They concluded that the evidence was inconclusive.137 Similarly, the current ERT review found no effect modi cation according to the presence of proteinuria (Supplementary Table S1297 ). The evidence that intensive BP reduction reduces the risk of progression to kidney failure is derived mainly from a prede ned subgroup analysis of MDRD (only 54 pa- tients with proteinuria >3 g/d, but large effect size)97,139 and long-term post-treatment follow-up from MDRD138 and A more recent meta-analysis of 11 RCTs of lower versus higher BP goals found that intensive BP reduction was associated with a reduction in kidney failure events (de ned as the composite of doubling of serum creatinine and a >50% reduction in eGFR or ESKD), with effect modi cation by Intensive BP control reduced the risk of kidney failure only among those with baseline proteinuria, de ned as a protein creatinine ratio (PCR) >220 mg/g (22 mg/mmol). The MDRD and AASK studies were major con- tributors to this evidence base. The REIN-2 study compared a higher DBP target of <90 mm Hg with a lower BP target of <130/80 mm Hg by adding felodipine to baseline ramipril therapy in patients with protei- nuric CKD (mean eGFR and proteinuria approximately 35 ml/ min and 3 g/d, respectively) without diabetes.99 no bene t of intensi ed BP control over a mean follow-up of approximately 19 months. However, the study was underpow- ered with a total of only 338 participants and had very small differences in achieved SBP and DBP of only 4 mm Hg and 2 mm Hg, respectively, during the intervention phase. The effects of intensive SBP lowering with target <120 mm Hg are only available in ACCORD and SPRINT. 