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|Title:||An elevated pro-inflammatory cytokine response is linked to development of amphotericin B-induced nephrotoxicity|
|Keywords:||Acute kidney injury|
|Citation:||Chai, L.Y.A., Netea, M.G., Tai, B.C., Khin, L.W., Vonk, A.G., Teo, B.W., Schlamm, H.T., Herbrecht, R., Donnelly, J.P., Troke, P.F., Kullberg, B.-J. (2013). An elevated pro-inflammatory cytokine response is linked to development of amphotericin B-induced nephrotoxicity. Journal of Antimicrobial Chemotherapy 68 (7) : 1655-1659. ScholarBank@NUS Repository. https://doi.org/10.1093/jac/dkt055|
|Abstract:||Objectives: The underlying mechanism for amphotericin B-induced acute kidney injury (AKI) remains poorly understood and may be immunologically mediated. We assessed whether the development of nephrotoxicity is linked to a distinct cytokine profile in patients receiving amphotericin B deoxycholate (AmBD). Patients and methods: In 58 patients who received AmBD, circulating serum interleukin (IL)-6, IL-8 and IL-10 were measured at baseline, week 1 and week 2 of antifungal treatment and correlated to the development of renal impairment. The Cox proportional hazards model approach was adopted for analysis. Results: The P value was 0.026 for the overall effect of IL-6 on time to development of AKI. An increasing or nonreceding IL-6 trend by week 1 of AmBD treatment (followed by a decreasing or non-receding IL-6 trend fromweek 1 to week 2) correlated with an increased likelihood of nephrotoxicity [hazard ratio (HR) 6.93, P value 0.005 and HR 3.46, P value 0.035, respectively]. Similarly, persistently increasing IL-8 levels were linked to a 3.84-fold increased likelihood of AKI. Conclusions: In patients receiving AmBD, persistence of an elevated pro-inflammatory cytokine milieu is associated with a predisposition to drug-related kidney injury. © The Author 2013. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved.|
|Source Title:||Journal of Antimicrobial Chemotherapy|
|Appears in Collections:||Staff Publications|
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