By clinical observations demonstrating a correlation between anti-dsDNA antibody titre and disease activity. Mesangial cells have a central location in the glomerulus. Not only do mesangial cells provide structural support to adjacent capillary loops but it is well established that they also participate actively in disease mechanisms through the production of inflammatory and fibrotic growth factors. Immunoglobulin deposition in the mesangial area, mesangial cell proliferation, and increase in mesangial matrix are constant features in renal biopsies of active LN. Our group has previously reported that antidsDNA isolated from patients with LN can bind to human mesangial cellsand such 20(S)-Notoginsenoside-R2 binding correlates with clinical Epimedoside-A activity in selected LN patients and could contribute to intra-renal disease pathogenesis. We also observed a correlation between anti-dsDNA and total IgG levels. In this study, we investigated whether the binding activity of total serum IgG and its subclasses to HMC might have clinical correlations in patients with LN, which have implications on the use of such binding as a biomarker for disease monitoring and further exploration into its pathogenic importance. SLE is characterized by the production of various autoantibodies. Previous studies have reported that different autoantibodies can bind to different renal components including podocytes, mesangial cells, endothelial cells, and renal tubular epithelial cells, and it has been speculated that such binding could have a pathogenic role in immune-mediated kidney injury. Mesangial cells are located strategically at the centre of glomeruli and are juxtaposed to the capillary loops. Mesangial immunoglobulin deposition and mesangial cell proliferation are cardinal histological features in LN. Our previous investigations showed that anti-dsDNA antibodies from patients with LN could bind to HMC and trigger cellular responses involved in inflammation and fibrosis, and that such binding correlated with total serum IgG level. The present study sought to investigate the potential clinical correlations of the in vitro findings. Our results showed a clear relationship between disease activity and HMC-binding by total serum IgG and IgG1 in LN, and the degree of binding was significantly increased in LN compared with healthy subjects and patients with non-lupus glomerular diseases. Also, the positive correlation of IgG HMC-binding with antidsDNA level, and negative relationship with C3 level, prompted us to investigate whether HMC-binding index might serve as a biomarker for disease activity monitoring. In this context, previous studies have also found that active LN patients had significantly stronger IgG binding to isolated rat glomeruli in an in vitro assay when compared to SLE patients without nephritis. That HMC-binding index of total IgG or IgG1 was not related to serum creatinine, serum albumin, or proteinuria was not a disadvantage since these clinical parameters represent a summative outcome of both active disease and prior chronic damage and are also subject to modulating factors distinct from the lupus disease process such as hypertensive renal damage. Conventional serological parameters C3 and anti-dsDNA levels have been reported to show sensitivity and specificity of 49�C79% and 
51�C74% respectively in the detection of disease flares. The present results from samples collected serially in LN patients showed that in the majority of cases increased HMC-binding.