Correspondence  |   November 2012
In Reply
Author Affiliations & Notes
  • H. Thomas Lee, M.D., Ph.D.
  • *College of Physicians and Surgeons of Columbia University, New York, New York.
Article Information
Correspondence   |   November 2012
In Reply
Anesthesiology 11 2012, Vol.117, 1143-1144. doi:
Anesthesiology 11 2012, Vol.117, 1143-1144. doi:
In Reply:
We thank Mayeur et al.  for their interest in our review on acute kidney injury and extra renal organ dysfunction.1 As stated in our review, “single-insult” kidney injury models including complete renal ischemia, nephrotoxins, nephrectomy, or renal hypoperfusion do not completely recapitulate the multifactorial causes of clinical acute kidney injury. Single-insult models of kidney injury, however, have been invaluable in demonstrating the effects of acute kidney injury-mediated remote and multiorgan dysfunction.2 We agree with Mayeur et al.  that the hemorrhage and resuscitation model is used to produce multiorgan injury as well as systemic inflammatory response syndrome.3,4 However, we disagree that it is a single-insult model of organ injury. The hemorrhage and resuscitation method is actually a “two-insult model” of multiorgan injury, as this model requires a period of controlled hemorrhage followed by resuscitation with shed blood. Resuscitation with shed blood exacerbates as well as causes multiorgan injury by promoting systemic inflammatory response, platelet activation, increased neutrophil recruitment and microthrombi formation.4 
*College of Physicians and Surgeons of Columbia University, New York, New York.
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