Key result
High arterial stiffness (tertile 3 vs 1) in hypertensive patients undergoing blood pressure lowering was associated with a higher incidence of kidney dysfunction (6.4% vs 0%; OR 2.23, 95% CI 0.84-5.95).
Why the study?
Intensive blood pressure lowering increased acute kidney injury risk despite cardiovascular benefits, prompting investigation into how treatment-induced blood pressure changes relate to kidney function decline while accounting for arterial stiffness.
Does intensive clinic blood pressure lowering increase kidney function decline in hypertensive patients with high arterial stiffness?
RCT (n=266)
Double-blind
randomized
Does intensive clinic blood pressure lowering increase kidney function decline in hypertensive patients with high arterial stiffness?
Odds Ratio: 2.23 (95% CI 0.84–5.95)
Absolute Event Rate: 6.4% vs 0%
Intensive blood pressure lowering in hypertensive patients with high arterial stiffness may lead to a greater decline in kidney function.
High arterial stiffness may signal greater kidney risk during BP lowering; leaves open whether it modifies intensive therapy effects.
BACKGROUND Intensive blood pressure (BP) lowering increased acute kidney injury risk, despite cardiovascular benefits. We investigated the association between treatment-induced BP changes and kidney function decline, while accounting for arterial stiffness. METHODS This post‑hoc analysis included 266 patients with hypertension from a 20‑week double‑blind trial treated with calcium-channel blockers. Kidney dysfunction was defined as an estimated glomerular filtration rate (eGFR) <60 ml/min·1.73 m2 or a decrease ≥30% from baseline. Arterial stiffness was measured as brachial-ankle pulse wave velocity (baPWV). RESULTS At baseline, systolic/diastolic BP (mean±SD, 153.2±9.3/91.8±9.5 mmHg) was associated positively (r = 0.20 [95% CI, 0.09 to 0.32]/0.23 [95% CI, 0.11 to 0.34]) with serum creatinine (72.1±16.2 μmol/l), and inversely (r=-0.25 [95% CI, -0.36 to -0.14]/-0.16 [95% CI, -0.28 to -0.04]) with eGFR (91.6±13.8 ml/min·1.73 m2). The associations with clinic systolic BP were weakened with higher baPWV, being observed in tertiles 1 and 2 (r ≥ 0.30 or ≤-0.27), but not tertile 3. After 20 weeks treatment, the incidence of kidney dysfunction was 0%, 4.8%, and 6.4%, respectively, in tertiles 1, 2 and 3 of baPWV (odds ratio for tertile 3 versus tertile 1, 2.23 [95% CI, 0.84-5.95]). In longitudinal analysis, the least square mean change from baseline in eGFR was -3.7 ml/min·1.73 m2 (95% CI, -4.3 to 1.1) in patients within tertile 3 of both baseline baPWV and treatment-induced clinic systolic BP changes. CONCLUSIONS In patients with stiffer arteries, kidney function at baseline was not associated with higher BP, and its decline during follow-up was greater when clinic BP was intensively reduced.
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Wang et al. (2026) conducted an RCT in hypertension (n=266). High arterial stiffness (tertile 3 baPWV) and intensive blood pressure lowering vs. Low arterial stiffness (tertile 1 baPWV) was evaluated on Kidney dysfunction (eGFR <60 ml/min·1.73 m2 or a decrease ≥30% from baseline) (OR 2.23, 95% CI 0.84-5.95). High arterial stiffness (tertile 3 vs 1) in hypertensive patients undergoing blood pressure lowering was associated with a higher incidence of kidney dysfunction (6.4% vs 0%; OR 2.23, 95% CI 0.84-5.95).
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