Ischemia reperfusion injury (IRI) has been associated with adhesion molecule induction in the injured tissue, but systemic consequences of this inflammatory response have not been well defined. Patients with ischemic acute renal failure often develop concomitant lung disease, therefore we hypothesized that renal IRI would lead to lung inflammation and induction of adhesion molecule expression. Male C57/BL6 mice were subjected to 45 min bilateral renal ischemia followed by reperfusion from 30 min to 72 h. Plasma creatinine increased from control levels of 0.3 to 3.25 mg/dl by 72 h, with concomitant rise in BUN from 20 to 150 mg/dl. Histologic evidence of tubular injury was apparent by 30 min reperfusion, progressing through 72 h. Induction of mRNA for E-Selectin and P-Selectin in kidney was demonstrated by 2 h reperfusion, with ICAM-1 upregulation by 3 h. Neutrophil infiltration could be identified by 12 h of reflow. In lungs harvested from these animals, E-Selectin was induced by 8 h of renal reperfusion, persisting through 72 h, whereas P-Selectin was not significantly upregulated. ICAM-1 mRNA was induced by 8 h, then declined by 72 h. Lung neutrophil infiltration was detected by 4 h of renal reperfusion, preceding upregulation of adhesion molecules. Neutrophil accumulation persisted through 48 h, but declined by 72 h. In conclusion, our findings suggest that in both the kidney and lung early injury or neutrophil accumulation respectively is independent of adhesion molecule induction. However, the later phase of kidney injury and lung inflammation induced by renal IRI is adhesion molecule dependent.