Association of serum 25-hydroxyvitamin D3, fibroblast growth factor-23, and C1q/tumor necrosis factor-related protein-3 with coronary artery calcification in nondialysis chronic kidney disease patients

Abstract

Objective To assess serum 25-hydroxyvitamin D3 (25(OH)D3), fibroblast growth factor 23 (FGF23), and C1q/tumor necrosis factor-related protein-3 (CTRP3) levels in nondialysis chronic kidney disease (CKD) patients and their relationship with coronary artery calcification (CAC). Methods One hundred and twenty-eight patients diagnosed with CKD were selected and all underwent cardiac computed tomography. CAC was assessed using the Agatston score, and coronary artery calcification score (CACs) >10 was identified as CAC. The differences in serum 25(OH)D3, FGF23, and CTRP3 levels between the CAC and non-CAC groups were analyzed. Their correlation with CACs was assessed by Spearman’s analysis, and logistic regression analysis was used to find risk factors for CAC. Results Compared to the non-CAC group, the CAC group was older (64.21 ± 9.68 years), with a higher percentage of hypertension (93.10%) and diabetes (63.80%) and higher levels of serum CTRP3 [1079.20 (644.4–1567.2) ng/mL]. However, there was no significant difference in serum 25(OH)D3 and FGF23 between these two groups. The high level CTRP3 group had a higher prevalence of CAC (61.5%). Logistic regression results showed that age, diabetes, decreased 25(OH)D3 (odds ratio (OR) = 0.95, p = .030) and high levels of CTRP3 (OR = 3.19, p = .022) were risk factors for CAC in nondialysis CKD patients. Conclusions Serum CTRP3 levels progressively increased with the progression of kidney disease, while 25(OH)D3 levels progressively decreased. Decreased 25(OH)D3 and high levels of CTRP3 are associated with CAC in patients with nondialysis CKD.

Exploring the mediating role of calcium homeostasis in the association between diabetes mellitus, glycemic traits, and vascular and valvular calcifications: a comprehensive Mendelian randomization analysis

“…By quantifying the mediation effect of altered calcium levels, we provide a potential pathway through which glycemic control may influence CAC and CAVS. This aligns with research showing that disrupted calcium metabolism in diabetes and chronic kidney disease patients contributes to vascular calcification [ 37 ]. Notably, decreased serum levels of 25OHD have been linked to increased vascular calcification risks, further substantiated by findings associating low vitamin D levels with poor cardiovascular outcomes [ 37 ].…”

“…This aligns with research showing that disrupted calcium metabolism in diabetes and chronic kidney disease patients contributes to vascular calcification [ 37 ]. Notably, decreased serum levels of 25OHD have been linked to increased vascular calcification risks, further substantiated by findings associating low vitamin D levels with poor cardiovascular outcomes [ 37 ]. However, in our study, calcium levels partially mediated the impact of T2DM on both types of calcifications, while 25OHD did not exhibit a mediation effect.…”

“…Our findings do not establish a direct causal relationship between FGF23 levels and cardiovascular calcifications in the general population. This discrepancy underscores the complexity of metabolic interactions in cardiovascular calcifications and highlights the potential for differential impacts across patient populations with varying degrees of renal function and metabolic health [ 37 ]. A quantitative measure is provided by the mediation effects observed for calcium on the relationship between T2DM and both types of calcifications.…”