DOI: 10.1097/CCM.0b013e318193054f
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PMID: 19112288
Issn Print: 0090-3493
Publication Date: 2009/01/01
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Excerpt
A multivariable regression analysis suggests that postoperative AKI is independently associated with death (5). A logical extrapolation from this observation is that prevention of AKI in this setting will save lives. Thus, a variety of agents have been investigated for their potential to reduce the incidence of AKI after open heart surgery (1). Several agents have been studied because of the interest they generated in the realm of radiocontrast-associated AKI. For example, Burns et al (6) evaluated N-acetylcysteine in patients undergoing open heart surgery, but found no effect on postoperative renal dysfunction. In contrast, a more recent but smaller study found that either N-acetylcysteine or fenoldepam, but not the combination, blunted the rise in serum creatinine concentration after cardiac surgery (7).
Sodium bicarbonate has gained repute as a renoprotective agent over the past 20 yrs or so. The theoretical appeal of bicarbonate derives from its effect to inhibit free radical generation, (8) thought to play a central role in the pathogenesis of AKI (9). Although one early rat study failed to show a protective effect of bicarbonate on ischemia-induced AKI (10), a subsequent study was more encouraging (11). More recently, there have been several positive trials in patients undergoing radiocontrast procedures (12–14). Sodium bicarbonate is inexpensive and has well-recognized side-effects. It is not surprising that it should be considered a promising candidate to prevent AKI in the high-risk, high-stakes setting of open heart surgery.
In this issue of Critical Care Medicine, Haase et al (15) report the results of the first randomized, double-blinded, controlled trial of sodium bicarbonate infusion in patients undergoing heart surgery. Compared with those patients who received sodium chloride infusion, fewer patients who got sodium bicarbonate reached the primary renal end point. Furthermore, the postoperative increase in urinary neutrophil gelatinase-associated lipocalin—an early marker of renal dysfunction in some settings (16)—was attenuated in the bicarbonate group.
These observations appear to offer some hope that sodium bicarbonate may protect the kidneys of patients undergoing open heart surgery, and it is tempting—very tempting—to wholeheartedly embrace what appears to be a safe intervention in order to prevent a dire outcome. Nonetheless, it is important to recognize the limitations of this study and to encourage the exercise of restraint in the application of this intervention.
First, this cannot really be considered a study of AKI. The definition of renal dysfunction in this study is extremely liberal. Patients could meet the primary renal end point with total increase in serum creatinine of only 0.3 mg/dL over the first five postoperative days; that is an increase of less than 0.1 mg/dL per day. Using a more stringent definition of AKI (a 50% increase in serum creatinine concentration), the investigators found no difference between groups. Furthermore, there was no difference between the treatment groups with respect to AKI of any “stage” when a consensus definition of AKI (17) was used. Thus, it would be a mistake to confuse the primary renal outcome in this study with AKI.
