The authors reply.

To the Editor: In a recent issue of Critical Care Medicine, Danziger et al (1) convincingly show that in critically ill patients, obesity is associated with acute kidney injury (AKI). This is an important and intriguing finding. The authors speculate about the underlying mechanisms that are probably multi-factorial. However, the authors do not include intra-abdominal pressure in their discussion. Body mass index is positively correlated with intra-abdominal pressure (2, 3). Normal intra-abdominal pressure is approximately 5–7 mm Hg, but baseline levels are higher at approximately 9–14 mm Hg in morbidly obese patients (4). A possible explanation for higher pressures in the obese is that there could be a direct mass effect of the abdominal adipose tissue on the measurement of intra-abdominal pressure (4). Even slight increases in intra-abdominal pressure lead to subtle signs of AKI (5). We therefore believe that increased intra-abdominal pressure may be one of the mechanisms involved in the development of AKI in obesity. Obesity is not a condition that can be treated on a short term, but independently associated with a normal blood lactate level. Unfortunately, we do not have details on the type, dosage, and time of the last drug taking, mainly because these data were not available in the medical files. However, if the hypothesis raised by Savas et al (1) was true, it is likely that the data adjustment according to the mortality would cancel the difference of blood lactate concentration observed between the two groups of patients. However, we are aware that our study has some limitations, mainly because it is retrospective, and only a prospective work could confirm our hypothesis regarding the effect of long-term β-blockers therapy on blood lactate concentration by an aerobic glycolysis-sparing-effect. The authors have disclosed that they do not have any potential conflicts of interest.