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Nephrol Dial Transplant (2004) 19: 1036-1040
Nephrol Dial Transplant Vol. 19 No. 5 © ERA-EDTA 2004; all rights reserved

Editorial Comment

Recurrent focal glomerulosclerosis in the era of genetics of podocyte proteins: theory and therapy

Gian Marco Ghiggeri1, Michele Carraro2 and Flavio Vincenti3

1Nephrology Section and Laboratory on Pathophysiology of Uremia, Giannina Gaslini Children Hospital, Genoa, Italy, 2University of Trieste, Trieste, Italy and 3University of California, San Francisco, CA, USA

Correspondence and offprint requests to: Gian Marco Ghiggeri, MD, Laboratory on Pathophisiology of Uremia, Istituto Giannina Gaslini, Largo Gaslini 5, Genoa, Italy. Email: labnefro@ospedale-gaslini.ge.it

Keywords: focal segmental glomerulosclerosis; inherited nephrotic syndrome; podocin; post-transplant recurrence of proteinuria; proteinuria

The first 150 words of the full text of this article appear below.



   Introduction
 
Focal segmental glomerulosclerosis (FSGS) is the most frequent cause of intractable proteinuria in children and adults and is emerging as a major glomerular cause of chronic kidney disease [1]. Most of the aspects related to its pathogenesis remain unknown, one major issue being post-transplant recurrence. Recent advances in molecular genetics of FSGS led to the identification of several genes responsible for familial forms. In general, they code for proteins of the podocyte and are specifically localized in the glomerular slit-diaphragm where they play a critical role in the control of glomerular permeability. The clinical implications of one of them, that is NPHS2 coding for podocin, are obvious as it's involvement has been extended to sporadic FSGS [2–4]. Experience with inherited sporadic FSGS due to NPHS2 mutations is accumulating and shows strong clinical homologies with idiopathic FSGS, in spite of clear pathogenic differences. This offers . . . [Full Text of this Article]



   Recurrent FSGS: the classical point of view
 


   Podocyte proteins as a clue for explaining proteinuria in inherited FSGS
 


   Homologies between genetic and ‘non-genetic’ conditions
 


   Post-transplant recurrence of FSGS in carriers of NPHS2 mutations
 


   Putative mechanisms for recurrence
 


   Current and future therapies of recurrent FSGS
 


   Conclusions
 

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