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Kidney Week

Abstract: SA-PO0429

Lipid Imbalance and Progression of Coronary Artery Calcification in CKD: A Differential Effect Across CKD Stages and Dialysis Modalities

Session Information

Category: Cardiovascular-Kidney-Metabolic Health

  • 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

  • Tsuruya, Kazuhiko, Nara Kenritsu Ika Daigaku, Kashihara, Nara Prefecture, Japan
  • Yoshida, Hisako, Osaka Koritsu Daigaku, Osaka, Osaka Prefecture, Japan
  • Yamada, Shunsuke, Kyushu Daigaku, Fukuoka, Fukuoka Prefecture, Japan
  • Nakano, Toshiaki, Kyushu Daigaku, Fukuoka, Fukuoka Prefecture, Japan
Background

Vascular calcification is a major complication of chronic kidney disease (CKD) and a strong predictor of cardiovascular outcomes. While CKD-mineral and bone disorder (CKD-MBD) has traditionally been implicated in its pathogenesis, the contribution of lipid-related pathways remains incompletely understood, particularly across different stages and treatment modalities of CKD, including non-dialysis-dependent CKD (ND-CKD), hemodialysis (HD), and peritoneal dialysis (PD).

Methods

Among 258 patients (106 with ND-CKD, 78 on HD, and 74 on PD) who underwent multi-detector computed tomography (MDCT), 187 (92 ND-CKD, 50 HD, and 45 PD) completed follow-up MDCT after 2 years and were included in the analysis. Changes in coronary artery calcification (CAC) scores were evaluated using the difference in square-root-transformed CAC scores (ΔCACS), defined as the difference between baseline and follow-up scans, with negative values truncated to zero. The annual change in CAC score (AC-CACS) was calculated as 365 × ΔCACS divided by the interval days between scans.

Results

The median (interquartile range) ΔCACS over two years and AC-CACS were 2.95 (0–8.02) and 1.46 (0–3.92), respectively. AC-CACS was significantly positively correlated with the low-density lipoprotein-to-high-density lipoprotein cholesterol ratio (L/H ratio). In multivariable linear regression analysis, a higher L/H ratio was independently associated with greater AC-CACS after adjustment for potential confounders, including CKD-MBD-related variables. A significant interaction was observed across patient groups, with a stronger association in PD patients, a modest association in ND-CKD patients, and little to no association in HD patients. In contrast, no significant associations were observed between AC-CACS and CKD-MBD markers, including calcium–phosphate product, whole parathyroid hormone, and fibroblast growth factor 23.

Conclusion

An increase L/H ratio was associated with accelerated progression of CAC in patients with CKD. This association was strongest in PD patients, modest in ND-CKD patients, and absent in HD patients. These findings suggest that lipid-related mechanisms may contribute to vascular calcification in CKD, particularly in PD patients, potentially to a greater extent than CKD-MBD-related pathways.