AIMS: Galectin-1 is an endogenous lectin that specifically binds to beta-galactoside structures. It has been associated with developmental mechanisms ranging from differentiation to apoptosis and exerts immunoregulatory functions in autoimmune diseases. The aim was to determine the immunohistochemical expression of galectin-1 in renal biopsy specimens of children with primary idiopathic proteinuric glomerulopathies. METHODS AND RESULTS: We examined 18 children with minimal change disease (MCD), 30 with diffuse mesangial proliferation (DMP) and 11 with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical protocol using a polyclonal antibody directed against galectin-1 was applied. Galectin-1 was detected in renal podocytes in DMP and FSGS cases, while control glomeruli and MCD were negative. Galectin-1 immunoreactivity was found within parietal epithelial cells in patients with FSGS. CONCLUSIONS: These results suggest a possible role for galectin-1 in the pathogenesis of primary glomerulopathies in children as a kind of podocyte-related self-protective activity and probably involvement of epithelial cells of Bowman's capsule in inflammatory processes. Immunohistochemistry using galectin-1 antibodies may further be helpful in histological distinction between MCD and DMP.
AIMS: Galectin-1 is an endogenous lectin that specifically binds to beta-galactoside structures. It has been associated with developmental mechanisms ranging from differentiation to apoptosis and exerts immunoregulatory functions in autoimmune diseases. The aim was to determine the immunohistochemical expression of galectin-1 in renal biopsy specimens of children with primary idiopathic proteinuric glomerulopathies. METHODS AND RESULTS: We examined 18 children with minimal change disease (MCD), 30 with diffuse mesangial proliferation (DMP) and 11 with focal segmental glomerulosclerosis (FSGS). An indirect immunohistochemical protocol using a polyclonal antibody directed against galectin-1 was applied. Galectin-1 was detected in renal podocytes in DMP and FSGS cases, while control glomeruli and MCD were negative. Galectin-1 immunoreactivity was found within parietal epithelial cells in patients with FSGS. CONCLUSIONS: These results suggest a possible role for galectin-1 in the pathogenesis of primary glomerulopathies in children as a kind of podocyte-related self-protective activity and probably involvement of epithelial cells of Bowman's capsule in inflammatory processes. Immunohistochemistry using galectin-1 antibodies may further be helpful in histological distinction between MCD and DMP.