Inhaled nitric oxide and acute kidney injury: new insights from observational data

Excerpt

The discovery of nitric oxide [1] generated excitement among intensivists because, as a therapeutic gas, it improved perfusion to ventilated lung units and increased arterial oxygenation without obvious systemic effects. Subsequent randomised trials in patients with acute respiratory distress syndrome (ARDS) found short-term improvements in oxygenation, with no effect on mortality and an unexpected increased risk of acute kidney injury (AKI) [2, 3]. In the absence of compelling biological mechanisms, one explanation could be that nitric oxide was used harmfully in trial protocols as opposed to clinician-directed practice. Although observational investigations can address this hypothesis, they are prone to bias and confounding that persist despite efforts at statistical ‘control’ during study design or analysis. However, empirical comparisons of treatment effects in randomised trials and observational studies have yielded mixed results [4, 5], and design alone does not determine the truth of study findings. …