Recently, interesting work was published by Farrar et al. [1] showing the interaction of fucosylated glycoproteins on stressed tubular epithelial cells with collectin-11 leading to complement activation via the lectin route of complement. This elegant work stimulated us to evaluate the dark side (bittersweet taste) of tubulo-interstitial glycans in kidney tissue damage. As will be discussed, glycans not only initiate tubular complement activation but also orchestrate tubulo-interstitial leucocyte recruitment and growth factor responses. In this review we restrict ourselves to tubulo-interstitial damage mainly by proteinuria, ischaemia-reperfusion injury and transplantation, and we discuss the involvement of endothelial and tubular glycans in atypical and Escherichia coli-mediated haemolytic uraemic syndrome. As will be seen, fucosylated, mannosylated, galactosylated and sialylated oligosaccharide structures along with glycosaminoglycans comprise the most important glycans related to kidney injury pathways. Up to now, therapeutic interventions in these glycan-mediated injury pathways are underexplored and warrant further research.
Keywords: complement; glycan; innate immunity; kidney; tissue remodeling; tubulo-interstitium.
© The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.