In kidney tubular epithelial cells, ACE2 is localized to the apical membrane and also appears in the cytoplasm [3, 10] . ACE2 is shed at its carboxy-terminus from the plasma membrane in cultured human embryonic kidney cells and airway epithelial cells, a process catalyzed by the enzyme ''a disintegrin and metalloproteinase-17'' (ADAM-17) [11] [12] [13] . Whether this process occurs in the proximal tubule is unclear, although soluble ACE2 has been detected in human urine [10] . In a recent study, urinary levels of ACE2 protein were significantly increased in humans with CKD (the majority with chronic glomerulonephritis), compared to healthy controls, as determined by enzyme-linked immunosorbent assay (ELISA) [14] . Urinary ACE2 was also higher in diabetics with CKD [14] . These results suggest that ACE2 may be shed into the urine, and could be a biomarker in CKD patients. However, the presence of urinary ACE2 has not been studied in renal transplant recipients, and the factors associated with elevated urinary ACE2 remain unclear. Accordingly, the principle objective of the present study was to determine if urinary ACE2 activity, protein, and mRNA can be detected in renal transplant patients, and to identify factors associated with the presence of ACE2. In addition, we examined factors associated with urinary ACE activity, protein and mRNA in these patients. Our data indicate that urinary ACE2 is increased in renal transplant recipients with diabetes, possibly due to increased shedding from tubular cells.