Abstract: Blockade of the renin–angiotensin system (RAS) is renoprotective beyond the effect of lowering blood pressure, especially in patients with mild-to-moderate chronic kidney disease (CKD).^1,2 However, such renoprotection is far more effective when patients with CKD have proteinuria.^1,2 As nephrologists, we struggle about whether to continue prescribing RAS inhibitors to patients with advanced (stage 4 or 5) CKD, given the perceived risks. We hope that stopping such treatment may lead to an increase (however modest) in the estimated glomerular filtration rate (eGFR), and we worry about possible drug-related hyperkalemia and other adverse events if RAS inhibition is continued. Although recent retrospective . . .