Diabetes mellitus (DM) may progress to diabetic nephropathy (DN) in approximately 40% of cases and it accounts for one of the most common causes of end-stage of renal disease (ESRD). The pathogenesis of DN involves complex interactions between metabolic and hemodynamic factors. DM type 1 has a dominant impact on morbidity and mortality after renal transplantation. We report a kidney transplantation patient with DM and DN as the etiology of end-stage renal disease and whose post-transplantation evolution over 19 years was remarkably atypical. DM was diagnosed at the age of 7 years and the patient suffered a rapid and aggressive progression of her disease with early development of DN and diabetic retinopathy. Nineteen years post-transplantation, the patient shows neither deterioration of graft function nor clinical reactivation of DN. There seems to be two quite distinct answers to the same injury supported by a group of factors that led to micro- and macrovascular lesions, all present before transplantation and potentially aggravated through some immunosuppressive therapy. This clinical evolution suggests the hypothesis that not only the graft but also the donor may have inherent characteristics that enabled him to display the resistance to DN despite the genetic susceptibility of the receptor. The answers to these questions would help to explain why some patients with diabetes progress to macro- and microvascular complications and others remain resistant to developing these vascular disorders. In this case, the resistance to DN is apparently a feature related to the donor.
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