الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Chronic kidney disease (CKD) is a global public health problem. Cardiovascular diseases (CVD) are the main cause of mortality in CKD patients. Traditional CVD risk factors do not adequately explain this disproportionate increase in risk and the role of non-traditional risk factors such as inflammation, oxidative stress and altered immune function have been explored. The kidney appears to be a major target organ for both the classical and non-classical actions of vitamin D, with the vitamin D receptor being appropriately highly expressed in this site. The non-classical effects of vitamin D may play a relevant role in the mortality and morbidity of patients with CKD, specifically affecting the possible progression of their renal disease and coexisting cardiovascular disease, which is the major cause of death in this population. Deficiency of vitamin D is associated with inflammatory activation, decreased arterial compliance and increased intima-media thickness. Increased inflammation, impaired endothelial function and central arterial stiffness are common in patients with CKD. Atherosclerotic plaques are inflammatory in nature, and the cell infiltrate consists mainly of T cells and macrophages. Both cell populations contribute to the growth and instability of the atherosclerotic lesion. In the early stages, T cells are involved in the initiation and progression of disease, while at the later stage, T cells may actively destabilize the plaque. CD4+ T cells are the dominant T cell population isolated from the atherosclerotic plaque. These T cells secrete proinflammatory cytokines such as IFN-γ and TNF-α and are enriched for CD28null T cells.
Evidence (in vitro & in vivo) suggests that CD4+CD28null T lymphocytes may be involved in the initiation and progression of atherosclerosis, whereas they subsequently contribute to the destabilization of atherosclerotic plaques. CD4+CD28null T cells may destabilize atherosclerotic plaques by several mechanisms. First, their secretion of proinflammatory cytokines such as IFN-γ may activate the local macrophages, promoting their differentiation into foam cells and the release of enzymes such as matrix metalloproteinases Second, the CD4+CD28null T cells may exert direct cytolytic activity against endothelial cells and vascular smooth muscle. Our study aimed to detect a link between 25(OH) vitamin D deficiency, inflammation and CD4+CD28null T-cell expansion, which might contribute to atherosclerosis in CKD subjects. This study was conducted on 40 chronic kidney disease patients and 30 normal individuals who served as control. All studied groups were subjected to the following: Full history taking Physical examination Investigations: Routine investigations: CBC , Kidney function, Serum electrolytes, Measurement of glomerular filtration rate(GFR), Liver function tests, Lipid profile Blood sugar, ECG. Special investigations: Highly sensitive C-reactive protein (hs CRP) by turbidimetry. Detection of expansion CD4+CD28- T lymphocytes by flowcytometry. Assay of 25 OH vitamin D (by ELISA technique).
Radiological investigations Pelvic-abdominal Ultrasound Estimation of common carotid artery intima – media thickness. The present study showed the following:- Serum 25 (OH) vitamin D level in the patients group was significantly lower than that of the controls group. Serum hs-CRP was highly significant higher in the patients group than that of the controls group. The CD4+ CD28 null T cells level in the CKD patients group showed higher levels when compared to the controls group. The CCA-IMT in the patients group was higher than that of the controls group. An association of vitamin D deficiency with inflammatory activation and expansion of the CD4+28null T-cell population, which has been implicated in the genesis of atherosclerosis, where 25 (OH) vitamin D level showed highly significant negative correlation with hs-CRP, CD4+ CD28 null T cells and CCA-IMT. CCA-IMT in CKD subjects was positively correlated with CD4+CD28null T cell frequency and hs-CRP level. In conclusion:- Based on these findings, we suggest that 25 (OH) vitamin D deficiency is associated with inflammatory activation, increased CD4+CD28null T-cell expansion and increased CCA-IMT, a preclinical marker of atherosclerosis in CKD patients