However, some important points merit discussion. First, it is unclear how much physiologic separation may have occurred between the 2 fluid administration groups. The authors did not report serum chloride data, which may have allowed an estimate of whether there was sufficient difference between the groups to permit a plausible effect on clinical outcomes. Second, the total exposure to these 2 fluids was minimal, approximately 2 L during the entire ICU stay. It is unlikely that this amount of fluid volume could have demonstrated a plausible hazard, and not in the study population that was at low risk for AKI or other adverse effects. Third, if the trial had been designed to test the efficacy of fluids on renal function, then the authors would have had to measure renal function or injury in a more granular fashion, perhaps including biomarkers or imaging studies. Prior studies in animals18 or healthy volunteers19 have shown important effects of fluids on the kidney. If the investigators had used the techniques used by Chowdhury et al,19 then they would most likely have demonstrated similar changes in renal blood flow and function, but these do not necessarily lead to an increase in moderate-severe AKI, as measured by changes in serum creatinine. In the healthy kidney, substantial functional reserve must be exhausted before serum creatinine increases.