Abstract
BackgroundThe pathophysiological mechanisms of cisplatin nephrotoxicity include the reduction of renal blood flow, as well as tubular epithelial cell toxicity. The objective of this study was to investigate the influence of lower blood pressure and decreased food intake on the incidence of cisplatin nephrotoxicity.MethodsWe conducted a retrospective cohort study at a university hospital between 2011 and 2012. We identified hospitalized adult patients with head and neck cancer, esophageal cancer, or gastric cancer, who received intravenous cisplatin administration. The primary outcome was the incidence of cisplatin nephrotoxicity defined as the increase in serum creatinine after cisplatin administration more than 1.5 times from baseline.ResultsThe study participants included 182 patients, in whom we observed a total of 442 cycles of cisplatin chemotherapy. The incidence of cisplatin nephrotoxicity was observed in 41 of 182 cycles with initial administration. Multivariate logistic regression analysis showed that systolic blood pressure was independently associated with cisplatin nephrotoxicity (adjusted odds ratio 0.75, 95% confidence interval 0.57 to 0.95 for each 10 mmHg). The use of renin-angiotensin system (RAS) inhibitors was also associated with cisplatin nephrotoxicity (3.39, 1.30 to 8.93). Among quartiles of systolic blood pressure in all cycles of chemotherapy, the incidence of nephrotoxicity in the lower blood pressure group was significantly higher than that in the higher blood pressure group for patients taking non-solid food (P = 0.037), while there was no significant difference for patients taking solid food (P = 0.67).ConclusionsLower blood pressure and the use of RAS inhibitors were associated with the incidence of cisplatin nephrotoxicity, and lower blood pressure had a greater influence on nephrotoxicity in patients who could not take solid food. Discontinuation of antihypertensive medication including RAS inhibitors before cisplatin chemotherapy should be considered, which may be beneficial for patients with lower blood pressure.
Highlights
The pathophysiological mechanisms of cisplatin nephrotoxicity include the reduction of renal blood flow, as well as tubular epithelial cell toxicity
We verified that lower blood pressure prior to cisplatin administration, and the use of reninangiotensin system (RAS) inhibitors were associated with the incidence of cisplatin nephrotoxicity
Our study showed that lower blood pressure, especially lower than 107 mmHg, prior to cisplatin administration was a significant risk for the incidence of cisplatin nephrotoxicity
Summary
The pathophysiological mechanisms of cisplatin nephrotoxicity include the reduction of renal blood flow, as well as tubular epithelial cell toxicity. Numerous approaches such as blocking inflammation, injury signaling, and cell death pathway have been reported in animal models or cultured cells [12,13,14]. Whether these approaches are applicable to human patients is still unknown [1, 10]. The pathophysiological mechanisms of cisplatin nephrotoxicity include its direct tubular epithelial cell toxicity as well as the reduction of renal blood flow as a consequence of endothelial dysfunction and vasoconstriction [15, 16]. We hypothesized that risk factors such as lower blood pressure and decreased food intake deteriorate cisplatin nephrotoxicity by reducing renal blood flow despite routine administration of hydration
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