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Nephrol Dial Transplant (2003) 18: 454-456
© 2003 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Mechanisms of oedema in nephrotic syndrome: old theories and new ideas

Georges Deschênes1,, Eric Feraille2 and Alain Doucet3

1 Hopital Trousseau, Service de Nephrologie Pediatrique, Paris, France, 2 Fondation pour Recherches Médicales, Laboratoire de Nephrologie, Genève, Switzerland and 3 FRE CNRS 2864, Institut Biomedical des Cordeliers, Paris, France

Keywords: aldosterone; endothelium; nephrotic syndrome; sodium; vasopressin

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

Interstitial oedema is a common clinical expression of nephrotic syndrome. Expansion of the interstitial compartment is secondary to the accumulation of sodium in the extracellular compartment, due to an imbalance between oral or parenteral sodium intake and urinary sodium output, along with alterations of fluid transfer across capillary walls.

Molecular mechanism of sodium retention

The intrarenal site of sodium retention was determined by an in vivo micropuncture study in the unilateral model of puromycin aminonucleoside (PAN)-induced proteinuria, which allows the study of a nephrotic and a normal control kidney within the same animal. Sodium delivery to the collecting duct was not different in the two kidneys while the urinary excretion of sodium was 3-fold lower in the nephrotic kidney compared with the control kidney, suggesting that stimulation of tubular sodium reabsorption originated in the collecting duct [1]. The molecular mechanisms of renal sodium avidity have been elucidated recently. The hydrolytic and transport activities . . . [Full Text of this Article]

Role of systemic factors

Mechanism of oedema generation


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