The kidneys are responsible for removing waste products from the blood and keeping protein molecules in the circulation. Normally very little protein is lost from the kidneys into the urine and protein loss is an early sign of kidney disease. There are an increasing number of people worldwide with protein losing kidney disease however there are limited treatment options. The research outlined in this proposal will look into the factors which allow the kidneys to lose protein molecules into the urine and what is involved in the development of protein losing kidney diseases so that it will be possible to consider ways in which new treatment could stop or even reverse kidney injury
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Registered Charity in England and Wales (505256)
Protein losing kidney disease affects both adults and children with an increasing worldwide incidence linked to the increase in obesity and type 2 diabetes. In many patients there is a relentless progression to kidney failure and the annual worldwide cost of managing these patients is ¬£55 billion. Targeted treatment of early kidney injury is a goal of the research community; however before such treatments are developed, it is necessary to understand the basic underlying mechanisms. The study of protein losing kidney disease in children has led to important developments in our understanding of the underlying mechanisms of the disease. Such discoveries have highlighted the importance of glomerular podocytes which are specialised epithelial cells with large cell bodies and foot processes which form a mesh like covering over the glomerular capillaries, which are the first place where urine is formed in the kidney and filters fluid from the blood. The space between adjacent podocyte foot processes is spanned by a slit diaphragm formed by several proteins including podocin and nephrin. We now understand that the complex of proteins connecting adjacent podocytes is critical for maintaining the integrity of the glomerular filtration barrier. Although evidence is evolving, there are still many unanswered questions about the regulation of the slit diaphragm protein complex, podocyte cell to cell and cell to extracellular matrix interactions. Historically, the study of podocytes in vitro has been limited by the loss of original properties in primary cells in culture. This problem has been overcome by the development of conditionally immortalised podocyte cell lines. Professor Moin Saleem at the University of Bristol established a unique resource of conditionally immortalised human podocytes. With this proposed research project we have a unique opportunity to use this valuable resource of cells and to interrogate podocyte interactions with the extracellular matrix in the setting of a world leading centre for cell matrix research. The research will look into podocytes proteins to determine what factors are needed to maintain normal podocyte function to prevent the loss of protein into the urine which leads to kidney disease so that it will be possible to consider ways in which new treatment could stop or even reverse kidney injury. The budget for the investigation into podocyte proteins in proteint losing kidney disease and the factors involved in why protein is lost into the urine will be ¬£22,200 over two years
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