About 40 % of renal graft losses over 10 years in Europe are caused by fibrosis. To explain the origin of interstitial fibroblasts, the epithelial-mesenchymal transition (EMT) theory has been recently ventured : under the effect of an aggression, tubular epithelial cells may change into fibroblasts, cross over the basal membrane, and join interstitium. This innovative hypothesis has been confirmed by the finding of a "fibroblast-specific" protein FSP-1 in the tubular epithelium, then by the detection of fibroblast-like FSP-1 expressing cells in the proximal tubule by confocal microscopy in a transgenic murine model in which fibrosis has been induced. In the renal graft, EMT markers such as FSP-1 and vimentin, have been detected in tubular epithelium in case of chronic allograft nephropathy, correlatively to the loss of expression of epithelial markers. The expression of EMT markers takes place very early, in the first months post-transplantation, in transplant patients whose renal function is not yet impaired, suggesting the existence of a patho-physiological link between EMT markers expression and graft fibrosis development.