AKI Is a Risk Factor for Elevated BP
Hospitalized patients who experienced AKI had a 22% increased risk of elevated BP after 2 years of follow-up.
Acute Kidney Injury (AKI) is an independent risk factor for the subsequent development of elevated blood pressure (BP), new findings suggest.
Chi-yuan Hsu, MD, of the University of California San Francisco, and colleagues studied 43,611 adult members of Kaiser Permanente Northern California hospitalized from 2008 to 2011. Of these, 2,451 experienced AKI. After a follow-up period of 2 years postdischarge, elevated BP—defined as values greater than 140/90 mm Hg— developed in a significantly greater proportion of AKI versus non-AKI patients (46.1% vs. 41.2%), Dr. Hsu's group reported online ahead of print in the Journal of the American Society of Nephrology. The difference between the groups was apparent within the first 180 days of follow-up (30.6% vs. 23.1%).
In multivariate analysis, AKI was independently associated with a significant 22% increased odds of developing elevated BP during 2 years of follow-up. The investigators observed higher adjusted odds with more severe AKI. For example, patients with stage 3 AKI had a significant 82% increased odds in adjusted analyses, whereas patients with stage 1 AKI had only a 9% increased odds.
The researchers defined AKI as a peak serum creatinine level during hospitalization that was 0.3 mg/dL or greater and/or 50% or greater than the baseline level.
“Our novel study provides the first result in adults of a connection between AKI and BP elevation, which could have important clinical and public health implications,” the researchers concluded.
The study population as a whole had a mean age of 56.1 years, with AKI patients being significantly older than the non-AKI patients (57.7 vs. 56 years). AKI was more likely to develop in men than women. Men made up 51.5% of the AKI group compared with 39.8% of the non-AKI group. Compared with the non-AKI group, a significantly higher proportion of the AKI group had diabetes mellitus (6.9% vs. 4.8%) and chronic heart failure (3.8% vs. 1%).
Dr. Hsu and colleagues noted that study strengths include the plausibility of the physiologic connection between AKI and subsequent BP level and an analysis of a large, contemporary community-based population with a wide diversity in age, sex, and race/ethnicity. In addition, the researchers used actual BP readings during follow-up to define elevated BP instead of administrative diagnostic codes regarding hypertension. They said they also carefully controlled for a wide range of potential confounders.
Regarding study limitations, the authors said that because their investigation was observational, association does not prove causality. “It would be unethical to randomly assign patients to develop AKI or not and follow subsequent BP levels,” they noted. In addition, because the study was based on data collected as part of routine clinical care, they were unable to determine BP levels at specific time points.