As far as I know, AT II constricts both the afferent and efferent arteriole. However, it contracts efferent more than afferent. This leads to less perfusion with increased plasma filtration fraction, and, therefore, increased Glomerular Filtration Rate.
So, in a diabetic that still does not have renal impairment, ACE inhibitors increase perfusion, but would decrease GFR if there were no compensatory mechanisms... But, as the exist, ACE inhibitors increase perfusion and don't change GFR, what is perfect to diabetic because its nephropathy is due to microvascular insufficiency.
Actually, a patient that donated its kidney is not insufficient because its other kidney nephrons have compensatory mechanisms that improves his renal function up to 80% of the original.
However, if your patient already has renal insufficiency, due to any cause, he lost nephrons and the remaining ones, althought they are working at maximum rate, are not able to compensate. If you give ACE inhibitors to this patient, you will increase perfusion and decrease GFR because, remember, - ATII contracts both arterioles, but efferent more - and - these nephrons are working at maximum capacity and, therefore, have no compensatory mechanisms to use. This leads to a best perfusion, but a decrease in renal function.
Because of this, ACE inhibitors are indicated to Hypertension and Diabetes coexistence, but contraindicated when there is Renal Insufficiency.
I'm sorry for english mistakes I hope I was clear.