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Pathophysiology of oedema in idiopathic nephrotic syndrome
Author(s) -
H. A. Koomans
Publication year - 2003
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfg1063
Subject(s) - medicine , oncotic pressure , nephrotic syndrome , pathophysiology , reabsorption , endocrinology , blood volume , nephron , blood pressure , edema , kidney , albumin
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 approximately 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.

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