Sialic acid expression in normal and diseased human kidney.

Three sialic acid-specific lectins, Tritrichomonas mobilensis (TML) (without linkage preference), Maackia amurensis leukoagglutinin (MAL) (alpha2,3) and Sambucus nigra agglutinin (alpha2,6 linkage-specific), were used for detection of sialylated glycoconjugates in normal and diseased human kidneys. Normal kidneys demonstrated strong podocyte positivity of alpha2,3 linked sialic acid and weaker sialic acid expression on capillary endothelium, which was alpha2,6 linked. Renal biopsies (45) representing a variety of diseases, e.g. minimal change disease, membranous, membranoproliferative glomerulonephritis, tubulointerstitial nephrosis or diabetic glomerulopathy showed increased sialic acid expression in glomerular capillaries, Bowman's capsule epithelium and on podocytes. In several different kidney diseases the glomerular endothelium expressed also alpha2,3 linked sialic acid along with increased TML-positivity of epithelial cells related to alpha2,6 linked sialic acid. No difference in sialic acid linkage expression was observed in the tubules, which expressed putative alpha2,6 linked sialic acid on the luminal surface of cells distal to the descending limb of Henle's loop. The study did not show changes characteristic of specific diseases. Rather, increased sialic acid expression on glomerular endothelium and podocytes was linked to a variety of pathological changes. It is assumed that changes in sialysation of glycoconjugates in the glomeruli represent nonspecific changes and do not reflect fundamental pathogenetic features of renal diseases.