Recovery from acute renal failure (ARF) requires the replacement of injured cells with new cells that restore tubule epithelial integrity. The new cells, which are seen to grow from the edges of the injured tubule, are actively engaged in DNA synthesis. The morphologic characteristics of the damage have been described, but not the cellular events that regulate this process. Pax-2 is a transcription factor that is normally expressed in the metanephric mesenchyme in the embryo and is limited to the collecting duct in adult kidney; however, immature regenerating cells express the Pax-2 damage (Imgrud et al. 1999). Other changes in gene expression have been reported in ARF but these studies have not investigated genes of nephrogenesis (Yoshida et al. 2002). We sougth to test the hyphotesis that tissue regeneration is characterized by re-expression of important developmental regulatory proteins. We used male Sprague-Dawley rats (n=5) with 30 min of bilateral ischaemic injury, followed by reperfusion. Animals were anaesthetised I.P. with a combination of ketamine:xylazine (25:2.5 mg kg^-1) and maintained at a temperature of 37°C. The rats were killed 24, 48, 72 and 96 h after ischaemia reperfusion and both kidneys were recovered. The expression of Lim 1/2, Noggin, Pax 2/5/8, BMP-7, Smads 2/3, p-Smad, Vimentin, NCam, ZO-1, VEGF, Tie-2, HIF-1 αand Engrailed protein was analysed by immunohistochemistry and Western blotting as previously done for other proteins (Rodriguez et al. 2004). The expression of CD34, haematopoietic stem cells were analysed by immunohistochemistry (replicates=5). All proteins were analysed 24, 48, 72 and 96h after I/R. To assess hypoxia the presence of HIF-1α protein and endothelial markers induced by hypoxia VEGF and TIE-2 were evaluated. We observed the expression of these markers in the kidney after bilateral ischaemia. To assess renal damage and regeneration the presence of ED-1, collagen III and α-actin were evaluated. Immunohistochemistry revealed the expression of the mesenchyme proteins Vimentin and Ncam; the latter is essential for kidney development. In addition this kidney also expressed Pax-2, Noggin, Lim1/2, BMP7 and Engrailed, all proteins with important roles during nephrogenesis. We observed a transient, temporally and locally restricted re-expression of these proteins that was not observed in control animals (p>0.05). We analysed the expression of transcription factors Smad and p-Smad, expressed by mesenchymal cells during kidney development. We observed the presence of these factors in regeneration of the kidney and not in control animals (p>0.05). We speculate that Smad may play specific roles in cell fate determination during kidney regeneration. To assess the presence of haematopoietic stem cells the marker CD-34 was analysed. We did not observe haematopoietic stem cells. These results indicate that the kidney after damage produced by bilateral ischemic injury can differentiate in a cellular type similar to metanephric mesenchymal cells and express morphogenic proteins before that differentiate into epithelia. This is a similar process to that seen in normal kidney development.