Non-dihydropyridine CCBs have the apparent addi- tional bene t of reducing proteinuria.170 If a 3-drug combina- tion of RASi, CCB, and diuretic at recommended doses is not adequate to control BP, additional therapy including a mineralocorticoid-receptor antagonist (MRA), long-acting alpha antagonist, or beta-blocker can be used, as well as dihy- dralazine, hydralazine, minoxidil, or centrally acting agents.171 Higher BP due to uid overload is common in CKD; therefore, diuretics are, in general, logical agents at appropriate dose to lower high BP, with or without the concomitant use of RASi. Outcome data in primary hypertension favor chlortha- lidone and indapamide over hydrochlorothiazide,2 although this has been questioned and there is an ongoing trial.172 174 Thiazide diuretics lose ef cacy in diuresis and BP lowering as GFR worsens, but several, including chlorthalidone, metola- zone, and indapamide appear to remain effective at . Loop diuretics are often effective at lower GFRs (i.e., <30 ml/min per 1.73 m2 ). When combined with a loop diuretic, thiazides are particularly effective in inducing diuresis, but they often lead to hypokalemia and hy- There are no data on clinical outcomes with loop diuretics in the treatment of high BP with or without CKD. 