It has been argued that the oedema of kwashiorkor is not caused by
hypoalbuminaemia because the oedema disappears with dietary treatment before the
plasma albumin concentration rises. Reanalysis of this evidence and a review of
the literature demonstrates that this was a mistaken conclusion and that the
oedema is linked to hypoalbuminaemia. This misconception has influenced the
recommendations for treating children with severe acute malnutrition. There are
close pathophysiological parallels between kwashiorkor and Finnish congenital
nephrotic syndrome (CNS) pre-nephrectomy; both develop protein-energy
malnutrition and hypoalbuminaemia, which predisposes them to intravascular
hypovolaemia with consequent sodium and water retention, and makes them highly
vulnerable to develop hypovolaemic shock with diarrhoea. In CNS this is
successfully treated with intravenous albumin boluses. By contrast, the WHO
advise the cautious administration of hypotonic intravenous fluids in
kwashiorkor with shock, which has about a 50% mortality. It is time to
trial intravenous bolus albumin for the treatment of children with kwashiorkor
and shock.