Our results support the hypothesis that transplant patients with diabetes exhibit increased urinary excretion of ACE2 protein. This was independent of eGFR as determined by multivariate analysis. Both soluble ACE2 and ACE have been detected in human urine [10] , and in humans with CKD, Mizuiri et al. reported increased urinary levels of ACE2 protein by ELISA, compared to healthy subjects [14] . Patients with diabetic nephropathy had higher urinary levels of ACE2 than those without diabetic nephropathy, and use of ACE inhibitor and/or angiotensin receptor blockers did not affect urinary ACE2 levels [14] . In our study, no subjects were taking inhibitors of the RAS. Using three independent assays for urinary ACE2 (enzyme activity, ELISA, and immunoblot), multiple linear regression revealed that diabetes was the only variable consistently predictive of higher urinary ACE2 levels. Age and gender had no influence on urinary ACE2 activity or protein levels. Similarly, in patients with CKD Mizuiri et al. found no difference in urinary ACE2 levels between males and females [14] .