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Updated: May 12, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Association of abdominal aortic calcification with cognitive impairment in peritoneal dialysis patients
Conghui Liu1, Yanan Shi1, Jiajie Cai1
1Department of Nephrology, Beijing Luhe Hospital, Capital Medical University, NO.82 Xinhua South Road, Tongzhou District, Beijing, 101100, China.
Background:
Patients on peritoneal dialysis (PD) frequently have cognitive impairment, which is linked to a poor prognosis. The purpose of this study was to determine whether abdominal aortic calcification (AAC) may have an impact on PD patients' cognitive function.
Methods:
In this cross-sectional study of 110 PD patients, cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), and AAC severity was quantified via lateral lumbar radiography (Kauppila method). Participants were stratified by AAC severity into high (HAAC; score ≥ 4) and low (LAAC; score < 4) groups.
Results:
Cognitive impairment (MoCA < 26) was present in 65.45% of patients. The HAAC group (71.8% of cohort) exhibited distinct metabolic profiles compared to LAAC: older age (63.2 ± 9.8 vs. 47.4 ± 12.1 years, P < 0.001), higher diabetes prevalence (68.4% vs. 22.6%, P < 0.001), elevated serum phosphorus (1.62 ± 0.45 vs. 1.30 ± 0.42 mmol/L, P < 0.001), and lower diastolic blood pressure (79.2 ± 10.8 vs. 86.6 ± 13.4 mmHg, P = 0.005). Notably, HAAC patients had reduced serum creatinine (898.4 ± 251.9 vs. 1190.7 ± 243.5 µmol/L, P < 0.001) and iPTH levels (142.5 vs. 218.0 pg/mL, P = 0.011), suggesting concurrent mineral bone disorder. Multivariate analysis identified AAC severity (OR = 1.28 per 1-point increase, 95%CI = 1.09-1.50) and age (OR = 1.12/year, 95%CI = 1.06-1.19) as independent predictors of cognitive impairment.
Conclusion:
AAC severity demonstrates a strong, dose-dependent association with cognitive dysfunction in PD patients, independent of traditional risk factors. The combination of elevated phosphorus and suppressed iPTH in high-AAC patients highlights the potential role of mineral metabolism dysregulation in both vascular calcification and neurocognitive decline.
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