various degrees of nephrotoxicity including hypertension, proteinuria, thrombotic microangiopathy, and acute and chronic kidney injury which resolved upon cessation of MTKI. Conclusions: Nephrologists and oncologists should be aware of the potential for toxic renal effects, and we recommend guidelines for early recognition and treatment of these conditions in patients receiving MTKI.

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Sunitinib and sorafenib in metastatic renal cell carcinoma patients with renal insufficiency

Cited by 51 publications

References 22 publications

Not All Patients with a Pancreatic Neuroendocrine Tumour Will Benefit from All Approved or Recommended Therapeutic Options: A Real-Life Retrospective Study

Not All Patients with a Pancreatic Neuroendocrine Tumour Will Benefit from All Approved or Recommended Therapeutic Options: A Real-Life Retrospective Study

Assessment of Vandetanib as an Inhibitor of Various Human Renal Transporters: Inhibition of Multidrug and Toxin Extrusion as a Possible Mechanism Leading to Decreased Cisplatin and Creatinine Clearance

Nephrotoxicities Associated with the Use of Tyrosine Kinase Inhibitors: A Single-Center Experience and Review of the Literature

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