Although gender did not influence urinary ACE2 activity or protein, in the present studies females had significantly higher urinary ACE2 mRNA levels. The gene for ACE2 is located on the X chromosome [2] , and in the rat renal wrap model of hypertension, intrarenal ACE2 activity and expression are upregulated by estrogens [23] , raising the possibility that female transplant recipients may express ACE2 mRNA at higher levels in the kidney compared to males. Female gender was also associated with higher urinary ACE mRNA levels, as was albuminuria, the latter being in agreement with studies in patients with diabetic nephropathy [24] . The cellular origin of urinary mRNA for ACE2 or ACE is unknown, although it has been speculated that proximal tubular cells may be the source, since they express all components of the RAS, and are found in the urine sediment [24] . However, the physiological significance of urinary ACE2 or ACE mRNA levels is unclear. In this regard, diabetes, albuminuria and eGFR did not influence urinary ACE2 mRNA levels in our transplant recipients, a result that differs from diabetic nephropathy patients, where proteinuria was found to correlate positively with urinary ACE2 mRNA, and eGFR to correlate negatively with ACE2 mRNA [24] . Factors related to transplant could therefore have an independent influence on urinary ACE2 mRNA. As one possibility, the use of immunosuppressive drugs in transplant subjects might regulate shedding of cells expressing ACE2 mRNA into the urine.