CIRCULATING LEUKOCYTE-ENDOTHELIAL ADHESION MOLECULES IN IGA NEPHROPATHY

There is accumulating evidence that leukocyte-endothelial adhesion mol ecules are important in inflammatory injury in being involved in the p rimary step of entrapment and migration of leukocytes to the site of i nflammation. We have used an antigen capture ELISA to measure the leve ls of circulating intercellular adhesion molecule-1 (cVCAM-1), vascula r cell adhesion molecule-1 (cVCAM-1) and E selectin (cE selectin) in t he peripheral blood of 33 patients with IgA nephropathy (IgAN) during clinical quiescence and 24 healthy controls. The serum levels of cICAM -1 and E selectin in IgA-nephritic patients were not different from th at of healthy controls but the cVCAM-1 level was significantly elevate d in IgAN despite a lack of clinical activity (p=0.008). The different ial rise of circulating leukocyte-endothelial adhesion molecules in Ig AN probably reflects the origins and nature of these molecules as well as the specific immunological profile of IgAN. There was no correlati on between the levels of these three circulating adhesion molecules. W hen the patients with IgA nephropathy were stratified according to the severity of their glomerular and interstitial lesions, there was an a pparent increase in cE selectin and cVCAM-1 associated with increased histopathologic grading. The changes in endothelial adhesion molecules during clinical exacerbation were studied in 10 patients. Coinciding with synpharyngitic macrohematuria, there was a significant rise of cV CAM-1 and cE selectin (p=0.046 and p=0.016, respectively) but no simil ar rise was observed in cICAM-1. Though probably of limited diagnostic significance, our findings tend to support the role of T lymphocyte i n the immunopathogenesis in IgAN and also indirectly reflect the activ e interaction between neutrophils/lymphocytes and vascular endothelial cells during the clinical exacerbation in IgAN.