An elevated pro-inflammatory cytokine response is linked to development of amphotericin B-induced nephrotoxicity

LYA Chai, MG Netea, BC Tai, LW Khin, Alieke Vonk, BW Teo, HT Schlamm, R Herbrecht, JP Donnelly, PF Troke, BJ Kullberg

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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). 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. The P value was 0.026 for the overall effect of IL-6 on time to development of AKI. An increasing or non-receding IL-6 trend by week 1 of AmBD treatment (followed by a decreasing or non-receding IL-6 trend from week 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. In patients receiving AmBD, persistence of an elevated pro-inflammatory cytokine milieu is associated with a predisposition to drug-related kidney injury.
Original languageUndefined/Unknown
Pages (from-to)1655-1659
Number of pages5
JournalJournal of Antimicrobial Chemotherapy
Issue number7
Publication statusPublished - 2013

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  • EMC MM-04-28-01

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