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Ann Thorac Surg 2004;78:1881-1882
© 2004 The Society of Thoracic Surgeons
Department of Anesthesiology, Duke University Medical Center, Department of Anesthesiology, Box 3094 DUMC, Durham, NC 27710, USA
staff002{at}mc.duke.edu
To the Editor:
We are interested in the comments of Dr Ranucci and colleagues in regard to our publication [1] in which we describe an inverse association between lowest hematocrit during cardiopulmonary bypass (in interaction with body weight) and postoperative acute renal injury.
A similar observation by Ranucci and colleagues [2] prompted actions to minimize circuit prime volume in their practice; these investigators have since noted reduced hemodilution and less average acute renal injury experienced by their patients. Interestingly, in their letter, these investigators describe lower degrees of acute renal injury predicted for any particular nadir hematocrit recorded relative to those reported in our study. Although Dr Ranucci and colleagues' observations are very interesting, we believe caution should be used in drawing broad conclusions from this comparison with data between institutions. Differences between Dr Ranucci and colleagues' most recent group and ours may be due to many factors other than avoidance of hemodilution, including comorbidities, difference in transfusion triggers (because transfusion itself can be associated with acute renal injury), and the profile of overweight patients between the two groups. In addition, because our patient sample was drawn from patients having surgery between 1995 and 1997, and the data from Ranucci and colleagues included patients from only the last 3 years, advances in overall care in the past few years may have improved patient outcomes.
Of the second point raised by Ranucci and colleagues regarding mechanisms to explain our findings, we wish to clarify our speculations on the interpretation of our observations. Although we speculate that a portion of the association of acute renal injury with hemodilution may be associated with reductions in oxygen delivery and medullary hypoxia, there are some aspects of this argument that are not consistent. For example, in our recent publication assessing acute renal injury in 300 patients randomized to normothermic or hypothermic cardiopulmonary bypass, we did not observe a difference in acute renal injury between the two groups [3]. This would suggest that differing oxygen demands due to changes in renal metabolic rate with temperature is not a major predictor of renal outcome. An alternate interpretation of the findings of the current study (given the interesting association of this effect with obesity) is a role of the inflammatory response to cardiopulmonary bypass. It is possible that gut ischemia due to hemodilution-related reduced tissue oxygen delivery may precipitate release of endotoxin and subsequent inflammatory kidney injury. In our article we outline how visceral fat is a key regulator for inflammation, and obesity is associated with an upregulated inflammatory state; these factors may explain the interactions of obesity with acute renal injury. In other words, hemodilution-mediated acute renal injury may be a consequence of inflammation-related injury. In this regard, a randomized prospective study of hemodilution and transfusion is required to assess the merit of tolerating extreme hemodilution relative to transfusion risk.
References
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