Epithelial-mesenchymal transition in the context of chronic fibrosis and function of kidney transplants

The principal cause of delayed renal failure after transplantation is interstitial fibrosis and tubular atrophy (IF/TA). Identification of all possible causes of IF/TA and improvement of the methods of specific treatment of such cases will be important issues for renal transplantation medicine in the future. Evidence to suggest that the epithelial-mesenchymal transition (EMT), alongside IF/TA, is a significant event in the process of damaging the patient’s own and transplanted kidneys has recently been appearing in the professional literature. In the course of the EMT, renal tubular cells undergo a process of gradual transformation into myofibroblasts. The presented review article discusses the molecular and cellular pathways of the EMT and the role they play in the progression of chronic fibrosis of the kidney transplant. The potential therapeutic options for the EMT are still a subject for discussion but many facts suggest that the EMT plays the principal role in the pathogenesis of chronic interstitial fibrosis and tubular atrophy (IF/TA), and as a consequence of chronic allograft dysfunction (CAD). The importance of the EMT involvement in kidney transplant fibrosis has not been elucidated. Many data are taken into account for the purpose of determining whether the EMT can be a useful marker in the assessment of chronic allograft dysfunction progression.