Association of serum 25-hydroxyvitamin D levels with indicators of target organ damage in patients with diabetes: a cross-sectional study.
To assess serum 25-hydroxyvitamin D [25(OH)D] in relation to indicators of target organ damage in patients with diabetes.
This analysis included 372 adults with diabetes who underwent serum 25(OH)D testing in the Department of Endocrinology at Jen Ching Memorial Hospital from January 1 to December 31, 2025. Data on demographic characteristics, medical history, laboratory parameters, carotid ultrasonography, and electrophysiological examinations were collected. We performed multivariable regression models to examine the associations of serum 25(OH)D levels with peripheral nerve dysfunction, carotid plaque, urinary microalbumin (mALB), cerebral infarction, and coronary heart disease (CHD). Restricted cubic spline (RCS), threshold effect, and sensitivity analyses were further employed.
Serum 25(OH)D was inversely associated with peripheral nerve damage and carotid plaque. After adjustment for all prespecified covariates, the corresponding odds ratios were 0.941 (95% CI, 0.905-0.976; P = 0.001) and 0.942 (95% CI, 0.906-0.977; P = 0.002), respectively. Serum 25(OH)D levels were also inversely associated with log-transformed mALB (β = -0.035, 95% CI, -0.057 to -0.013; P = 0.002). In continuous-variable models, higher serum 25(OH)D was additionally associated with lower odds of cerebral infarction (OR = 0.896, 95% CI, 0.816-0.971; P = 0.013) and CHD (OR = 0.902, 95% CI, 0.835-0.966; P = 0.006) after full adjustment. RCS and exploratory threshold analyses suggested nonlinear associations of serum 25(OH)D with peripheral nerve damage and mALB. Sensitivity analyses yielded consistent results.
Among patients with diabetes, lower serum 25(OH)D levels were associated with peripheral nerve damage, carotid plaque, and higher mALB levels. These findings support an association between serum 25(OH)D and indicators of diabetes-related target organ damage, but prospective studies are needed to clarify the temporal and clinical significance of these associations.
This analysis included 372 adults with diabetes who underwent serum 25(OH)D testing in the Department of Endocrinology at Jen Ching Memorial Hospital from January 1 to December 31, 2025. Data on demographic characteristics, medical history, laboratory parameters, carotid ultrasonography, and electrophysiological examinations were collected. We performed multivariable regression models to examine the associations of serum 25(OH)D levels with peripheral nerve dysfunction, carotid plaque, urinary microalbumin (mALB), cerebral infarction, and coronary heart disease (CHD). Restricted cubic spline (RCS), threshold effect, and sensitivity analyses were further employed.
Serum 25(OH)D was inversely associated with peripheral nerve damage and carotid plaque. After adjustment for all prespecified covariates, the corresponding odds ratios were 0.941 (95% CI, 0.905-0.976; P = 0.001) and 0.942 (95% CI, 0.906-0.977; P = 0.002), respectively. Serum 25(OH)D levels were also inversely associated with log-transformed mALB (β = -0.035, 95% CI, -0.057 to -0.013; P = 0.002). In continuous-variable models, higher serum 25(OH)D was additionally associated with lower odds of cerebral infarction (OR = 0.896, 95% CI, 0.816-0.971; P = 0.013) and CHD (OR = 0.902, 95% CI, 0.835-0.966; P = 0.006) after full adjustment. RCS and exploratory threshold analyses suggested nonlinear associations of serum 25(OH)D with peripheral nerve damage and mALB. Sensitivity analyses yielded consistent results.
Among patients with diabetes, lower serum 25(OH)D levels were associated with peripheral nerve damage, carotid plaque, and higher mALB levels. These findings support an association between serum 25(OH)D and indicators of diabetes-related target organ damage, but prospective studies are needed to clarify the temporal and clinical significance of these associations.