Key result
Intensive BP control is not linked to inpatient AKI but is associated with outpatient AKI.
Why the study?
Adjudication of inpatient AKI in SPRINT was based on billing codes and notes, and the effect of intensive versus standard BP control on creatinine-based AKI and its association with CVD and mortality was unclear.
Does intensive blood pressure control increase the risk of AKI, and is incident AKI associated with cardiovascular disease and mortality?
Observational (n=3,644)
Yes
Does intensive blood pressure control increase the risk of AKI, and is incident AKI associated with cardiovascular disease and mortality?
EHR-based creatinine ascertainment demonstrates that intensive BP control increases the risk of outpatient AKI, which is subsequently associated with increased all-cause mortality.
Answers are grounded in this paper and cite their sources.
Intensive BP control may warrant outpatient AKI monitoring; leaves open whether creatinine-defined events predict outcomes in observational cohorts.
Background: Adjudication of inpatient AKI in the Systolic Blood Pressure Intervention Trial (SPRINT) was based on billing codes and admission and discharge notes. The purpose of this study was to evaluate the effect of intensive versus standard BP control on creatinine-based inpatient and outpatient AKI, and whether AKI was associated with cardiovascular disease (CVD) and mortality. Methods: We linked electronic health record (EHR) data from 47 clinic sites with trial data to enable creatinine-based adjudication of AKI. Cox regression was used to evaluate the effect of intensive BP control on the incidence of AKI, and the relationship between incident AKI and CVD and all-cause mortality. Results: A total of 3644 participants had linked EHR data. A greater number of inpatient AKI events were identified using EHR data (187 on intensive versus 155 on standard treatment) as compared with serious adverse event (SAE) adjudication in the trial (95 on intensive versus 61 on standard treatment). Intensive treatment increased risk for SPRINT-adjudicated inpatient AKI (HR, 1.51; 95% CI, 1.09 to 2.08) and for creatinine-based outpatient AKI (HR, 1.40; 95% CI, 1.15 to 1.70), but not for creatinine-based inpatient AKI (HR, 1.20; 95% CI, 0.97 to 1.48). Irrespective of the definition (SAE or creatinine based), AKI was associated with increased risk for all-cause mortality, but only creatinine-based inpatient AKI was associated with increased risk for CVD. Conclusions: Creatinine-based ascertainment of AKI, enabled by EHR data, may be more sensitive and less biased than traditional SAE adjudication. Identifying ways to prevent AKI may reduce mortality further in the setting of intensive BP control.
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Drawz et al. (2022) conducted an observational in Hypertension (n=3,644). Intensive BP control vs. Standard BP control was evaluated on Creatinine-based inpatient AKI (HR 1.20, 95% CI 0.97 to 1.48). Intensive BP control did not significantly increase the risk of creatinine-based inpatient AKI compared to standard control (HR 1.20; 95% CI 0.97-1.48), though it increased outpatient AKI.
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