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Mannose-Binding Lectin and Mortality in Type 2 Diabetes
Troels Krarup Hansen, MD, PhD;
Mari-Anne Gall, MD, DMSc;
Lise Tarnow, MD, DMSc;
Steffen Thiel, PhD;
Coen D. Stehouwer, MD, PhD;
Casper G. Schalkwijk, MD, PhD;
Hans-Henrik Parving, MD, DMSc;
Allan Flyvbjerg, MD, DMSc
Arch Intern Med. 2006;166:2007-2013.
Background Inflammation and complement activation initiated by mannose-binding lectin (MBL) may be implicated in the pathogenesis of diabetic vascular complications. We evaluated the relationship between serum MBL and mortality and development of albuminuria in type 2 diabetes.
Methods Levels of MBL and C-reactive protein (CRP) were measured at baseline in 326 patients with type 2 diabetes who attended the Steno Diabetes Center, Gentofte, Denmark, for control. Urinary albumin excretion was determined annually, and the vital status of all patients was traced after more than 15 years of follow-up.
Results During follow-up, 169 patients died. The risk of dying was significantly higher among patients with MBL levels greater than or equal to 1000 µg/L than among patients with levels less than 1000 µg/L (hazard ratio, 1.5; 95% confidence interval, 1.1-2.1; P = .005). After adjustment for known confounders, MBL remained a significant risk factor for death from any cause. It added to the predictive power of CRP, and mortality was significantly higher among patients with both high MBL ( 1000 µg/L) and high CRP (above the median, 3.6 mg/L) levels than among patients with both low MBL and low CRP levels (hazard ratio, 2.7; 95% confidence interval, 1.7-4.3; P<.001). Normoalbuminuric patients with both high MBL and high CRP levels at baseline had a significantly increased risk of developing microalbuminuria or macroalbuminuria compared with patients with both low MBL and low CRP levels (hazard ratio, 2.6; 95% confidence interval, 1.5-4.4; P<.001).
Conclusion In patients with type 2 diabetes, measurements of MBL alone or in combination with CRP can provide prognostic information on mortality and the development of albuminuria.
Author Affiliations: Immunoendocrine Research Unit, Medical Department M and Medical Research Laboratories, Aarhus University Hospital, Aarhus, Denmark (Drs Hansen and Flyvbjerg); Steno Diabetes Center, Gentofte, Denmark (Drs Gall, Tarnow, and Parving); Department of Medical Microbiology and Immunology (Dr Thiel) and Faculty of Health Science (Drs Parving and Flyvbjerg), University of Aarhus; and Department of Medicine, University Hospital Maastricht and Maastricht University, Maastricht, the Netherlands (Drs Stehouwer and Schalkwijk).
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