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Vascular calcification in diabetic foot and its association with calcium homeostasis

Introduction: Vascular calcification (VC), long thought to result from passive degeneration, involves a complex process of biomineralization resembling osteogenesis, frequently observed in diabetes and is an indicator of diabetic peripheral vascular disease with variable implications. Aim and Objective: To study the association between vascular calcification and calcium homeostasis in diabetic patients with foot ulcers without stage 4, 5 chronic kidney disease. Materials and Methods: A total of 74 patients with diabetic foot ulcer were enrolled, and VC was detected by X-ray and Doppler methods. Serum calcium, phosphate, alkaline phosphatase (ALKP), fasting and post-prandial glucose levels, and glycosylated hemoglobin (HbA1C) were recorded. Serum iPTH and 25 (OH) vitamin D were estimated by immune radiometric assay and radioimmunoassay, respectively. Data was analyzed by SPSS 16.0. Results: Vascular calcification was present in 42% of patients. Significant difference in the mean (±SD) of vitamin D, HbA1C, and eGFR was observed in VC +ve compared to VC –ve. There was no significant association of age, duration, BMI, PTH, Ca, PO4, ALKP with that of VC incidence. Severe vitamin D deficiency was more common in VC +ve (51.6%) compared to in VC –ve (18.6%). Sub-group analysis showed that the risk of VC was significantly higher (RR = 2.4, P < 0.05, 95% C.I. = 0.058-2.88) in patients with vitamin D < 10 ng/ml compared to others. Conclusion: Vitamin D deficiency could be a risk for vascular calcification, which possibly act through receptors on vascular smooth muscle cells or modulates osteoprotegerin/RANKL system like other factors responsible for VC in diabetic foot patients.