期刊
DIABETOLOGIA
卷 57, 期 10, 页码 2201-2207出版社
SPRINGER
DOI: 10.1007/s00125-014-3332-7
关键词
Albuminuria; Complement; Diabetic nephropathy; Ficolin-3; H-ficolin; Type 1 diabetes
资金
- Novo Nordisk Foundation
- Danish Diabetes Academy
- Novo Nordisk Fonden [NNF13OC0003820] Funding Source: researchfish
Aims/hypothesis Increasing evidence links complement activation through the lectin pathway to diabetic nephropathy. Adverse complement recognition of proteins modified by glycation has been suggested to trigger complement auto-attack in diabetes. H-ficolin (also known as ficolin-3) is a pattern recognition molecule that activates the complement cascade on binding to glycated surfaces, but the role of H-ficolin in diabetic nephropathy is unknown. We aimed to investigate the association between circulating H-ficolin levels and the incidence of microalbuminuria in type 1 diabetes. Methods We measured baseline H-ficolin levels and tracked the development of persistent micro- and macroalbuminuria in a prospective 18 year observational follow-up study of an inception cohort of 270 patients with newly diagnosed type 1 diabetes. Results Patients were followed for a median of 18 years (range 1-22 years). During follow-up, 75 patients developed microalbuminuria, defined as a persistent urinary albumin excretion rate (UAER) above 30 mg/24 h. When H-ficolin levels were divided into quartile groups an unadjusted Cox proportional hazards regression model showed a significant association with risk of incident microalbuminuria during follow-up (HR, fourth vs first quartile, 2.45; 95% CI 1.24, 4.85) (p=0.01). This remained significant after adjusting for HbA(1c), systolic blood pressure, smoking and baseline UAER (HR 2.09; 95% CI 1.03, 4.25) (p=0.04). Conclusion/interpretation Our data suggest that high levels of the complement activating molecule H-ficolin are associated with an increased risk of future progression to microalbuminuria in patients with newly diagnosed type 1 diabetes.
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