Calcitriol exerts reno-protective effects to attenuate CKD progression induced by excessive angiotensin II by (1) counteracting ADAM17/TGFα signals, (2) inducing ACE2/Angiotensin 1-7/MAS receptor activity at the cell surface by preventing ACE2 shedding in the setting of increased ADAM17 activity in uremia and, (3) by preventing excessive renal inflammation through the simultaneous suppression of the vicious TNFα/ADAM17 feed-forward loop. Here, AGT is linked to uremia.