Abstract 3263
Background
Risk factors of cisplatin induced acute kidney injury (AKI) patients has been well described. In HNSCC, an incidence of cisplatin induced AKI was observed in 34.2%. Most studies reported AKI as a surrogate endpoint. However, delayed cisplatin induced nephrotoxicity and long-term renal outcomes were not well studied.
Methods
Locally advanced HNSCC patients treated between 1/2007 and 12/2018 who underwent definitive or post-operative chemoradiotherapy (CRT) with cisplatin were identified. Patient characteristics, treatments, creatinine at baseline, during, 3, 6, and 12 months after CRT completion were retrospectively reviewed. Acute kidney disease (AKD) was defined by (i) estimated glomerular filtration rate (eGFR) <60 ml/min/ 1.73 m2 for <3 months, or (ii) decrease in eGFR by ≥ 35 %, or (iii) increase in serum creatinine by > 50 % for <3 months.
Results
A total of 509 patients were analyzed. Overall AKD occurred in 27.9% patients. Most patients (95%) had prophylactic feeding. ECOG of 0 was more prominent in AKD patients (p = 0.017) and hypertension (p < 0.001). Most patients received definitive CRT (83%) with mean cumulative dose of cisplatin during CRT and entire treatment of 189 mg/m2, and 400 mg/m2, respectively. There was no statistical difference in cumulative dose, delay, dose reduction, termination, and hospitalization. In AKD patients, eGFR started to decline significantly during CRT (-36%) and worsened at 3 months (-39%) after CRT. The eGFR started to improve at 12 months after CRT (-29%), but did not recover to baseline nor non-AKD patients. In multivariate analysis, ECOG of 0 (OR = 1.77), and hypertension (OR = 2.25) were a significant predictive factor for AKD.
Conclusions
Almost one third of locally advanced HNSCC patients who underwent CRT with cisplatin developed AKD with peak incidence at 3 months after CRT. After 1 year, eGFR of patients with AKD had not recovered, and remained at -30% below baseline. ECOG 0 and hypertension were a predictor for AKD. Hypertension might reflect underlying kidney disease which leads to susceptibility to kidney injury. Moreover, physician’s awareness of AKD and underestimation of potential complications in fit patients might explain these findings.
Clinical trial identification
Editorial acknowledgement
Legal entity responsible for the study
The authors.
Funding
Has not received any funding.
Disclosure
All authors have declared no conflicts of interest.
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