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Nephrol Dial Transplant (2003) 18: VI30-VI32
© 2003 European Renal Association-European Dialysis and Transplant Association

Pathophysiology of oedema in idiopathic nephrotic syndrome

Hein A. Koomans

Department of Nephrology and Hypertension, University Medical Center Utrecht, Room F03.226, PO Box 85500, 3508 GA Utrecht, The Netherlands

Correspondence and offprint requests to: Professor H. A. Koomans MD, Department of Nephrology and Hypertension, PO Box 85500, 3508 GA Utrecht, The Netherlands. Email: h.a.koomans{at}digd.azu.nl

Abstract

The decrease in plasma protein and colloid osmotic pressure (COP) in the nephrotic syndrome is accompanied by a decrease in tissue-fluid protein and COP. The latter protects against a fall in blood volume. However, the range and speed of this protective mechanism are limited, and a decrease in blood volume can be expected if plasma COP is below ~10 mmHg, or (temporarily) if the protein loss starts very fast. In addition, due to this protective mechanism volume retained by the kidneys cannot effectively expand blood volume, explaining that hypertension is rarely grave and pulmonary congestion unusual, whereas peripheral oedema can be gross. The renal derangement leading to volume retention involves a decreased filtration per nephron, increased tubular reabsorption, and decreased sensitivity to ANP but the relation between these changes is incompletely resolved.

Keywords: nephrotic syndrome; oedema; pathophysiology


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