Association of abdominal aortic calcification with cognitive impairment in peritoneal dialysis patients.

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Tác giả: Tingting Bai, Jiajie Cai, Jingjing Li, Zhongxin Li, Conghui Liu, Yanan Shi, Lingju Yue

Ngôn ngữ: eng

Ký hiệu phân loại: 617.559 *Hernias in abdominal region

Thông tin xuất bản: England : BMC nephrology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 686473

 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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