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Association Between Mannose-Binding Lectin and Vascular Complications in Type 1 Diabetes

¹ Immunoendocrine Research Unit, Medical Department M and Medical Research Laboratories, Aarhus University Hospital, Aarhus, Denmark
² Steno Diabetes Center, Gentofte, Denmark
³ Department of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark
⁴ Regional Centre for Blood Transfusion and Clinical Immunology, Aalborg Hospital, Aalborg, Denmark
⁵ Institute of Cardiovascular Research, Vrije Universiteit Medical Centre, Amsterdam, the Netherlands
⁶ Faculty of Health Science, University of Aarhus, Aarhus, Denmark

Complement activation and inflammation have been suggested in the pathogenesis of diabetic vascular lesions. We investigated serum mannose-binding lectin (MBL) levels and polymorphisms in the MBL gene in type 1 diabetic patients with and without diabetic nephropathy and associated macrovascular complications. Polymorphisms in the MBL gene and serum MBL levels were determined in 199 type 1 diabetic patients with overt nephropathy and 192 type 1 diabetic patients with persistent normoalbuminuria matched for age, sex, and duration of diabetes, as well as in 100 healthy control subjects. The frequencies of high- and low-expression MBL genotypes were similar in patients with type 1 diabetic and healthy control subjects. High MBL genotypes were significantly more frequent in diabetic patients with nephropathy than in the normoalbuminuric group, and the risk of having nephropathy given a high MBL genotype assessed by odds ratio (OR) was 1.52 (1.02–2.27, P = 0.04). Median serum MBL concentrations were significantly higher in patients with nephropathy than in patients with normoalbuminuria: 2,306 µg/l (interquartile range [IQR] 753–4,867 µg/l) vs. 1,491 µg/l (577–2,944 µg/l), P = 0.0003. In addition, even when comparing patients with identical genotypes, serum MBL levels were higher in the nephropathy group than in the normoalbuminuric group. Patients with a history of cardiovascular disease had significantly elevated MBL levels independent of nephropathy status (3,178 µg/l [IQR 636–5,231 µg/l] vs. 1,741 µg/l [656–3,149 µg/l], P = 0.02). The differences in MBL levels between patients with and without vascular complications were driven primarily by pronounced differences among carriers of high MBL genotypes (P < 0.0001). Our findings suggest that MBL may be involved in the pathogenesis of micro- and macrovascular complications in type 1 diabetes, and that determination of MBL status might be used to identify patients at increased risk of developing these complications.

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