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al., could potentially have contributed to renoprotection.Higher norepinephrine doses (0.60 g kg -1 min -1 ) have been shown to impair medullary oxygenation, 5 but since the doses used in the present study were less than 0.15 to 0.20 g kg -1 min -1 , we consider this explanation less likely.We have previously shown that, in patients with norepinephrine-dependent vasodilatory shock following cardiac surgery 6 and liver transplantation, 7 increasing the norepinephrine dose to raise mean arterial pressure from 60 to 75 mmHg increased renal blood flow and renal oxygen delivery, improving the renal oxygen supply-demand relationship.Desebbe et al. also question the clinical relevance of the attenuated release of the tubular injury marker N-acetyl-d-glucosaminidase observed in the high-flow group.We agree that our study was not designed to assess postoperative clinical outcomes, such as the incidence of AKI, but, rather, to investigate the (patho)physiologic effects of high CPB flow on renal perfusion, function, and oxygenation.Consequently, it remains to be determined, in a randomized clinical trial, whether higher-than-normal CPB flow translates into improved renal outcomes.Our group is currently conducting such an outcome study (ClinicalTrials.gov
Mahmoud Daoud (Mon,) studied this question.