Diabetic nephropathy consists in the Non Enzymatic Glucolization (NEG) of the vascular basal membrane (B.M) with the efferent arteriole being more affected than the afferent.
NEG basically means Glucose attaching to amino acids. This results in hyaline arteriolosclerosis (lumen narrows) --> HTN of the Glomerulus (remember this is happening in the efferent arteriole first)
Another thing that constricts the efferent is Angiotensin II so extra pressure in the glomerulus. By using ACE I or ARB you inhibit AT II activity (not explaining their mechanisms, bet you are very clear on that)
So we basically reduce that "extra tension", protecting the Glomerulus