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Department of Anesthesiology, Duke University Medical Center, Box 3094 DUMC, Durham, NC 27710
(Email: staff002{at}mc.duke.edu).
The grave prognosis associated with post-cardiac surgery acute kidney injury (AKI) may be due, at least in part, to the distant effects of AKI on other organ function. An AKI requiring dialysis occurs in as many as 5% of cardiac surgery patients, while an additional 8% to 15% have moderate kidney injury (eg, >1.0 mg/dL peak creatinine rise in serum creatinine). Lesser renal injuries are even more common with as many as 50% of postoperative cardiac surgery patients in some studies having a 25% or greater rise in serum creatinine. The AKI in many settings, including cardiac surgery, has been independently linked with in-hospital mortality, even after adjustment for comorbid diseases and other complications [1]. All degrees of AKI are associated with short-term mortality and other adverse outcomes [2]. However, only a few previous studies have focused on the relationship of perioperative AKI with long-term survival.
Brown and colleagues [3] compare mortality rates and postoperative renal dysfunction in a population of 13,593 isolated coronary artery bypass graft procedures in terms of lowest postoperative estimated glomerular filtration rate (eGFR). What is particularly elegant in the current study relative to any of the other studies in this area is that the authors have a sufficiently large dataset to demonstrate an association with long-term survival, even when this outcome is separated from short-term in-hospital, 30-day mortality. Their finding, linking eGFR rates less than 60 mL/min with decreased long-term survival (after 30 days postoperatively) is yet further validation of the importance of postoperative renal dysfunction, including AKI. As early biomarkers start to provide better information than serum creatinine and become validated as clinical tools to diagnose AKI, the hope is that early recognition and prompt intervention similar to the strategies developed for acute myocardial infarction (AMI) may redefine the therapeutic approach to AKI and potentially, as with AMI, lead to the development of interventions that may improve outcome including long-term survival. Studies such as the one from Brown and colleagues [3] that provide measurable endpoints associated with AKI may become the benchmarks against which such renoprotective interventions are compared.
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