Aggressive Systolic Blood Pressure Management as a Risk Factor of Acute Kidney Injury in Patients with Intracerebral Hemorrhage

Background Intensive systolic blood pressure (SBP) reduction is routinely employed to limit hematoma expansion in spontaneous intracerebral hemorrhage (ICH). However, the renal consequences of sustained aggressive SBP lowering in real-world clinical practice remain incompletely characterized. Methods We conducted a retrospective cohort study of adults admitted to the intensive care unit with spontaneous ICH between 2011 and 2023. Hourly SBP measurements over the first 7 days were standardized and clustered using k -Shape time-series clustering to identify distinct shape-based SBP trajectories. Acute kidney injury (AKI) was defined using Kidney Disease: Improving Global Outcomes (KDIGO) criteria. Multivariable logistic regression assessed associations between SBP trajectory cluster and AKI, adjusting for demographics, baseline illness severity, renal function, and nephrotoxic medication exposure. Results Among 233 patients (mean age 61.2±14.1 years), two distinct SBP trajectories were identified: Cluster 1 (rebound SBP trajectory), a progressive upward SBP trajectory with gradual rebound, and Cluster 2 (rapid-drop SBP trajectory), a lower SBP trajectory characterized by rapid early reduction and sustained levels below 140 mm Hg. Overall, 70.4% developed AKI of any stage. Patients of Cluster 1 (rebound SBP trajectory) had significantly higher odds of AKI compared to those of Cluster 2 (rapid-drop SBP trajectory) (adjusted OR 1.97; 95% CI, 1.03–3.78). Higher maximum nicardipine dose was independently associated with AKI (OR 1.14 per mg/h; 95% CI, 1.03–1.26). SBP trajectory cluster was not significantly associated with hematoma expansion (defined as a binary outcome based on physician-documented expansion vs. no expansion), neurological outcomes, or 1-year mortality. Conclusions In ICH patients, rapid early decline in SBP followed by relative stabilization at lower levels (<140 mm Hg) is associated with increased risk of AKI without clear neurological benefit. These findings highlight the importance of balancing cerebral hemorrhage control with renal perfusion and support cautious implementation of intensive BP targets in clinical practice.