Glomerulonephritis is a common cause of irreversible renal failure leading to the need for dialysis and transplantation. We aim to discover the fundamental causes of these diseases, in addition to the mechanisms that mediate renal inflammation. Our basic research program has used experimental models of glomerulonephritis to explore these mechanisms. In recent years we have dissected the role of the innate immune system and in particular how Toll-like receptors interact with the adaptive immune system and lead to tissue damage. We have also explored the role of specific IgG subclasses and Fc receptors in glomerular inflammation.

We are currently developing a specific interest in one form of glomerulonephritis, namely anti-neutrophil cytoplasmic antibody associated vasculitis (AAV). We are pursuing research based both on experimental models of AAV and on patient samples. Myeloperoxidase (MPO) is one of the major autoantigens in AAV and a model of AAV based on the knockout mouse has been published by others. We are using both this model and other novel systems to dissect both the mechanisms of capillary injury and the origin of autoimmunity in AAV. We are also collecting blood samples from newly presenting patients with AAV in order to examine how their white blood cells differ from controls, and to develop new markers of disease activity.