Valérie Besse-Eschmann

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Excessive proteinuria due to loss of glomerular permselectivity in nephrotic syndrome can cause disturbances in renal salt and water handling with edema formation. Apart from oncotic and hydrostatic mechanisms associated with hypoalbuminemia, primary derangements in renal tubular sodium transport may contribute to the pathogenesis of nephrotic edema.(More)
BACKGROUND Nephron loss is a major determinant of renal failure in glomerular diseases. The prevalent concept stresses the role of the toxicity of filtered proteins and/or of interstitial inflammation in tubular degeneration. However, whether that concept is compatible with the actual histopathological features of nephron loss has not been investigated(More)
Recent observations suggest a central role of podocytes in crescent formation. In experimental glomerulonephritis podocytes disrupt the parietal epithelial layer and attach on its basement membrane, thus forming bridges between the tuft and Bowman’s capsule, and they are a major constituent of crescents. In order to explain these findings we hypothesize(More)
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