Glyceraldehyde-3-phosphate dehydrogenase of induces infection-related glomerulonephritis .

Infection-related glomerulonephritis (IRGN) was previously thought to be due mostly to species, but is now known to be caused by a variety of other pathogens. Nephritis-associated plasmin receptor (NAPlr) was originally isolated from group A streptococci as the protein responsible for acute poststreptococcal glomerulonephritis, and was shown to be identical to streptococcal glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Here, we describe a 7-year-old boy diagnosed with IRGN presenting with acute nephritic syndrome. Laboratory data revealed a significant increase in serum anti- antibody titer. Renal biopsy revealed diffuse global endocapillary proliferation and cellular crescents in 5/43 glomeruli examined. Although antistreptolysin O antibody titer and serum complement C3 level were within the respective normal ranges, glomeruli showed positive staining for NAPlr and upregulation of plasmin activity. In addition, positive staining for NAPlr in the glomeruli was abolished by preabsorption of anti-NAPlr antibody with recombinant GAPDH. Western blotting analysis revealed anti-NAPlr antibody reactivity with a band at around the predicted size of GAPDH in the protein isolate of (37 kDa). Furthermore, immobilized GAPDH bound to anti-NAPlr antibody as well as plasmin in vitro. These data suggest that GAPDH has a function similar to streptococcal GAPDH (NAPlr) and may induce plasmin-related glomerular damage in IRGN. NAPlr could be a marker of glomerulonephritis related to infection not only by streptococci but also by &.