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 . . .