Of 445 patients included in the study, 25.2% developed stage I AKI after cardiac surgery, defined as a ≥26.5 µmol/l or 50% increase in serum creatinine concentration within 72 h of surgery. Patients who developed AKI had a longer hospital stay, were more likely to develop postoperative atrial fibrillation, were more likely to develop pneumonia and had a higher risk of death at 30 days than did patients who did not develop AKI. After adjustment for baseline risk factors for AKI, the odds of AKI increased by 26.5% per 5 kg/m2 increase in BMI.
When the investigators measured markers of oxidative stress, antifibrinolysis and inflammation, they found that levels of F2-isoprostanes were significantly higher at baseline and during surgery in patients who developed AKI than in those who did not develop AKI. By contrast, baseline levels of IL-6 and PAI-1 did not predict AKI although intraoperative concentrations of PAI-1 were higher in patients who developed AKI. For any given BMI, intraoperative levels of F2-isoprostanes were higher in patients with AKI than in those without AKI. BMI no longer predicted AKI after adjustment for the effect of F2-isoprostanes, whereas IL-6 and PAI-1 did not alter the association between BMI and AKI. Relationships between BMI, candidate pathway biomarkers and AKI were examined by deconstructing the total effect of BMI on AKI into direct effects and indirect effects. “Our data suggest that the association between obesity and kidney injury is partially mediated by the effect of BMI on oxidative stress but not inflammation or antifibrinolysis”, comments Billings.
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