Prevention of acute kidney injury by intravenous sodium bicarbonate: the end of a saga

The systematic review and meta-analysis of prospective randomized trials reported by Tie and colleagues [1] in a previous issue of Critical Care provide evidence that intravenous sodium bicarbonate (SBIC) administration does not reduce the incidence of cardiac surgery-associated (CSA) acute kidney injury (AKI) but prolongs the duration of mechanical ventilation and of hospital stay. The conclusions of the authors are corroborated by a recent comprehensive systematic review [2] demonstrating that the administration of SBIC to patients at risk for CSA-AKI, contrast-induced nephropathy, septic AKI, or pigment nephropathy has no additional benefit compared with saline but adds to in-hospital morbidity and mortality. The authors do not discuss the mechanisms underlying possible harms of SBIC. In cardiac patients, this type of fluid may precipitate volume overload and acute pulmonary edema. Alkalosis-induced hypoventilation may be associated with myocardial ischemia aggravating decreased cardiac contractility and may cause arrhythmia by inducing hypokalemia [3,4]. The principal intervention with proven efficacy for the prevention of AKI is adequate fluid administration. Definitively, SBIC is not the optimal fluid.