While RAS blockade and SGLT2 inhibition both reduce hyperfiltration via their hemodynamic actions, angiotensin II, the primary effector molecule of the RAS, also exerts several other effects that contribute to the ability of ACE inhibitors and ARBs to reduce interstitial fibrosis, tubular atrophy and glomerulosclerosis [19, 42, 43]. Here, ACE is linked to glomerulosclerosis.