Impact of primary diabetic nephropathy on arteriolar hyalinosis lesions in patients following kidney transplantation.

AimArteriolar hyalinosis (AH) is a common lesion in allograft biopsies taken following kidney transplantation. Recent studies have shown that severe AH may predict transplant outcomes and provide information about previous exposure to certain drugs, such as calcineurin inhibitors (CNI). However, the incidence of AH as a direct result of diabetic nephropathy (DN) after kidney transplantation has not been fully evaluated. This study aimed to assess the impact of primary DN on the development of AH lesions in patients who underwent kidney transplantation. MethodsEighty-three patients who underwent living-donor kidney transplantation between April 2005 and June 2015 were enrolled in this study. A total of 33 patients had DN prior to transplantation. Allograft biopsies were scored according to the Banff classification, and the relationship between the individual histological lesions and clinical baseline data was assessed. ResultsAt early biopsy (3-12 months), there were no differences in the rates of AH lesions between the DN group and the non-DN group (ah 1: 37% vs. 41.3%, P = 0.719; aah 1: 14.8% vs. 6.5%; P = 0.453). However, there were significant differences between the groups in biopsies taken more than 3 years after the transplant (ah 2: 83.3% vs. 36.8%, P = 0.013; aah 2: 66.7% vs. 21.1%, P = 0.011). Multivariable analysis showed that both the length of time after transplantation and the presence of DN were independent risk factors for ah 2 (odds ratio [OR]: 2.55, 95% confidence interval [CI]: 1.47-19.54, P = 0.011) and aah 2 (OR: 7.55, 95% CI: 1.49-38.33, P = 0.015). ConclusionThis is the first report showing that the presence of primary DN disease contributes to the development of severe AH late in the course after kidney allografts. SUMMARY AT A GLANCE Arteriolar hyalinosis developing after kidney transplantation is a major complication. We found that primary diabetic nephropathy was closely associated with the development of severe arteriolar hyalinosis evident in late allograft biopsies. Better control of hyperglycaemia may ameliorate arteriolar hyalinosis progression.