Lowering of BP was explicitly not the aim of those trials. Kidney disease pro- gression was reduced with RASi compared to placebo or other antihypertensive agents with a suggestion of effect modi ca- tion by urine protein excretion.166 RASi also reduced CV outcomes as compared to placebo in high-risk populations, particularly in subgroups with CKD,166,167 independent of the presence or absence of high BP.165,167,168 That said, there is limited evidence to use speci c antihy- pertensive agents to treat high BP to target in CKD, and almost no evidence comparing antihypertensive combination therapies in CKD from outcome trials. Many people with CKD and BP of at least 20 mm Hg above the target will need combinations of several antihypertensive drugs. Starting antihypertensive ther- apy in such people with antihypertensive drug combinations is suggested. There are, however, no RCTs comparing different drug combinations in CKD, as there are no RCTs on antihy- pertensive classes other than RASi, beta-blockers, and CCBs. A recent network meta-analysis by Xie et al., including 119 RCTs (n 64,768), examined the bene ts of treating with RASi compared to placebo or active therapy in patients with CKD for kidney and CVoutcomes and included studies with and without diabetes and albuminuria (A1 A3). The results demonstrated improved precision with narrower con dence intervals than smaller meta-analyses reported below.169 Both ACEi and ARBs reduced the risk of kidney failure (de ned as a composite of any of the following: doubling of serum creatinine, 50% decline in GFR, or ESKD) by 39% and 30%, respectively, compared to placebo with high certainty; and 35% and 25%, respectively, against active controls with moderate certainty. 