Our study has a number of strengths, including the reliability and reproducibility of the assays, the inclusion of data on mRNA, protein, and ACE2/ACE products, and the use of multiple linear regression to adjust for confounding variables. Limitations include the relatively small number of subjects, the absence of plasma ACE2 or ACE measurements, and the single time point for urinary ACE2, ACE and peptide assays. Furthermore, it is possible that diabetes alone may contribute to increased urinary ACE2 levels, independent of transplant status. Studies in patients with diabetes and normal kidney function are required to answer this question. Larger studies are also needed to determine if urinary ACE2 or ACE are biomarkers of transplant function or if they may predict responsiveness to blockade of the RAS.