43 2 CISPLATIN-INDUCED ACUTE KIDNEY INJURY | PART ONE data on adherence to antiemetics used in days 2 to 4, due to the retrospective design of this study. We were also unable to determine the severity of nausea or vomiting using an assessment tool in this retrospective study. Despite these limitations in the study, there seems to be a clear need for further improvements in the management of CINV to minimize its negative impact. The benefit of olanzapine in controlling nausea and emesis has been suggested in previous trials, which showed that nausea and emesis were significantly reduced when olanzapine was added to guideline-directed prophylactic agents [28,29]. This antiemetic regimen should be further explored in patients treated with CRT including high-dose cisplatin for LA-SCCHN. Our results confirm previous observational studies’ findings that AKI is an independent risk factor for the development of chronic kidney disease [30,31]. Decline of renal function was observed in both AKI and non-AKI patients at three and twelve months posttreatment. However, long-term decline in renal function was significantly more severe in AKI patients. In the current study, AKI did not have a negative impact both in terms of DFS and DSM. On the contrary, DSM and disease recurrence rates were numerically (but not statistically) higher in non-AKI patients. This could have several reasons. First, in this retrospective study of electronic medical records, we did not have access to survival and disease recurrence data of all patients, which could have led to underreporting mortality and disease recurrence in the present study. Second, due to the retrospective nature of this study, patients were not stratified by prognostic risk factors, like primary tumor site, tumor stage, age or comorbidity at diagnosis, which may have resulted in unbalanced groups. Third, the follow-up period of 29 months was relatively short. Patients with AKI did not have inferior survival rates compared to non-AKI patients. In addition to the arguments already mentioned, this could also be explained by our data, which show that the majority of AKI and non-AKI patients (94%) received cisplatin with a cumulative dose of ≥ 200 mg/m2; only in 6% of patients cisplatin was discontinued after one cycle. Median cumulative dose of cisplatin was >250 mg/m2 in both groups and not statistically different between treatment groups. This was well above the minimum dose of 200 mg/m2, which confers a survival benefit in LA-SCCHN patients treated with high-dose cisplatin-based concurrent CRT [32]. One of the strengths of our study was that associations between potential risk factors for AKI and outcome were studied in a well-characterized study population. AKI was also defined and graded according to KDIGO criteria, making it possible to identify low grade – but nevertheless clinically relevant – AKI. This study identifies a strong association between AKI and CINV, which is an important and potentially modifiable risk factor. Limitations were the single center retrospective nature of the study, and the relatively short follow up period of 2.5 years. Also, possible dose-response associations between the stage of AKI and outcome was not assessed. Finally, the effect of AKI and CINV on patients’ quality of life, and patients’ adherence to antiemetics could not be assessed due to the study’s retrospective design.
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