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NDT Advance Access originally published online on July 5, 2005
Nephrology Dialysis Transplantation 2005 20(9):1777-1779; doi:10.1093/ndt/gfh961
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Editorial Comment

Slit or pore? A mutation of the ion channel TRPC6 causes FSGS

Gerd Walz

Renal Division, University Hospital Freiburg, Germany

Correspondence and offprint requests to: Gerd Walz, Renal Division, University Hospital Freiburg, Germany. Email: gerd.walz@uniklinik-freiburg.de

Keywords: focal segmental glomerulosclerosis (FSGS); hereditary; nephrotic syndrome; TRP channel; TRPC6

The first 10% of the full text of this article appears below.



   Introduction
 
Podocytes are delicate creatures that, together with the basement membrane and the fenestrated capillary endothelium of the renal glomerulum, ensure that waste products exit the circulation via the kidney, retaining essential plasma constituents such as albumin. The task is formidable; 180 liters of plasma need to be depleted of albumin and other plasma proteins every day. Failure to get this job done results in a loss of protein with the urine. Typically, a proteinuria of >3.5 g/day causes a nephrotic syndrome characterized by hypoalbuminaemia, oedema and hyperlipidaemia.



   The nephrin–podocin complex
 
The podocyte attaches to the glomerular basement membrane via foot processes and, in almost all instances of proteinuria, these processes are lost, a disturbance termed foot process effacement by the renal pathologist. Although several agents are known to trigger . . . [Full Text of this Article]



   Podocyte protection against apoptosis and detachment
 


   TRPC6, a new player from the family of TRP cation channels
 


   Relation between TRPC6's gain of function and FSGS
 

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