Endothelial dysfunction and low-grade inflammation and the progression of retinopathy in Type 2 diabetes

Aims To study whether microalbuminuria, endothelial dysfunction and low‐grade inflammation are associated with the presence and progression of diabetic retinopathy. Methods Patients with Type 2 diabetes (n = 328) attending a diabetes clinic were followed for 10 years and examined annually during the last 7 years. Retinopathy was assessed after pupillary dilatation by direct ophthalmoscopy (baseline) and two‐field 60° fundus photography (follow‐up). Urinary albumin excretion, and markers of endothelial function (von Willebrand factor, tissue‐type plasminogen activator, soluble E‐selectin (sE‐selectin), and soluble vascular cell adhesion molecule 1) and inflammatory activity (C‐reactive protein and fibrinogen) were determined. Results The prevalence of retinopathy was 33.8%. The median diabetes duration at baseline was 7 years (interquartile range 2–12 years). The highest tertiles of baseline urinary albumin excretion and glycated haemoglobin (HbA1c) were associated with prevalent retinopathy: odds ratio (OR) 95% confidence interval (CI) 2.80 (1.44–5.46) and 2.19 (1.11–4.32), respectively. Progression of retinopathy occurred in 188 patients. The second and third tertiles of baseline sE‐selectin were associated with progression of retinopathy [1.44 (1.04–2.01) and 1.61 (1.19–2.18)] but not independently of HbA1c. None of the other markers was significantly associated with the presence or progression of retinopathy. High baseline HbA1c was significantly associated with progression of retinopathy: 1.65 (1.21–2.25). Conclusions In this population of patients with Type 2 diabetes who attended a diabetes clinic, there was some evidence for a role of endothelial dysfunction in the progression of retinopathy. We could not demonstrate a role for low‐grade inflammation. Our study emphasizes the importance of glycaemic control in the development and progression of retinopathy.