Assessing Cardiac Surgery–Associated Acute Kidney Injury in Pediatric Patients

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In a secondary analysis of the previous Safe Pediatric Euglycemia After Cardiac Surgery (SPECS) trial, Blinder et al (1), in a recent issue of Pediatric Critical Care Medicine, show that tight glycemic control does not reduce the occurrence rate of cardiac surgery–associated acute kidney injury (CS-AKI) in pediatric patients. Indeed, the SPECS trial has the numerous strengths to assess the influence of tight glycemic control on morbidity after pediatric cardiac surgery. In this secondary analysis, furthermore, the authors had used appropriate statistical methods to identify the risk factors of CS-AKI and determine the associations of CS-AKI with postoperative adverse events and mortality. In designing the SPECS trial, however, CS-AKI was not used as a primary endpoint (2). When using data of the SPECS trial to assess the influence of tight glycemic control on the occurrence of CS-AKI, thus, there are several possible limitations in the study design.
First, in view of the relatively low serum creatinine (sCr) levels in study population, CS-AKI of any stage was defined using the modified acute kidney injury Network (AKIN) criteria, which required an increase in sCr from baseline of greater than 0.1 mg/dL. However, the readers were not provided the time window of postoperative sCr measurement, though the AKIN criteria require a 48-hour time window from the date of surgery. Furthermore, it was unclear whether the sCr levels used for diagnosis and staging of postoperative acute kidney injury (AKI) in this analysis had been corrected based on perioperative fluid balance. It has been shown that not adjusting sCr levels for fluid balance may underestimate incidence of CS-AKI as a positive perioperative fluid balance may dilute sCr (3).
Second, perioperative hemoglobin levels and blood management were not provided. It has been shown that preoperative anemia and postoperative hemoconcentration (hemoglobin level increase > 3 g/dL from preoperative level) are independent risk factors for AKI after congenital cardiac surgery in infants and children (4). Furthermore, intraoperative transfusion of blood products is significantly associated with AKI in children undergoing cardiac surgery with cardiopulmonary bypass (5). In addition, hematologic dysfunction, such as platelet count less than 80,000/mm3 or a decline of 50% from the highest value recorded over the last 48 hours, has been identified as an independent risk factor for AKI after cardiac surgery in children (6).
Third, the SPECS trial did not provide the occurrence of intraoperative hypotension, a known causative factor of postoperative AKI, and perioperative use of vasoactive drugs and fluid. The available evidence shows that reduced renal perfusion pressure by a lower mean arterial blood pressure and a higher central venous pressure is a significant predictor of AKI after pediatric cardiac surgery (7), especially high-grade AKI. Furthermore, vasoactive inotrope score has been significantly associated with the increased risk of AKI after cardiac surgery in children (8). In addition, pediatric patients with fluid overload have been shown a higher incidence of CS-AKI (9).
We are concerned that the above unknown factors in the SPECS trial would have confounded the true influence of tight glycemic control on the development of pediatric CS-AKI in this secondary analysis.

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