1988 Volume 30 Issue 1 Pages 49-58
Helix pomatia agglutinin (HPA) recognizes terminal N-acetyl-D-galactosamine residues, which are "masked" by sialic acid in normal rat glomeruli. Digestion in vitro or in vivo with neuraminidase (NRD) resulted in exposure of HPA receptors on the surface of glomerular endothelial cells (GEN). Experimental glomerulonephritis (GN) was induced by intravenous injection of rabbit-anti-HPA serum (AHPAS) before perfusion, ex vivo perfusion of left kidney with NRD and HPA (perfusate was recovered from the renal vein), reestablishment of blood circu-lation, and intravenous injection of AHPAS after perfusion. 15 minutes after revasculization, accumulation of platelets in the glomeruli was seen and immune deposits containing rabbit IgG, rat C3 and HPA were present in the sub-endothelial space. 2 days later, immune deposits were recognized mainly in the sub-epithelial space in finely granular pattern. 7 days after revasculization, these subepithelial deposits increased in their size and mild GBM thickening was observed. In the rats which were not treated with NRD, immune deposits localized in the mesangium and were not observed in GBM 2 or 7 days after revasculization. In the rats which were not treated with HPA, or in the rats treated with normal rabbit serum instead of AHPAS, no immune deposits were formed. Only the group of rats treated with AI-IPAS, NRD and HPA developed mild to moderate proteinuria. Rat IgG was negative in glomeruli throughout the experiment. These results suggested that this experimental model was characterized by (1) initiation of immune reaction on the surface of GEN, (2) movement of immune deposits across GBM from luminal side to epithelial side. Glomerular filtration pressure, NRD treatment, and mediators from platelets might contribute to the immunopathologic change in this model.
