Abstract
It has recently become clear that initial glomerular injury affects glomerular visceral epithelial cells (also called as podocytes) as important target cells for progression of chronic kidney disease (CKD) and end-stage kidney disease. Podocytes are injured in many human kidney diseases including minimal change disease, focal segmental glomerulosclerosis, diabetic nephropathy, membranous nephropathy and lupus nephritis. Podocytes are highly specialized epithelial cells that cover the outer layer of the glomerular basement membrane (GBM). Podocytes serve as the final barrier to urinary protein loss through the special formation and maintenance of foot-processes and an interposed slit-diaphragm. Chronic podocyte injury may cause podocyte detachment from the GBM, which leads to glomerulosclerosis. The elucidation of podocyte biology during the last 15 years has significantly improved our understanding of the pathophysiologic processes of proteinuria and glomerulosclerosis. In this review, we highlight some of new data including our recent findings for translating podocyte biology into new examinations and therapies for podocyte injury.
