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Focal and segmental glomerulosclerosis

Focal and segmental glomerulosclerosis An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cellular and Molecular Life Sciences Springer Journals

Focal and segmental glomerulosclerosis

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References (51)

Publisher
Springer Journals
Copyright
Copyright © 2006 by Birkhäuser Verlag, Basel
Subject
Life Sciences; Biomedicine general; Life Sciences, general; Biochemistry, general; Cell Biology
ISSN
1420-682X
eISSN
1420-9071
DOI
10.1007/s00018-006-6171-y
pmid
16952054
Publisher site
See Article on Publisher Site

Abstract

An increasing cause of end-stage renal disease is the pathological lesion focal and segmental glomerulosclerosis (FSGS). FSGS is characterized by proteinuria and frequently nephrotic syndrome with ensuing renal failure. The etiology remains unknown in the majority of individuals. The idiopathic form of FSGS is most common; however, secondary forms of FSGS do exist. There is a form of FSGS that is fulminant that frequently recurs after renal transplantation with an estimated frequency of approximately 30%, suggesting that the pathogenesis is not solely a result of intrinsic kidney disease. Recently, hereditary forms of the disease were recognized as well as those associated with other congenital syndromes. Known genetic causes of the hereditary form of this disease have been suggested to account for upwards of 18% of cases. This review will address recent discoveries of the genetic mechanisms of hereditary FSGS and the current interpretations of their interactions at the slit diaphragm.

Journal

Cellular and Molecular Life SciencesSpringer Journals

Published: Sep 4, 2006

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