suPAR as an Inflammatory and Preclinical Atherosclerotic Marker in Hypovitaminosis D

The mechanistic link between inflammation and atherosclerosis highlights the critical role of immune modulation in cardiovascular disease. The soluble urokinase plasminogen activator receptor (suPAR), an immune-derived factor, has recently emerged as a non-specific inflammatory marker across chronic diseases and infections. All cells within the atherosclerotic arterial wall can express uPAR and release urokinase, which plays a key role in the etiology of atherosclerosis. Hypovitaminosis D and dyslipidemia are well-recognized risk factors for atherosclerosis; however, the relationship between plasma vitamin D levels and suPAR in apparently healthy individuals has not yet been fully characterized. This study aimed to explore the utility of suPAR as a potential marker of preclinical atherosclerosis and systemic inflammation in the context of hypovitaminosis D. Ninety apparently healthy individuals aged 25–55 years were categorized into three groups (n = 30 each) based on plasma vitamin D levels: sufficient, insufficient, and deficient. The deficient group was further subdivided into moderately and severely deficient subgroups. Lipid profile was assessed spectrophotometrically, C-reactive protein (CRP) and suPAR by enzyme-linked immunosorbent assay (ELISA), and vitamin D by electrochemiluminescence immunoassay (ECLIA). The neutrophil-to-lymphocyte ratio (NLR) was derived from complete blood count data. suPAR levels were significantly elevated in the vitamin D-deficient group compared to the insufficient and sufficient groups (p < 0.01 and p < 0.001, respectively). Severe vitamin D deficiency was associated with the highest suPAR levels and significant elevations in atherogenic indices, including TC/HDL-C and non-HDL cholesterol. A progressive and significant rise in inflammatory biomarkers, CRP, NLR, and suPAR, was observed across the spectrum from vitamin D sufficiency to deficiency. In conclusion, elevated suPAR levels may serve as an early indicator of vascular inflammation and preclinical atherogenesis in individuals with vitamin D deficiency, supporting its potential utility as a biomarker for subclinical cardiovascular risk stratification.