Pedicels interdigitate, thereby giving rise to thin gaps called filtration slits. The slits are covered by slit diaphragms which are composed of a number of cell-surface proteins including nephrin, podocalyxin, and P-cadherin, which restrict the passage of large macromolecules such as serum albumin and gamma globulin and ensure that they remain in the bloodstream. Proteins that are required for the correct function of the slit diaphragm include nephrin, NEPH1, NEPH2, podocin, CD2AP. and FAT1. Small molecules such as water, glucose, and ionic salts are able to pass through the filtration slits and form an ultrafiltrate in the tubular fluid, which is further processed by the nephron to produce urine. Podocytes are also involved in regulation of glomerular filtration rate (GFR). When podocytes contract, they cause closure of filtration slits. This decreases the GFR by reducing the surface area available for filtration. Clinical significance A loss of the foot processes of the podocytes (i.e., podocyte effacement) is a hallmark of minimal change disease, which has therefore sometimes been called foot process disease. Disruption of the filtration slits or destruction of the podocytes can lead to massive proteinuria, where large amounts of protein are lost from the blood. An example of this occurs in the congenital disorder Finnish-type nephrosis, which is characterised by neonatal proteinuria leading to end-stage kidney failure. This disease has been found to be caused by a mutation in the nephrin gene. Presence of podocytes in urine has been proposed as an early diagnostic marker for preeclampsia. See also List of human cell types derived from the germ layers References External links - "Mammal, renal vasculature (EM, High) - ". Ultrastructure of the Cell: podocytes and glomerular capillaries" podocyte.ca at Samuel Lunenfeld Research Institute Kidney anatomy Human cells Epithelial cells