ACE2 is expressed at relatively high levels in the kidney, particularly in the proximal tubule, and is thought to be renoprotective via its ability to reduce Ang II levels. ACE2 also increases production of Ang-(1-7), which can oppose the delete- rious non-hemodynamic actions of Ang II in tubular cells [19] . Kidney expression of ACE2 is reduced in experimental models, including the remnant kidney model of CKD [16, 20, 21] . In humans with diabetic nephropathy, expression of ACE2 is decreased in glomeruli and proximal tubules [22] , suggesting a predisposition to Ang II-mediated injury.