Oedema
There is a large body of clinical evidence against the theory that the hypoalbuminaemia is the driving
force for oedema formation.
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Analbuminaemic patients
have only minimal or no oedema, despite low plasma oncotic pressure.
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In children with
steroid-sensitive nephrotic syndrome, natriuresis starts at the same time as
proteinuria ceases, before the serum albumin has risen.
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Blood volume does not
correlate with plasma oncotic pressure in nephrotic patients.
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When children relapse,
21% display hypertension, but only 4% exhibit circulatory collapse. Only 1%
display hypovolaemia, whereas 17% manifest hypervolaemia.
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Intravenous
administration of albumin leads to volume expansion but only minimal natriuresis.
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Blockade of mineralo-corticoid
receptors or inhibition of angiotensin-converting enzyme has no effect on
natriuresis in most patients.
This has led to the
identification of other possible mechanisms for oedema formation. Click
here.
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