Syndecan-1 can impede leukocyte adhesion to the endothelium by inhibiting the interaction of β2 integrin on leukocytes to ICAM-1 on endothelial cells.
In patients with renal disease including LN, syndecan-1 present on tubular epithelial cells can bind L-selectin and MCP-1, and the degree of binding is associated with leukocyte infiltration (93).
LN patients with active disease have increased serum syndecan-1 level compared to patients in remission and the level correlated with serological and clinical parameters of disease including anti-dsDNA antibody titre, proteinuria, serum creatinine level and both SLEDAI-2K and renal SLEDAI-2K scores (56, 105, 106).
Serum syndecan-1 level was also higher in LN patients with active disease compared to SLE patients with extrarenal manifestations (53, 56) and this may be attributed, at least in part, to a loss of syndecan-1 from the glomerular endothelial glycocalyx and downstream glomerular injury.
Serum syndecan-1 level showed a higher sensitivity rate (85.91%) than anti-dsDNA antibody titre (75.00%) and C3 level (62.07%) in distinguishing patients with active LN from quiescent LN patients, while the specificity rate was comparable between all three markers (86.21%, 91.67% and 96.43% respectively) (53).
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