Recovery from acute renal failure (ARF) requires the replacement of injured cells by new cells that are able to restore tubule epithelial integrity. We have recently described the expression of nephrogenic proteins (Vimentin, Ncam, bFGF, Pax-2, BMP-7, Noggin, Smad 1-5-8, p-Smad, HIF-1, VEGF), in a time frame similar to that observed in kidney development, after ischemic ARF induced in an ischemia/reperfusion (I/R) model. Furthermore, we shown that basic fibroblast growth factor (bFGF), a morphogen involved in mesenchyme/epithelial transition in kidney development, induces a re-expression of morphogenic proteins in an earlier time frame and accelerates the recovery process after renal damage. Herein we confirm that renal morphogenes are modulated by bFGF, and hypothesized that a decrease in bFGF receptor 2 (bFGFR2) levels by the use of antisense oligonucleotides, diminish the expression of morphogenes. Male Sprague-Dawley rats submitted to ischemic injury, were injected with 112 µg/kg bFGFR2 antisense oligonucleotide (bFGFR2-ASO) followed by reperfusion. Rats were sacrificed and the expression of nephrogenic proteins and renal marker damage were analyzed by immunohistochemistry and immunoblot. Animals subjected to I/R treated with bFGFR2-ASO showed a significant reduction in morphogen levels (P<0.05). In addition we observed an increase in markers of renal damage: macrophages (ED-1) and interstitial -smooth muscle actin. These results confirm that bFGF participates in the recovery process and that treatment with bFGFR2-ASO induces an altered expression of morphogen proteins.