Literature DB >> 10773749

Nephrotic syndrome: molecular and genetic basis.

A Fogo1.   

Abstract

Nephrotic syndrome results from varying injuries to the capillary wall of the glomerulus. The components of the capillary wall, including the endothelial cell, glomerular basement membrane and glomerular visceral epithelial cell all may be targets of injury and contribute to proteinuria. These mechanisms of injury include immune complexes, cytotoxins, abnormal protein deposition, metabolic abnormalities, reactive oxygen species, growth factors, hemodynamic stress, and genetic abnormalities. We review mechanisms of glomerular permselectivity, with focus on emerging new understanding of the functions of the glomerular visceral epithelial cell. The significance and consequences of proteinuria and possible pathogenic mechanisms and the effect of interventions in clinical renal disease on these factors are considered. Copyright 2000 S. Karger AG, Basel

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Year:  2000        PMID: 10773749     DOI: 10.1159/000045623

Source DB:  PubMed          Journal:  Nephron        ISSN: 1660-8151            Impact factor:   2.847


  2 in total

1.  Sulodexide ameliorates early but not late kidney disease in models of radiation nephropathy and diabetic nephropathy.

Authors:  Michele Rossini; Takashi Naito; Haichun Yang; Michael Freeman; Ellen Donnert; Li-Jun Ma; Stephen R Dunn; Kumar Sharma; Agnes B Fogo
Journal:  Nephrol Dial Transplant       Date:  2010-01-07       Impact factor: 5.992

2.  Urinary immunoglobulin G to albumin ratio and N-Acetyl-Beta-D-Glucosaminidase as early predictors of therapeutic response in ANCA-associated glomerulonephritis.

Authors:  Marija Mravljak; Alenka Vizjak; Dusan Ferluga; Jernej Pajek; Damjan Kovac; Andrej Skoberne; Andreja Ales Rigler; Radoslav Kveder; Andrej Kosir; Jelka Lindic
Journal:  PLoS One       Date:  2013-12-13       Impact factor: 3.240

  2 in total

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