Role of Intercellular Adhesion Molecule-1, Lymphocyte Function-associated Antigen-1, and Macrophages in ddY Mouse Nephropathy

ddY mouse nephropathy is an animal model of human IgA nephropathy that is characterized by spontaneous IgA deposition in the glomerular mesangium, mesangial cell proliferation, and matrix expansion. We investigated the involvement of intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and macrophages in the pathogenesis of ddY mouse nephropathy. Five mice each underwent urinalysis, light microscopic examination of the kidneys, immunofluorescent detection of immunoglobulins and complement, and immunohistochemical examination for intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and infiltrating macrophages at 5, 10, 20, 30, 40, 50, 60, and 70 weeks of age. Albuminuria was observed from the age of 20 weeks and all mice showed albuminuria by 70 weeks. Histological glomerular damage was significantly related to the appearance of albuminuria (p<0.01). In the glomeruli, positivity for intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1, as well as the number of infiltrating macrophages, were significantly increased in mice with nephropathy compared to pre-nephropathy mice (p<0.01). These results suggest that intercellular adhesion molecule-1, lymphocyte function-associated antigen-1, and infiltrating macrophages are involved in the progression of histological damage in ddY mouse nephropathy.