It has previously been shown that MBL-mediated complement activation is associated with IgA nephropathy and Henoch-Schonlein purpura nephritis [17, 19], and our group have previously shown that there is a clear association between high serum levels of MBL and increased risk of developing microalbuminuria and diabetic nephropathy [7, 26, 27]. The gene discussed is MBL2; the disease is IgA glomerulonephritis.