2011 NephCure Award Recipients
Jeremy Duffield, M.D., Ph.D.
University of Washington
The Role of Pentraxin-2/Serum Amyloid P in preventing glomerulosclerosis and interstitial fibrosis in mouse models of glomerular injury
Fibrosis is the irreversible scarring of tissue due to injury or disease that reduces the ability of organs such as the kidney to function properly. The progression of this condition in FSGS cannot be stopped with traditional medications and may lead to ESRD, requiring dialysis or a kidney transplant for survival. Dr. Duffield is testing the efficacy of a compound called Pentraxin-2 (PTX-2) in mouse models that express two types of glomerular injury. Preliminary studies have found that PTX-2 has an anti-fibrotic effect and may be potentially useful for the treatment and prevention of fibrotic diseases, such as FSGS.
Alessia Fornoni, M.D., Ph.D.
University of Miami
Novel Targets of Rituximab in FSGS
Dr. Fornoni demonstrated that rituximab (a specialized drug primarily used for cancer treatment) can help reduce the percentage of patients with post-transplant recurrence of FSGS to 26 percent, compared with 64 percent for those who did not take the drug. Using kidney biopsies and blood from patients with FSGS, Dr. Fornoni continues to study the mechanism by which rituximab protects podocytes. This may pave the way for the development of a new generation of therapies for recurrent FSGS and for the development of an assay to be used before transplant to identify patients at risk for recurrent FSGS disease.
Peter Mundel, M.D.
Massachusetts General Hospital
Cell and molecular biological analysis of synaptopodin
Determining the mechanisms by which podocytes maintain structural and functional integrity is of critical importance in understanding how to sustain normal glomerular filtration. Previous studies demonstrated that a protein called synaptopodin plays a role in stabilizing the kidney filter. Dr. Mundel is testing how the activation of an enzyme in podocytes (tyrosine kinase Src) changes podocyte cells by degrading synaptopodin leading to proteinuria. His research will provide a better understanding of the biological mechanism underlying the dynamic re-organization of the podocyte in normal and proteinuric kidneys and, in the long term, enable the development of therapies that protect podocytes.