Search tips
Search criteria 


Logo of ccforumBioMed CentralBiomed Central Web Sitesearchsubmit a manuscriptregisterthis articleCritical CareJournal Front Page
Crit Care. 2010; 14(Suppl 1): P522.
Published online 2010 March 1. doi:  10.1186/cc8754
PMCID: PMC2934552

Pressure-controlled hemorrhagic shock in mice: a new model of acute kidney injury


At the present time, mice models have failed to reproduce human acute kidney injury (AKI) and new relevant models of AKI are required [1]. In this study we developed a model of AKI in mice based on pressure-controlled hemorrhagic shock that closely reproduces hypotension involved in most of human ischemic AKI.


We first determined shock and resuscitation modalities in a C57/Bl6 mice population. A femoral arterial catheter was used for pressure control and bleeding and a central jugular catheter for anesthesia and resuscitation. We secondly explored renal repercussions of a 2-hour shock duration at 35 mmHg mean arterial pressure. We assessed successively the glomerular filtration rate (GFR), histological kidney injury score and performed real-time PCR after the procedure. The shock group was compared with sham mice and with a control group that underwent no procedure (n = 5 in each group).


The shock group GFR was decreased 2 (D2) and 6 (D6) days after shock when compared with control and sham (Figure (Figure1).1). This AKI was intrinsic as showed by the Na/K urinary ratio increase and the decrease in urine concentration ability. Tissular damage prevailed in the outer medulla with a maximal expression at D6 (paucicellular tubular epithelium, intratubular casts) (Figure (Figure2).2). These lesions are associated with an increase of tissular KIM-1 and HIFs mRNA. Despite GFR normalization, the shock group showed discreet defect in urine concentration ability and a slight peritubular fibrosis 3 weeks after shock.

Figure 1
Glomerular filtration rate 2 (D2), 6 (D6) and 21 (D21) days after the procedure.
Figure 2
Tubular injury score at H3, D2, D6 and D21. *P < 0.05 and ** P < 0.01.


This new model of AKI based on hypotension opens new perspectives in the field of short-term and long-term kidney function following AKI.


  • Rosen S, J Am Soc Nephrol. 2008. [PubMed]

Articles from Critical Care are provided here courtesy of BioMed Central