This acute eGFR decrease with BP lowering may be mediated, at least in part, by intrarenal hemodynamic changes. This hypothesis is supported by the following observations: (i) Single-nephron GFR decreases when glomerular blood ow rate drops below the level that can be sustained by (ii) Urinary excretion of various tubular biomarkers during intensive SBP treatment in SPRINT was not indicative of (iii) Albuminuria during follow-up was lower, instead of higher, in the intensive SBP arm than in the standard SBP treatment arm in SPRINT. Similar observations have been reported in ACCORD participants.133 Nonetheless, the overall rate of decline of eGFR was higher rather than lower on intensive treatment in SPRINT in both and non-CKD subgroups,134 In both ACCORD and SPRINT, participants assigned to intensive BP target also developed more incident CKD during follow-up than those assigned to standard BP target.128,134 There was no difference in the rate of doubling of serum creatinine between intensive and standard SBP treatment in SPRINT, but the small number of these discrete events pre- cludes rm conclusions. The difference in the rate of decline of eGFR in SPRINT after the initial 6 months was small (0.47 /yr in the intensive and standard arms, respectively). If this slope persisted long-term, it would take 20 years to cause a 3 ml/min per 1.73 m2 difference in eGFR between intensive and standard SBP treatment. Taking both the bene cial effect on albuminuria and the adverse effect on eGFR into account, the long-term effects of intensive SBP lowering on the kidney cannot be determined from these relatively short-term, on-treatment observations. Progression to kidney failure and effect modi cation by proteinuria. Prior to SPRINT, the largest RCTs addressing the effects of intensive BP control in CKD were MDRD,97 The primary outcome of these 3 trials was progression of kidney disease. 