Endothelial cell–selective adhesion molecule in diabetic nephropathy

Abstract

Endothelial cell-selective adhesion molecule (ESAM) contributes to the integrity of tight junctions and modulates endothelial function. ESAM has been linked to experimental diabetic nephropathy; its soluble fraction is related to atherosclerosis in humans. In this cross-sectional observational study, we describe for the first time serum ESAM in type 2 diabetic patients with different stages of chronic kidney disease (CKD) and its relationship to vascular endothelial growth factor-A (VEGF-A). Materials and methods We included diabetic patients with different stages of CKD and controls. History, laboratory evaluation, serum ESAM and VEGF-A and urinary albumin/creatinine ratio were obtained. Endothelial cell-selective adhesion molecule was higher in non-CKD diabetic patients 13.80 (6.15-18.70) ng/mL (n=45) than controls 7.30 (4.60-9.40) ng/mL (n=48), P=0.001. VEGF-A had a similar pattern: 71.3 (54.75-120.70) vs. 43.20 (30.1-65.90) pg/mL, P<0.0001. ESAM was 10.4 (5.6-17.4) ng/mL in predialysis CKD patients (n=59) and 22.35 (8.55-29.95) ng/mL in dialysis patients (n=36), P<0.001. Patients with glomerular filtration rate (GFR)<15 mL/min had the highest ESAM (P=0.003). ESAM was similar in normoalbuminuric, microalbuminuric and proteinuric patients. ESAM was directly correlated with the duration of diabetes (r(2)=0.048, P=0.009), C-reactive protein (r(2)=0.028, P=0.05), VEGF-A (r(2)=0.040, P=0.01) and inversely with HbA1C (r(2)=0.036, P=0.03), haemoglobin (r(2)=0.062, P=0.005) and albumin (r(2)=0.0·40, P=0.026). In multiple regression diabetes duration, HbA1C and VEGF-A were significant predictors of ESAM. In controls, ESAM was inversely related to VEGF (r(2)=037, P=0.01). Endothelial cell-selective adhesion molecule and VEGF-A are higher in patients with diabetes than in controls. The highest ESAM is found in dialysis patients. ESAM correlates with diabetes duration and control, inflammation and VEGF-A in patients with diabetes, but not in controls.