Molecular mechanism of edema formation in nephrotic syndrome

Archives de pédiatrie : organe officiel de la Sociéte française de pédiatrie
G DeschênesAlain Doucet

Abstract

Nephrotic edema are the clinical feature of isolated interstitial expansion. Expanded interstitial compartment compensates sodium accumulation in the extracellular volume due to inappropriate renal sodium retention. Renal sodium retention is brought about by an activation of the molecular structures responsible for the reabsorption of sodium along the cortical collecting duct: amiloride-sensitive epithelial sodium channel at the apical face and sodium pump at the basolateral face of the principal cell. This activation is independent of aldosterone and vasopressin. The asymmetry of expansion between interstitium and plasma compartments is due to impaired Starling forces and increased fluid transfer through the capillary wall. The lack of significant changes in transcapillary oncotic and hydrostatic gradients suggests that increased hydraulic conductivity due to transconformation of endothelial intercellular junctions drives the leakage of fluid into the interstitium and allows to understand the mobility of nephrotic edema. Consistently with the site of renal sodium retention and the activation of the epithelial sodium channel, the association of amiloride and furosemide is efficient to increase urinary sodium excretion, to rever...Continue Reading

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Citations

Jun 8, 2007·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Alain DoucetGeorges Deschênes
Mar 19, 2013·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·René F AndersenSøren Rittig
Mar 27, 2013·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Detlef Bockenhauer
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Aug 21, 2015·American Journal of Physiology. Renal Physiology·Chia Wei TeohDamien Gerard Noone
Jun 29, 2017·Pflügers Archiv : European journal of physiology·Per SvenningsenBoye L Jensen

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