We have read with interest the review by Yap et al .1on acute kidney injury and extra renal organ dysfunction. We agree with their comments on the limitations of previously described models based on nephrotoxicants to explore acute kidney injury in animals. Surprisingly the authors wrote that ““severe and prolonged hypotension in rats does not typically induce renal injury and is therefore not suitable for use as a ‘‘single insult’’ animal model.”” Indeed, in a recent experimental study in mice, we have shown that a 2- hr pressure control hemorrhagic shock in mice induces prolonged decrease in glomerular filtration rate, histological lesions, and molecular hypoxic impact.2Moreover, 3 weeks after injury, sparse renal fibrosis and persistent tubular function abnormalities are present. In many respects and despite the limits of such anthropomorphism, this single-insult model reproduces closely both functional and histologic features of human ischemic acute kidney injury. This work and others sustain the potential interest of such a model.3 

Nicolas Mayeur M.D.,* Vincent Minville M.D., Ph.D.,

Ivan Tack M.D., Ph.D.* Université Paul Sabatier, Toulouse, France. nicolas.mayeur@inserm.fr

Yap SC, Lee HT. Acute kidney injury and extrarenal organ dysfunction: New concepts and experimental evidence. Anesthesiology. 2012;116:1139–48
Mayeur N, Minville V, Jaafar A, Allard J, Al Saati T, Guilbeau-Frugier C, Fourcade O, Girolami JP, Schaak S, Tack I. Morphologic and functional renal impact of acute kidney injury after prolonged hemorrhagic shock in mice. Crit Care Med. 2011;39:2131–8
van Meurs M, Kurniati NF, Wulfert FM, Asgeirsdottir SA, de Graaf IA, Satchell SC, Mathieson PW, Jongman RM, Küümpers P, Zijlstra JG, Heeringa P, Molema G. Shock-induced stress induces loss of microvascular endothelial Tie2 in the kidney which is not associated with reduced glomerular barrier function. Am J Physiol Renal Physiol. 2009;297:F272–81