146 PART THREE | DELIRIUM recovery from AKI with minimalization of any residual functional impairment [35]. Various hydration regimens and supplementation strategies are used to prevent cisplatin-induced AKI. However, concrete recommendations regarding the exact hydration type, volume / duration, supplementation, and use of forced diuresis remain unavailable [36]. Guideline-consistent CINV prophylaxis reduces the incidence of CINV after highly emetogenic chemotherapy, such as high-dose cisplatin [37]. However, the present study clearly shows that CINV was poorly controlled in a significant number of patients, despite the use of guideline-consistent antiemetic therapy. Future randomized clinical trials (RCTs) investigating more potent antiemetic regimens are much needed with the ultimate goal of gaining complete control of CINV after CRT containing high-dose cisplatin for patients with LA-SCCHN. Olanzapine as compared with placebo, significantly improved nausea prevention in patients receiving cisplatin ≥70 mg/m2 [38]. In addition, due to insufficient patient tolerance, various weekly low-dose schedules of cisplatin (≤50 mg/ m2) are increasingly used in clinical practice, although three-weekly high-dose cisplatin is still considered the standard systemic regimen given concurrently with postoperative or definitive radiotherapy in LA-SCCHN [39]. Prior to its implemention in routine clinical practice, the low-dose weekly approach should be prospectively compared for efficacy and safety with the standard three-weekly high-dose schedule. In the present study, renal function in both AKI and non-AKI patients was impaired at 3 and 12 months after CRT compared to baseline values. Renal function was significantly more impaired in AKI patients at 3 months (p = 0.01) and at 12 months (p = 0.01) compared to non-AKI patients. With a median follow-up of 2.5 years, disease free survival (DFS) and disease-specific mortality (DSM) were not significantly affected by the onset of AKI during treatment. Our results are largely consistent with those reported in a meta-analysis by Coca et al [40] showing that patients who experienced AKI had an almost 9-fold higher adjusted risk of chronic kidney disease (pooled adjusted hazard ratio [HR] 8.8, 95% CI 3.125.5) and a 3-fold higher adjusted risk of progressing to end-stage renal disease (pooled adjusted HR 3.1, 95% CI 1.9–5.0) compared to those without AKI. Chertow et al [41] found that an increase of SCr of 40.3 mg/dl (426.5 μmol/l) was independently associated with higher mortality. Similarly, Lassnigg et al [42] saw, in a cohort of patients who underwent underwent cardiac surgery, that either an increase of SCr ≥0.5 mg/dl (≥44.2 μmol/l) or a decrease 40.3 mg/dl (426.5 mmol/l) was associated with worse survival. For reasons that are not entirely clear, even small changes in SCr lead to an increase in hospital mortality. Possible explanations include the untoward effects of decreased kidney function such as volume overload, retention of uremic compounds, acidosis, electrolyte disorders, increased risk for infection, and anemia [43]. The relatively short follow-up period for assessing mortality, as well as the incompleteness of follow-up, may explain why differences in treatment outcomes could not be demonstrated in our study.
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