A decrease in podocyte number contributes to the development of glomerulosclerosis in most forms of glomerular disease [1,2,3,4,5]. Traditionally, it has been argued that this decrease may be caused by the inability of podocytes to proliferate and replace those lost following immune, metabolic, toxic or hemodynamic injury. These data contrast with recent studies showing that podocytes are able to enter the cell cycle after injury, to progress through the different phases of the cell cycle and even enter mitosis. However, experimental and human data suggest that entry of podocytes into the cell cycle may result in reduced adhesion to the glomerular basement membrane with subsequent loss of podocytes into the urine and excretion of both viable and apoptotic podocytes. Viable urinary podocytes can be cultivated ex vivo for up to 2–3 weeks and in experimental models precede the onset of proteinuria. More importantly, podocyturia can decrease despite persistent proteinuria. The latter observation suggests that podocyturia may serve as the first non-invasive marker of ‘active’ glomerular damage and might thus drive therapeutic interventions in the future. However, at present technical issues still prevent a broad clinical application of podocyturia detection in clinical practice.

Keywords:
‘Crossing the bridge’, Podocyte detachment, Glomerulonephritis, Proteinuria, Apoptosis
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© 2007 S. Karger AG, Basel
2007
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