Ascorbic Acid May Be Seen as a Nephroprotective Agent in the Prevention of Colistin-Induced Nephrotoxicity Free

To the Editor—We appreciate the contribution of Dalfino and colleagues, whose prospective study in a recent issue of CID evaluated Colistin-associated acute kidney injury (AKI) in severely ill patients: a step toward a better renal care? A prospective cohort study [1]. They reported that clinical resolution rate of infections was 77%, and 6 of the patients died. But they did not describe the death term of 30 days or 90 days or hospital survival or intensive care unit use and the relation between death and colistin-associated AKI. We believe that the term of outcome assessment is important. Also, they reported that compared to AKI and non-AKI, age median 70 vs 50, Sequential Organ Failure Assessment score on day 1 of colistin treatment, median (interquartile range) 9 (7–10) vs 7 (5–9), baseline renal impairment, 13 (41.9%) vs 5 (12.8%) varied significantly. Though using Aminoglycosides were 11 (35.5%) vs 6 (15.4%) in the patients, there was not at the same time any significance on nephrotoxicity [2]. Besides, aminoglycoside-class antibiotics have a significant well-known effect on nephrotoxicity. Recently, Temocin et al assessed the risk factors for colistin-associated nephrotoxicity and reported that advanced age and concomitant aminoglycoside-class antibiotic use were significantly associated with nephrotoxicity in their multivariate analysis [3]. So aminoglycosides may increase for colistin neurotoxicity and lead to ascorbic acid as a nephroprotective agent in this study. We believe that ascorbic acid may be useful as a nephroprotective agent, but it needs more research and analysis.

Note

Potential conflicts of interest. All authors: No reported conflicts. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed.

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