Increased syndecan-1 in serum is related to early nephropathy in type 1 diabetes mellitus patients

Abstract

To the Editor: Hyperglycaemia is associated with increased inflammatory activity, endothelial dysfunction and microvascular complications in patients with type 1 diabetes mellitus. Low-grade inflammation and changes in functions of different constituents of the capillary wall may contribute to the development of complications. The endothelium is covered by a protective glycocalyx consisting of proteoglycans, hyaluronan, glycoproteins and plasma proteins. The transmembrane proteoglycan syndecan-1 is a component of this cell coat. Through its glycosaminoglycan chains, syndecan-1 has the ability to bind numerous ligands and by such interactions to modulate important cellular functions like receptor binding and regulation of inflammation [1]. The syndecan-1 ectodomain can be released from the endothelial cell surface by a highly regulated proteolytic cleavage at a juxtamembrane site of the protein core. Syndecan-1 concentrations found in sera from healthy individuals are low. Shed syndecan-1 levels are often increased in tissue injury and certain cancers. In this study we tested for associations between early kidney damage, as evidenced by persistent microalbuminuria, and shedding of syndecan-1, measured by determining serum concentrations of soluble syndecan-1 in patients with type 1 diabetes mellitus. In an initial study, patients with type 1 diabetes mellitus were recruited from Aker University Hospital and nearby paediatric Departments [2]. The inclusion criteria in this study were persistent microalbuminuria, defined as an AER between 15 and 200 μg/min in at least two out of three overnight urine samples taken during 1 year, and diabetes