145 8 DELIRIUM | PART THREE stage III/IV LA-SCCHN treatedwith radiotherapy concurrent with either 3-weekly or weekly cisplatin. They observed that 53.7% of all patients developed AKI. In 2007, the Acute Kidney Injury Network (AKIN) group proposed a modified version of the RIFLE criteria, which aimed to improve the sensitivity of AKI diagnostic criteria [13]. There were several changes: an absolute increase in SCr of at least 0.3 mg/dL (26.5 μmol/L) was added to stage 1; the glomular filtration rate (GFR) criterion was removed; patients starting renal replacement therapy (RRT) were classified as stage 3, irrespectively of SCr values; and outcome classes were removed. The latest classification of AKI proposed by the Acute Kidney Injury Working Group of KDIGO [14], is based on the previous two classifications, and has the aim of unifying the definition of AKI. Comparing to the AKIN criteria, KDIGO classifies patients initiating RRT into stage 3 AKI, but removes the threshold of a 0.5 mg/dl (44.2 μmol/l) increment for SCr >4 mg/dl (353.7 μmol/l) in the criteria of stage 3 AKI. KDIGO is more sensitive for detecting low stage AKI than previous AKI classifications [15-17]. This explains the higher incidence of cisplatin-induced AKI in the current study compared to studies that did not apply the KDIGO criteria for AKI. The variation in AKI incidences between the different classification systems highlights the challenges in optimizing sensitivity and specificity for providing accurate prognostic information. Early identification of nephrotoxicity will improve current point-of-care by enabling dose and regimens adjustments before the development of overt renal dysfunction. The current diagnostic approach of AKI is based on an acute decrease of GFR, as reflected by an acute rise in SCr levels and/or a decline in urine output over a given time interval, and has low sensitivity and specificity. Novel biomarkers have been shown to detect AKI earlier and are more sensitive than SCr [18-20]. It is not clear, whether a single or multiple biomarker approach is needed to diagnose the complicated and multifactorial aspects of AKI [21-23]. The role of biomarkers other than SCr in the early diagnosis, differential diagnosis, and prognosis of AKI patients needs to be further explored. For any prevention strategy to be effective, patients with high risk for cisplatin-induced AKI need to be identified before insults result in kidney damage. Determining the risk factors for cisplatin nephrotoxicity may assist clinicians in selecting these high-risk patients. Several studies have reported risk factors for predicting cisplatin-induced AKI, such as old age, female sex, smoking, hypoalbuminemia, hypokalemia, hypomagnesemia, a high body surface area, the frequency of cisplatin treatment, the combined use of cisplatin and paclitaxel, advanced cancer, the total dose of cisplatin administered, cardiovascular disease and diabetes mellitus [24-29]. In agreement with our findings, hypertension has been associated with heightened risks of AKI in several clinical settings [30]. The present study clearly demonstrates that CINV is a highly significant risk factor for cisplatin-induced AKI. When poorly controlled, CINV leads to dehydration, anorexia, weight loss, electrolyte disturbances, and diminished quality of life (QoL) [31-34]. Decreased renal perfusion associated with intravascular volume depletion from vomiting results in a reduced GFR. It is accepted that optimization of the hemodynamic status and correction of any volume deficit will have a salutary effect on kidney function, will help minimize further extension of the kidney injury, and will potentially facilitate
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