Association Between Ankle-Brachial Index and Coronary Artery Calcification Score in Patients Beginning Hemodialysis

Patients initiating hemodialysis (HD) face a markedly increased risk of cardiovascular disease (CVD). The ankle-brachial index (ABI) is a simple, non-invasive marker reflecting distinct vascular calcification patterns: low ABI indicates intimal arterial calcification (IAC), while high ABI may reflect medial arterial calcification (MAC). Coronary artery calcium score (CACS), measured by computed tomography, represents coronary atherosclerosis but does not distinguish between IAC and MAC. Although several studies have examined ABI–CACS associations in maintenance dialysis, evidence at the time of HD initiation remains limited. This study aimed to clarify the relationship between ABI and CACS in patients at the start of HD.

We conducted a single-center, cross-sectional study including 204 patients who underwent both ABI measurement and coronary CT within 30 days of HD initiation between November 2013 and December 2023. Patients with ischemic heart disease or prior peritoneal dialysis were excluded. Participants were categorized into three groups: low ABI (≤0.90), normal ABI (0.91–1.30), and high ABI (>1.30). CACS was compared across ABI groups using the Wilcoxon rank-sum test. Restricted cubic spline (RCS) models with three knots were used to evaluate nonlinear associations between ABI and log-transformed CACS. Logistic regression was applied to identify factors associated with high CACS (>400), adjusting for age, sex, diabetes, BMI, smoking history, estimated glomerular filtration rate (eGFR), serum albumin, C-reactive protein (CRP), calcium, phosphate, and statin use. Subgroup analyses were performed by sex and diabetes status.

Median CACS values were 930.5 (IQR 159.3–2241.1) for the low ABI group, 315.7 (58.5–1046.6) for the normal ABI group, and 54.3 (0.0–413.5) for the high ABI group. Compared with the normal ABI group, CACS was significantly higher in the low ABI group (p=0.037) and lower in the high ABI group (p=0.002). RCS analysis demonstrated a nonlinear, inverse relationship between ABI and CACS, with a steeper decline beginning around an ABI of 1.1–1.2. After adjustment, the spline curve in the low ABI range shifted downward compared with the unadjusted model. In logistic regression, low ABI was associated with high CACS in the unadjusted model (odds ratio [OR] 2.74, p=0.029), but this association became non-significant after full adjustment (adjusted OR 1.29, p=0.651). High ABI showed consistently lower odds of high CACS (unadjusted OR 0.48, p=0.070; adjusted OR 0.41, p=0.067), though not statistically significant. Subgroup analyses by sex and diabetes status revealed consistent directional trends, and no significant interactions were observed.

Among patients at the initiation of HD, low ABI (≤0.9) was associated with higher CACS, but this association was attenuated after adjustment, suggesting that it was largely explained by age and other comorbid factors. In contrast, high ABI (>1.3) consistently showed lower CACS across models. Although the mechanism remains speculative, one possible explanation is that high ABI may reflect a distinct vascular phenotype with delayed progression of medial arterial calcification from peripheral to coronary arteries.