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Updated: May 23, 2026

Assessment of Vascular Function in Patients With Chronic Kidney Disease
Published on: June 16, 2014
Vitamin D deficiency, CD4+CD28null cells and accelerated atherosclerosis in chronic kidney disease
Ashok Kumar Yadav1, Debasish Banerjee, Anupam Lal
1Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Insights
Vitamin D deficiency is linked to atherosclerosis in chronic kidney disease (CKD) patients. Lower vitamin D levels correlate with inflammation and abnormal T cells, contributing to cardiovascular disease risk in CKD.
Area of Science:
- Nephrology
- Cardiology
- Immunology
Background:
- Cardiovascular disease (CVD) is a primary cause of mortality in chronic kidney disease (CKD) patients.
- The specific role of vitamin D in CVD development within the CKD population remains unclear.
- Investigating the interplay between vitamin D, immune cells, inflammation, and atherosclerosis is crucial for CKD management.
Purpose of the Study:
- To evaluate the relationship between 25-hydroxyvitamin D levels, T helper cell subsets (CD4+CD28null), systemic inflammation (hsCRP), and atherosclerosis (CCA-IMT) in CKD patients.
- To determine if vitamin D deficiency is associated with preclinical atherosclerotic changes in individuals with stage 4-5 non-dialysis CKD.
- To explore potential links between vitamin D metabolism, T cell modulation, and atherosclerosis development in CKD.
Main Methods:
- A cross-sectional study involving 101 stage 4-5 non-dialysis CKD patients and 40 healthy controls.
- Measurement of common carotid artery intima media thickness (CCA-IMT) via ultrasound.
- Quantification of serum 25(OH) vitamin D, hsCRP, and circulating CD4+CD28null T cells using ELISA and flow cytometry.
Main Results:
- CKD patients exhibited significantly higher CCA-IMT, hsCRP levels, and CD4+CD28null cell frequency compared to controls.
- CKD subjects had markedly lower 25(OH) vitamin D levels.
- Serum 25(OH) vitamin D showed a strong inverse correlation with CCA-IMT and correlated with CD4+CD28null cell frequency and hsCRP in CKD patients. Multiple regression analysis identified 25(OH) vitamin D, diabetes, and CD4+CD28null cell frequency as independent predictors of IMT.
Conclusions:
- Vitamin D deficiency, heightened systemic inflammation, and an increased frequency of CD4+CD28null T lymphocytes are associated with preclinical atherosclerosis in the CKD population.
- These findings suggest a potential link between impaired vitamin D metabolism and aberrant T cell function, both contributing to atherosclerosis in CKD.
- Targeting vitamin D supplementation and immune modulation may offer therapeutic strategies to mitigate cardiovascular risk in CKD patients.
Aim:
Cardiovascular disease (CVD) is the leading cause of death among chronic kidney disease (CKD) patients. The role of vitamin D remains controversial in this process. We evaluated the relationship between 25-hydroxyvitamin D, abnormal T helper cells (CD4+CD28null cells), systemic inflammation and atherosclerosis in CKD patients.
Methods:
A total of 101 stage 4-5 non-dialysis CKD patients and 40 healthy controls were studied. Common carotid artery intima media thickness (CCA-IMT) was measured with an ultrasound system. 25(OH) vitamin D and highly sensitive C-reactive protein (hsCRP) were measured in serum by enzyme linked immunosorbent assay. The frequency of circulating CD4+CD28null cells was evaluated by flowcytometry.
Results:
CKD subjects exhibited higher CCA-IMT (0.71 ± 0.01 vs 0.56 ± 0.01 mm, P < 0.0001), hsCRP (90.7 ± 5.8 vs 50.1 ± 8.6 µg/mL, P < 0.0001), CD4+CD28null cell frequency (9.1 ± 0.9 vs 3.6 ± 0.5%, P < 0.0001) and lower 25(OH) vitamin D levels (17.9 ± 1.9 vs 26.9 ± 3.5 ng/mL, P < 0.0001). In CKD subjects, serum 25 (OH) vitamin D level showed a strong inverse correlation with CCA-IMT (r = -0.729, P < 0.0001) and correlated with CD4+CD28null cell frequency (r = -0.249, P = 0.01) and hsCRP (r = -0.2, P = 0.047). We also noted correlation of IMT with patient age (r = 0.291, P = 0.004) and CD4+CD28null cells (r = 0.34, P = 0.001). On multiple regression analysis, 25(OH) vitamin D level, diabetic status and CD4+CD28null cell frequency exhibited independent association with IMT in CKD subjects.
Conclusions:
Vitamin D deficiency, inflammatory activation and higher frequency of CD4+CD28null T lymphocyte population correlate with preclinical atherosclerotic changes in CKD population. These findings suggest possible linkage between vitamin D metabolism and T cell modulation - abnormalities that may contribute to development of atherosclerosis in CKD.
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