Studying the Prevention of Acute Kidney Injury

cute kidney injury (AKI) complicates approximately 5 to 15% of hospitalizations, depending on its defini- tion (1-3), and is independently associated with a five-fold or more increase in in-hospital mortality rates (3-5). AKI also extends length of stay, obligates excess hospital ex- penditures, and may exert long-term adverse effects, including an increased risk for ESRD. Several known mechanisms contribute to the development of AKI, including ischemia, vasoconstriction, toxic injury related to selected endogenous substances (e.g., myoglobin), radiocon- trast and drugs (e.g., amphotericin B), and microcirculatory changes, as observed with sepsis and other inflammatory states (6). Given the dire consequences that are associated with AKI, efforts at prevention seem desirable and worthy of intense investigation. Unfortunately, most episodes of AKI cannot be predicted readily, either from clinical criteria or from the timing of events. The vast majority of prevention trials in kidney disease have been conducted in the setting of radiocontrast exposure. Sev- eral recently published studies in AKI prevention have at- tracted significant attention and have changed practice consid- erably (7-11). In this report, we scrutinize three of these studies, focusing on issues related to effect estimates and statistical power, and incorporate principles of Bayes' Theorem in our interpretation of study results. More general, we provide a cautionary note regarding the interpretation of "positive" stud- ies with an insufficient sample size and a "significant" (P 0.05) result.