34 PART ONE | CISPLATIN-INDUCED ACUTE KIDNEY INJURY Chemotherapy Cisplatin (100 mg/m2 ) was administered intravenously on day 1 of a three-weekly cycle for a total of three courses, with pre-hydration containing 2000 mg magnesium sulfate and 20 milliequivalents per Liter (mEq/L) of potassium chloride in 1000 mL of 0.9% normal saline over a 2-hours period, and post-hydration containing 2000 mg magnesium sulfate and 20 mEq/L of potassium chloride in 4000 mL of 0.9% normal saline over a 20-hours period. Prophylactic antiemetic therapy to prevent chemotherapy-induced nausea and vomiting (CINV) was prescribed according to international guidelines [13,14], containing a threedrug regimen, which included dexamethasone, the serotonin receptor antagonist (5HT3 RA) ondansetron, and the neurokinin-1 receptor antagonist (NK1 RA) aprepitant intravenously before administration of cisplatin (day 1), followed by aprepitant on days 2 and 3, and dexamethasone on days 2 to 4 taken orally. The use of rescue antiemetics was allowed and reported in the EMR. Measurements Demographic and tumor characteristics, tumor and nodal stage (seventh edition of the American Joint Committee on Cancer (AJCC) TNM classification of malignant tumors), medical history, weight and height, age-adjusted Charlson Comorbidity Index (CCI) [15], and Eastern Cooperative Oncology Group (ECOG) performance status score were derived from the EMRs of the included patients. Information on the use of potentially nephrotoxic co-medications was obtained by medical prescription history from the week before start of treatment until the last day of chemoradiation. The drugs documented included all categories of diuretics, angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, non-steroidal anti-inflammatory drugs (NSAIDs), proton-pump inhibitors, lithium, haloperidol, and intravenous contrast media. Data on early termination of cisplatin or dose reductions, radiotherapy delay or truncations, occurrence of CINV, the use of rescue antiemetics, and the number and length of emergency hospitalizations were also obtained, including the reason for treatment modifications and emergency admissions. Serumcreatinine (sCr) valueswere derived fromthe clinical laboratory database at baseline (day before start CRT), weekly during CRT, at least every other day during (emergency) hospitalizations, and three and twelve months after completion of CRT. The criteria for AKI based on the KDIGO criteria were applied [11]. AKI (stage 1) was defined by sCr rise of greater than or equal to 26.5 µmol/l within 48 hours, or sCr increase greater than or equal to 1.5-fold from the baseline reference value. Stage 2 AKI was defined as a greater than or equal to 2.0- to 2.9 fold increase from baseline reference sCr. Stage 3 AKI was defined as a greater than or equal to threefold increase from baseline reference sCr, or increase of 354 µmol/l, or commenced on renal-replacement therapy irrespective of stage of AKI. The reference sCr is defined as the lowest creatinine value recorded within 3 months of the event, or from repeat sCr within 24 hours, or estimated from the nadir sCr value if a patient recovers from AKI. The urine output criterion was not used in this study. Disease free survival (DFS) and disease-specific mortality (DSM) were assessed from the last day of radiotherapy until disease recurrence or death, respectively.
RkJQdWJsaXNoZXIy MjY0ODMw