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| Podocyte | |||
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Renal corpuscle structure:
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| Glomerulus. (Diagram in French, but "Membrane basale glomerulaire et ses podocytes" labeled near center.) | |||
| Dorlands/Elsevier | Podocyte | ||
Podocytes (or visceral epithelial cells ) are cells of the visceral epithelium in the kidneys[1] and form a crucial component of the glomerular filtration barrier, contributing size selectivity and maintaining a massive filtration surface.
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Adjacent podocytes interdigitate to cover the basal lamina which is intimately associated with the glomerular capillaries, but the podocytes leave gaps or thin 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 ensure that large macromolecules such as serum albumin and gamma globulin remain in the bloodstream.
Small molecules such as water, glucose, and ionic salts are able to pass through the slit diaphragms and form an ultrafiltrate[2] 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.
Structural features of podocytes indicate a high rate of vesicular traffic in these cells. Many coated vesicles and coated pits can be seen along the basolateral domain of the podocytes.
In their cell bodies, podocytes possess a well-developed endoplasmic reticulum and a large Golgi apparatus, indicative of a high capacity for protein synthesis and post-translational modifications.
There is also growing evidence of a large number of multivesicular bodies and other lysosomal components seen in these cells, indicating a high endocytic activity.
"Pedicels" (or "foot processes") extend from the podocyte and increase the surface area.[3]
Disruption of the slit diaphragms 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 renal failure. This disease has been found to be caused by a mutation in the nephrin gene.
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