However, there were increased risks for hy- pokalemia (HR: 1.87; 95% CI: 1.02 3.43) and hyperkalemia (HR: 1.36; 95% CI: 1.01 1.82), presumablybecause of the greater use of antihypertensive medications in the intensive BP arm. Acute kidney injury. In the entire ACCORD cohort and SPRINT cohort (and in the SPRINT CKD subgroup), there were higher rates of AKI in the intensive SBP arms, although most of these were AKI Stage 1 and showed full recovery.150 The biomarker data described above suggest that at least some of the fall in eGFR seen with intensive BP treatment could be due to intrarenal hemodynamic changes rather than structural dam- age. In a post hoc analysis of SPRINT, there was a signi cant interaction between baseline eGFR and SBP lowering, such that patients with a baseline eGFR <45 ml/min per 1.73 m2 had an increased risk of AKI in the intensive BP arm but no reduction in the primary CVoutcome.151 Hence, the risk bene t ratio for kidney outcomes in the intensive SBP arm may not be as favorable in this subgroup as in the subgroup with higher baseline eGFR. However, caution should be used in interpreting these non-prespeci ed post hoc ndings in relatively small subgroups. In 2 other post hoc analyses of SPRINT, the respective risks of AKI were marginally increased with the intensive BP target in people $75 years old (HR: 1.41; 95% CI: 0.98 2.04) and increased in people $80 years old (HR: 2.12; 95% CI: 1.37 3.26). These data collectively suggest that inten- sive BP lowering increased the risk of AKI in people with moderate CKD and advanced age, but the episodes were rather infrequent, affecting less than 4% of SPRINT participants and tended to be mild and reversible (Supplementary Polypharmacy. 