It was a Retrospective study and residual confounding. Angiotensin-converting enzyme (ACE) inhibitors and renin-angiotensin-aldosterone system (RAAS) blockers were proven to slow the worsening of Chronic Kidney Disease (CKD). They may, however, have caused hyperkalemia. For a study, researchers wanted to examine the relationship between stopping RAASi after a hyperkalemia episode and clinical outcomes in individuals with chronic kidney disease. Adults in Manitoba (7,200) and Ontario (n=71,290) with an episode of de novo RAASi-associated hyperkalemia (serum potassium ≥ 5.5 mmol/L) and CKD. The major outcome was all-cause mortality. CV mortality, fatal and non-fatal CV events, dialysis initiation, and a negative control result (cataract surgery) were secondary outcomes. Cox proportional hazards models were utilized to compare the effect of RAASi continuation (vs. cessation) on outcomes using an intention-to-treat approach. Sensitivity analyses were performed in the main study and included time-dependent, dose-dependent, and propensity matching. An average potassium and average eGFR were 5.8 mEq/L and 41 ml/min/1.73m2 in Manitoba and 5.7 mEq/L and 41 ml/min/1.73m2 in Ontario. RAASi discontinuation was related with a higher risk of all-cause mortality [hazard ratio (HR) 1.32, 95% CI: 1.22-1.41 in Manitoba, and HR: 1.47, 95% CI: 1.41-1.52 in Ontario] and cardiovascular mortality [HR: 1.28, 95% CI: 1.13-1.44 in Manitoba, and HR: 1.32, 95% CI: 1.25-1.39 in Ontario]. Raasi discontinuation was associated with an increased risk of dialysis initiation in both cohorts (Manitoba: HR, 1.26 [95% CI, 0.89-1.78] and Ontario HR, 1.11 [95% CI, 1.08-1.16]). In patients with hyperkalemia and chronic kidney disease, removal of the drug RAASi is linked to increased mortality and cardiovascular problems when compared to continued usage. Maintaining RAASi therapy after an episode of hyperkalemia may improve patient outcomes in those with CKD.