Background The etiology of steroid-resistant nephrotic syndrome, which manifests as FSGS,
is not completely understood. Aberrant glycosylation is an often underestimated factor for
pathologic processes, and structural changes in the glomerular endothelial glycocalyx have
been correlated with models of nephrotic syndrome. Glycans are frequently capped by sialic
acid (Sia), and sialylation's crucial role for kidney function is well known. Human podocytes
are highly sialylated; however, sialylation's role in podocyte homeostasis remains unclear …