The overarching goal of the Nephrology Research Laboratory is to prevent renal fibrogenesis and improve allograft and patient survival of kidney transplant patients. We investigate the mechanisms of injury to kidney transplants using state-of-the-art techniques in immunology, histology, and molecular biology. The major research areas of our lab are described below.
Pathogenesis of acute and chronic kidney allograft rejection
The main cause of kidney transplants is rejection. A major goal of our lab is to better understand how the immune system causes acute and chronic rejection and damages the transplanted kidney so that effective therapies can be developed. We investigate acute and chronic active antibody-mediated rejection in in vivo models of kidney transplantation.
Role of B cells and B cell survival cytokine (BAFF and APRIL) in promoting the immune response in kidney transplantation
Currently, there are no FDA-approved therapies to treat antibody-mediated rejection. B cells and B cell survival cytokines are major contributors to antibody-mediated rejection in transplantation. B cells and B cell survival cytokines represent innovative therapeutic targets. We are investigating novel targeted therapeutics and genetic strains in B cells, BAFF, and APRIL.
Mechanisms of injury to glomerular endothelial cells
Endothelial cells in the kidney transplant are the first target of the immune system in rejection. We use endothelial cell culture and histology to investigate endothelial injury that occurs during rejection in the kidney transplant.
Role of heat shock protein 27 (HSP27) and NADPH oxidase 2 (Nox2) in kidney fibrogenesis
We use genetically modified straines of HSP27 and Nox2 to understand the pathogenesis of renal fibrogenesis in murine models of obstructive nephropathy, lupus nephritis, calcineurin inhibitor nephrotoxicity, allograft rejection, and ischemia reperfusion injury.