Ambulatory arterial stiffness index (AASI), derived from ambulatory blood pressure monitoring (ABPM), reflects arterial stiffness via blood pressure fluctuations over 24-hours. AASI correlates with pulse wave velocity, a marker of arterial stiffness and cardiovascular risk. However, data on AASI in pediatric and transplant patients are limited.
A single-center retrospective chart review of pediatric kidney transplant recipients (2017–2023) with post-transplant ABPMs and echocardiograms was performed. Analyses included t-tests, Spearman correlation, and multivariable regression.
The study included 78 patients (mean age 14.9 ± 4.40 years); 50% (n=39) were male, and 86% (n=67) had deceased donor transplants.
Higher AASI associated with wake and sleep systolic HTN compared to those without hypertension on ABPM (Fig 1). AASI was 0.409 ± 0.130 in patients with vs. 0.298 ± 0.117 in those without wake systolic HTN, p = 0.015. Sleep systolic HTN group also had higher AASI, 0.345 ± 0.128 vs. 0.285 ± 0.115 those without HTN, p = 0.048. No significant associations were found between AASI and diastolic hypertension. In multivariable regression, wake SBP remained a significant predictor of AASI (β = 0.396, 95% CI: 0.236–0.554, p = 0.043).
AASI was higher with inadequate (<10%) nocturnal dipping (ND) (mean AASI = 0.328 ± 0.135; n = 55) than in those with adequate (≥10%) ND (0.270 ± 0.078; n = 23), with a trend toward significance (p = 0.075) (Fig 1).  

There was no difference in AASI between those with and without left ventricular hypertrophy (LVH); mean AASI was 0.326 ± 0.135 in the no LVH group (n = 44) and 0.279 ± 0.109 in the LVH group (n = 16) (p = 0.279). Spearman correlation between AASI and LVMI was non-significant (ρ = -0.13, p = 0.34). In multivariable regression, higher AASI was associated with lower odds of LVM (OR = 0.0011, 95% CI: 0.0001–0.58, p = 0.036). Male sex linked to higher odds of LVH (OR = 6.88, 95% CI: 1.56–30.45, p = 0.013), and lower wake systolic percentile to decreased odds of LVH (OR = 0.08, 95% CI: 0.003–0.56, p = 0.021). Age was not significant (p = 0.57).
AASI was associated with systolic HTN and inadequate nocturnal dipping but did not show a strong relationship with LVH or LVMI. The paradoxical link between higher AASI and lower LVMI/LVH may reflect timing of echocardiography relative to ABPM. Longitudinal studies may determine whether persistent AASI elevations contribute to cardiac remodeling and adverse outcomes.