P155: Correlation of Soluble Receptor for Advanced Glycation End Products and S100–A1 on Arterial Stiffness in Normotensive Patients with Diabetes

Abstract

Background

Accumulation of advanced glycation end products (AGEs) are involved in several pathophysiological processes in the vessel wall, that may cause premature atherosclerosis and arterial stiffening (1). A soluble form of RAGE (sRAGE), which is a splice variant of full-length RAGE has been considered to be protective against diseases originating from RAGE activation since sRAGE can bind and sequester RAGE ligands and reduce RAGE activation (2). S100A1 is the most abundant calcium-binding protein in myocardial tissue and is a major determinant of cardiac function. This circulating ligand of the RAGE is known as a pro-inflammatory factor in diabetes. Aberrant expression levels of S100A1 surfaced as molecular key defects, driving the pathogenesis of cardiovascular diseases (3).

Objective

This study was design to explore the relationship between serum levels of sRAGE and S100A1 on arterial stiffness in non-hypertensive patients with diabetes.

Methods

Using a cross-sectional design, a total of 20 non-hypertensive patients with diabetes were recruited. A fasting blood sample, medical history and arterial stiffness parameters were collected.

Results

In bivariate analysis, sRAGE positively correlated with time evolution of diabetes (r = 0.503, p < 0.024) and negatively correlated with systolic (r = −0.457, p = 0.043) and diastolic blood pressure (r = −0.527, p = 0.017). S100A1 positively correlated with creatinine (r = 0.724, p< 0.000) and negatively correlated with peripheral and central hemodynamics, including augmentation index (r = −0.469, p = 0.037), as shown in Table 2.

Table 2 Correlation of sRAGE with metabolic, hemodynamic and arterial stiffening variables.

Conclusion

This study shows a significant correlation of serum sRAGE and S100–A1 on peripheral and central hemodynamics in non-hypertensive diabetic patients.