The major histocompatibility complex molecules are the primary antigens responsible for causing graft rejection, and T-cell recognition of alloantigens is the cardinal event initiating cellular rejection. Current concepts suggest that direct allorecognition mediates acute rejection, whereas indirect allorecognition mediates chronic rejection. In biopsy tissue of rejecting human renal allografts, several cytotoxic T-lymphocyte molecules are upregulated. The net result of cytokine release and the acquisition of cell surface receptors is the emergence of antigen-specific and graft-destructive T cells. Acute rejection is more frequent in children than in adults. By the end of the first year posttransplantation, 45% of living donor recipients and 60% of cadaver donor recipients will have an episode of rejection. In recent years, with improved immunosuppressive therapy, the incidence of acute rejection is decreasing at a rate of about 8% each year, however, chronic rejection graft loss has increased to 41% of all graft losses in the last 2 years. The mechanisms leading to chronic rejection and attempts to reduce acute rejections should provide a better half-life to children postrenal transplantation.