Both early and long-term outcomes of kidney transplantation are improving steadily, which should be attributed to a modern and effective immunosuppression, as well as an increasing experience of transplant surgeons and comprehensive care provided to the graft recipients. According to the data of United States Renal Data System (USRD) from 1999 (1), median cadaveric graft survival improved from 5.2 years in the mid-1980s to 10.2 years the mid-1990s, and the European data from the Collaborative Transplant Study (CTS) (2005) revealed that the expected graft half-life exceeded 15 years (2). Despite that, still about 5% of patients return every year to the hemodialysis treatment due to graft function loss. The main reason is chronic allograft dysfunction (CAD), the pathogenesis of which is complex, and the prevention of and treatment have not been very effective so far. The chronic allograft dysfunction may be sometimes diagnosed as soon as a few months after transplantation, but it usually develops move than a year from the surgery. Clinical manifestation of this process involves gradual decline of the glomerular filtration rate (GFR), accompanied by hypertension and proteinuria. Morphological signs of CAD involve progressive vascular changes of endarteritis proliferativa type with myofibroblast hyperplasia and vascular wall fibrosis, resulting in arteriole stenosis and invariably leading to secondary ischemic changes within the graft. These changes are of concentric nature and involve interlobar, arcuate and interlobular arteries. Sometimes they also affect the afferent glomerular arterioles. The internal elastic membrane remains intact. These alterations are accompanied by the markers of ongoing inflammation within interstitial tissue and tubules (tubulitis), mediated by infiltration of immunologically competent cells in the course of cellular response to alloantigens (3).