LAUSR

In the recent article by Oh et al. [1] assessing the renal safety of using 6% hydroxyethyl starch (HES) 130/0.4 for volume resuscitation during cardiac surgery with cardiopulmonary bypass in paediatric patients, the authors concluded that use of 6% HES 130/0.4 up to 30 ml.kg 1 was not associated with postoperative acute kidney injury (AKI). In this study, many things were done well; for example, a prospective, randomised controlled design was applied, and two commonly used diagnostic criteria (paediatric risk, injury, failure, loss, end-stage renal disease (pRIFLE) and Acute Kidney Injury Network (AKIN) criteria) were chosen to evaluate the occurrence of postoperative AKI. Furthermore, the authors tried to control most of the known the peri-operative factors affecting postoperative AKI development, such as age, pre-operative RACHS score, renal function, albumin level, operative and cardiopulmonary bypass times, intraoperative blood loss and transfusion, minimum haemoglobin level and mean urine output during cardiopulmonary bypass, etc [2]. To determine the effect of one intervention on the primary endpoint in a randomised controlled trial, however, all of the other factors have to be standardised for avoidance of potential bias. However, we think that several important issues were not well addressed in this study. Firstly, the readers were not provided with the time windows of the pRIFLE and AKIN criteria used for diagnosis of postoperative AKI, although they are significantly different. Moreover, the duration of the observed period was not included in the methods section. It has been reported that the median time for the HES-induced AKI is 16 days [3]. We are concerned that use of the improper time windows for the pRIFLE and AKIN criteria combined with a short observation period in this study might have resulted in an incorrect assessment of HES-induced AKI. Secondly, intra-operative urine output and fluid input differed significantly between the two groups, but postoperative fluid balance was not provided in the results. Importantly, it was unclear whether the serum creatinine levels used for diagnosis of postoperative AKI had been corrected based on the postoperative fluid balance. The available literature indicates that not adjusting serum creatinine levels for postoperative fluid balance can underrate the incidence of AKI after cardiac surgery, as a positive fluid balance may dilute serum creatinine [4]. We are concerned that this factor might have underor overestimated the incidence of AKI reported in this study. Thirdly, the authors did not provide intra-operative hemodynamic data, especially the occurrence of intra-operative hypotension, a known causative factor of postoperative AKI [5]. Furthermore, reduced renal perfusion pressure due to lower mean arterial pressure and high central venous pressure has also been identified as a significant predictor of AKI after paediatric cardiac surgery [6]. In addition, it was unclear whether vaso-active and inotrope drugs were required to maintain stable haemodynamics during surgery. If needed, the dosages and duration of intra-operative vaso-active and inotrope drugs should be compared between groups. It has been shown that intra-operative vaso-active inotropes are associated with an increased risk of AKI after cardiac surgery in children [7]. We believe that addressing the above issues would further clarify the transparency of this study and improve interpretation of its findings.