Renal podocytes are important for glomerular biology and pathology. Podocytes are terminally differentiated cells that line the outer aspect of the glomerular basement membrane. Podocytes therefore form the final barrier to protein loss, which explains why podocyte injury is typically associated with marked proteinuria. Podocytes play a key role in the development and progression of most glomerular diseases including minimal change disease, congenital nephrotic syndrome, familial and secondary forms of focal segmental glomerulosclerosis, diabetic nephropathy, and HIV-associated glomerulopathy.

Podocyte foot processes (FP) and the interposed slit diaphragms (SD) form the final barrier to protein loss. The highly dynamic FP actin cytoskeleton is linked to the SD and proteins regulating podocyte actin dynamics are therefore of critical importance for structural maintenance and sustained function of the glomerular filter.

From the standpoint of progressive glomerular disease, it is important to recognize that if the early structural changes are not reversed, severe and progressive glomerular damage develops. Loss of podocytes is a hallmark of progressive renal disease. Studies in human diabetic nephropathy (type I and II), in the chronic puromycin model of glomerulosclerosis and TGF-beta 1 transgenic mice collectively provided convincing evidence for a correlation between the loss of podocyte and the progression of glomerular diseases.

Research in glomerular biology in the Division of Nephrology is focused on three major topics including the dynamic regulation of the podocyte actin cytoskeleton in renal development and under nephrotic conditions, the role of TGF-beta in podocyte differentiation and apoptosis as well as the downstream effects of HIV-1 infection on podocytes.