Background: Data regarding the most efficacious and least toxic schedules for the use of colistin are scarce. The\r\naim of this study was to determine the incidence and the potential risk factors of colistin-associated nephrotoxicity\r\nincluding colistin plasma levels.\r\nMethods: A prospective observational cohort study was conducted for over one year in patients receiving\r\nintravenous colistin methanesulfonate sodium (CMS). Blood samples for colistin plasma levels were collected\r\nimmediately before (Cmin) and 30 minutes after CMS infusion (Cmax). Renal function was assessed at baseline, on\r\nday 7 and at the end of treatment (EOT). Severity of acute kidney injury (AKI) was defined by the RIFLE (risk, injury,\r\nfailure, loss, and end-stage kidney disease) criteria.\r\nResults: One hundred and two patients met the inclusion criteria. AKI related to CMS treatment on day 7 and at\r\nthe end of treatment (EOT) was observed in 26 (25.5%) and 50 (49.0%) patients, respectively. At day 7, Cmin (OR, 4.63\r\n[2.33-9.20]; P < 0.001) was the only independent predictor of AKI. At EOT, the Charlson score (OR 1.26 [1.01-1.57];\r\nP = 0.036), Cmin (OR 2.14 [1.33-3.42]; P = 0.002), and concomitant treatment with = 2 nephrotoxic drugs (OR 2.61\r\n[1.0-6.8]; P = 0.049) were independent risk factors for AKI. When Cmin was evaluated as a categorical variable, the\r\nbreakpoints that better predicted AKI were 3.33 mg/L (P < 0.001) on day 7 and 2.42 mg/L (P < 0.001) at EOT.\r\nConclusions: When using the RIFLE criteria, colistin-related nephrotoxicity is observed in a high percentage of patients.\r\nCmin levels are predictive of AKI. Patients who receive intravenous colistin should be closely monitored and Cmin might\r\nbe a new useful tool to predict AKI.
Loading....