The evidence on the effects of intensive BP lowering, namely the <120 mm Hg SBP target, on critical clinical outcomes such as CV events and all-cause mortality is considered to be moderate due to study limitations, while the effect on kidney failure is weak. For CV events and all-cause mortality, the evidence is primarily derived from SPRINT, in which the sample size was large, the effects of intensive BP lowering on clinical outcomes were strong, and there was no heterogeneity in the effects between the CKD and non-CKD subgroups. Results from the subgroup analysis of ACCORD, as well as the joint analysis of the ACCORD and SPRINT data, lend further support, although there were relatively few participants with CKD in ACCORD (Supplementary Table S1191 93 ). TherenoprotectiveeffectsofBPlowering inCKDareprimarily derived from MDRD and AASK trials. The evidence is considered tobeoflowqualityduetostudylimitationsandinconsistency.The effects were seen in only the proteinuric subgroups, and in the case of AASK, the effects were seen only during the long-term post-trial follow-up (Supplementary Table S1297 99,135,138 and Supplementary Table S1391,92,95,97 99,135,138,143,146 148 ). Further, SPRINTshowed a short-term acute decline in eGFR and no long- term bene cial effect on eGFR with intensive SBP lowering. Therefore, collectively, these studies did not show convincingly that intensive BP lowering is renoprotective. chapter 3 www.kidney-international.org Values and preferences. The Work Group places high value on decreasing the risks of CV events and all-cause mortality by intensive SBP lowering, although the renoprotective effects are more tenuous. The reduction in the absolute risk of all-cause mortality in the CKD subgroup in SPRINT was 0.6% per year (1.61% and 2.21% in the intensive and standard SBP group, respectively). If this trend continues linearly, the risk reduction would be substantial over 20 or 30 years. 