ACEi are good for CKD for a variety of reasons:
1) overall systemic blood pressure control
2) decreases hydrostatic pressure in the glomerulus leading to lower single nephron GFR and (varying degrees) of overall GFR which reduces maladaptive hyper filtration in diabetic kidney disease and virtually all other renal diseases
3) biologic effects that aren't completely understood but AngII is a bad player in the genesis of renal fibrosis by directly stimulating TGF-B production in the kidney and heart and probably other organs, these are probably the most important effects as CKD patients don't die from renal disease per se, rather cardiovascular complications
ACEi are bad in situations that stress renal auto regulation: volume contraction, coexisting diuretics and NSAIDs, CNIs, systemic hypotension. Though the effects may be mild or negligable in patients without renal issues who can auto regulate RBF well, in a patient who is "stressed" with a chronic disease at baseline: renovascular disease (hyalin arteriosclerosis of afferent arterioles), advanced CKD (lower reserve), HF, cirrhosis, and nephrosis (chronic prerenal state), the effect can be dramatic and ACEi can help precipitate ischemic tubular injury.