مشخصات پژوهش

Chronic kidney disease (CKD) is a major global health problem characterized by progressive loss of renal function and disturbances in calcium–phosphate metabolism. Vitamin D deficiency is highly prevalent among CKD patients, resulting from impaired renal hydroxylation and reduced vitamin D receptor (VDR) activation. Low vitamin D status is linked to mineral bone disorder (CKD-MBD), secondary hyperparathyroidism, cardiovascular risk, and inflammation. The VDR gene encodes a nuclear receptor that mediates the biological actions of calcitriol. Genetic polymorphisms in the VDR gene, particularly FokI (rs2228570) and BsmI (rs1544410), have been shown to influence vitamin D metabolism, receptor activity, and disease susceptibility. Variations in these loci may contribute to differences in serum 25-hydroxyvitamin D [25(OH) D] levels and related biochemical abnormalities in CKD patients. However, data from Middle Eastern populations, including Iraq, remain scarce