Principal investigator: Abdalla Rifai, PhD
The pathogenesis of IgA nephropathy, the most common form of glomerulonephritis in the world, is still largely unknown. Utilizing an experimental model of IgA immune complex-mediated nephropathy, our laboratory is focused on elucidating in vivo the cellular and molecular mechanisms that are associated with glomerular IgA immune deposits. Identification of the early molecular events induced by glomerular IgA deposition includes establishing a profile of proinflammatory cytokines, chemokines and growth factors that initiate renal tissue injury.
In addition, differential expression of extracellular matrix genes involved in the progressive stages of renal fibrosis is being characterized in a chronic model of this disease. This approach promises to provide an opportunity to develop rational therapies for IgA nephropathy.