42 PART ONE | CISPLATIN-INDUCED ACUTE KIDNEY INJURY as was applied in our study. Hypomagnesemia can upregulate OCT-2, leading to increased cisplatin transport to the kidneys, resulting in nephrotoxicity [19]. Several systematic reviews suggest that magnesium supplementation (8-16 milliequivalents [mEq]) may limit cisplatin-induced nephrotoxicity [18,20]. In this study, 2000 mg (= 16 mEq magnesium) was administered to all patients according to protocol. Potassium supplementation was also included in the protocol. Several other approaches have been evaluated to prevent cisplatin-induced nephrotoxicity, including N-acetylcysteine, anti-inflammatory drugs and antioxidant supplements, but none have an established role in patients being treated with cisplatin. Amifostine is the only FDA-approved agent for the reduction of cumulative renal toxicity in advanced ovarian and non–small-cell lung cancer patients receiving cisplatin [21]. However, use of this drug is limited by side effects (nausea, vomiting, hypotension). In addition, concerns about possible interference with the antitumor activity of cisplatin limit its use to clinical trials in tumors other than advanced ovarian and non–small-cell lung cancer patients. Another strategy to prevent dehydration and cisplatin-induced nephrotoxicity, is to perform prophylactic percutaneous endoscopic gastrostomy (PEG) tube placement in those patients deemed at greatest risk of becoming malnourished or dehydrated during the course of treatment. The indication for prophylactic PEG placement is discussed in the multidisciplinary tumor board on a case-by case basis. Malnutrition, dysphagia and bilateral neck irradiation are among factors considered. In this retrospective study, 90 patients (73%) were treated with prophylactic PEG placement. During treatment, patients were monitored by a nutritionist, and if indicated a nasogastric feeding tube was placed in patients without PEG, or with PEG, in the case of PEG-related complications or dysfunction. In this study, 20 patients (10 patients without PEG; 10 patients with PEG) were treated with (short-term) nasogastric feeding tube placement. Despite nastrogastric feeding tube placement, AKI occurred in 17 of these patients. Prophylactic PEG and feeding tube placement were not associated with a lower risk of AKI. Reported predictors of cisplatin-induced AKI included older age and hypertension [2224], female sex [22,25], smoking, black ethnicity [22,26], hypokalemia, hypoalbuminemia [23-25], concomitant use of other anticancer drugs, and single dose versus fractionated dose radiotherapy [27]. This retrospective study confirms the association of hypertension with cisplatin-induced AKI. No significant association with female sex was found, although both sexes were adequately represented in the study. The association of older age with AKI could not be confirmed, because elderly patients were underrepresented in this study (median age 60 years, range 30 to 74). Ethnicity could not be selected as a primary variable; included patients were predominantly white in this study. This also applied to serum albumin values, which were not measured in this study. This study clearly demonstrates that CINV remains poorly controlled in a significant number of patients receiving CRT with high-dose cisplatin for LA-SSCHN, despite the use of guideline-consistent antiemetic therapy. Adherence to antiemetics in order to optimize CINV control for patients undergoing emetogenic chemotherapy is important, because adequate control of emesis prevents intravascular depletion of fluids and electrolytes, and therefore decreases the potential for cisplatin-induced nephrotoxicity. We have no
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