A secondary analysis published September 3 in *Hypertension Research* found that intensive systolic blood-pressure control reduced cardiovascular events across data from two major randomized trials while increasing a composite measure of adverse kidney outcomes.
The apparent tradeoff was not uniform across categories of baseline kidney risk. However, the study was a post hoc reanalysis rather than a newly randomized comparison, and one key statistical test for differences in cardiovascular benefit between risk groups narrowly missed the conventional threshold for significance.
What the researchers analyzed
The investigators used participant-level data from SPRINT and from ACCORD-BP participants who met SPRINT-style eligibility criteria. The original trials compared an intensive systolic blood-pressure target below 120 mm Hg with a standard target below 140 mm Hg.
SPRINT enrolled 9,361 adults at elevated cardiovascular risk who did not have diabetes. ACCORD-BP enrolled 4,733 adults with type 2 diabetes and high cardiovascular risk, although the new analysis used only its SPRINT-eligible subset.
Researchers classified participants as having low, moderate, or high to very high risk under the Kidney Disease: Improving Global Outcomes framework. KDIGO categories combine estimated glomerular filtration rate, a measure of kidney filtration, with urinary albumin, a marker of kidney damage.
The cardiovascular endpoint combined nonfatal heart attack, nonfatal stroke, fatal or hospitalized heart failure, and cardiovascular death. The kidney endpoint combined a sustained decline of at least 40% in estimated glomerular filtration rate with end-stage kidney disease.
Cardiovascular events fell as kidney events rose
Across the analyzed population, intensive blood-pressure control was associated with a 32% lower relative hazard of the cardiovascular composite than standard control. The hazard ratio was 0.68, with a 95% confidence interval from 0.59 to 0.78.
The estimated cardiovascular benefit became smaller at higher KDIGO risk, but the overall interaction test produced a P value of 0.055. That result does not meet the commonly used 0.05 threshold and should not be presented as definitive proof that kidney-risk category changes the total cardiovascular effect. Interactions for nonfatal heart attack and fatal or hospitalized heart failure were statistically significant.
The pattern moved in the opposite direction for the kidney composite. Intensive control was associated with an 88% higher relative hazard, with a hazard ratio of 1.88 and a 95% confidence interval from 1.52 to 2.33. That increase appeared mainly in the low- and moderate-risk categories, and the interaction across KDIGO groups was statistically significant.
Crucially, the kidney result was driven by sustained declines in estimated filtration. There was no detectable increase in end-stage kidney disease alone: its hazard ratio was 1.05, with a confidence interval from 0.74 to 1.48.
A filtration decline is not necessarily kidney failure
Lowering blood pressure can alter pressure within the kidney’s filtering units and reduce estimated filtration without necessarily causing the same structural injury that drives progressive kidney disease. The composite endpoint therefore should not be translated into a claim that intensive control nearly doubled kidney-failure risk.
The unchanged end-stage kidney disease result is reassuring but not conclusive. Its confidence interval permits both a meaningful reduction and a meaningful increase, indicating limited precision for this less frequent outcome.
Relative hazard ratios also do not communicate how many additional or prevented events occurred. Absolute risks, treatment burden, adverse effects and a patient’s starting cardiovascular and kidney risks are needed to judge the clinical balance.
Why the subgroup findings remain provisional
Randomization in SPRINT and ACCORD-BP supports comparisons between their original treatment groups. It does not eliminate uncertainty introduced by retrospectively sorting participants into kidney-risk categories and testing multiple interactions.
The source trials also enrolled different populations: SPRINT excluded diabetes, while ACCORD-BP specifically studied people with type 2 diabetes. SPRINT ended its intervention early after cardiovascular benefit emerged, and its standardized blood-pressure measurements may not correspond directly to routine readings taken under different conditions.
The analysis strengthens the evidence that intensive pressure control can prevent major cardiovascular events in high-risk adults. It also shows why a single target cannot be interpreted apart from kidney function, albuminuria and measurement method. The findings inform risk assessment; they do not establish a self-directed or universally appropriate blood-pressure goal.
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This article provides general information, not diagnosis or treatment advice. Consult a qualified clinician before making medical decisions.