Hypoalbuminaemia and transcapillary pressures have role in nephrotic syndromeBMJ 1999; 319 doi: https://doi.org/10.1136/bmj.319.7213.852 (Published 25 September 1999) Cite this as: BMJ 1999;319:852
- Nadeem E Moghal, consultant paediatric nephrologist ()
EDITOR—In their article on understanding oedema Diskin et al have overlooked an important body of work that challenges the traditional pathophysiological explanation for the development of oedema in the nephrotic syndrome secondary to renal disease.1 Animal as well as several human studies have shown that sodium retention seems to occur as a primary phenomenon in the nephrotic syndrome as a result of increased sodium reabsorption in the collecting duct.2–4 This in turn may be due to resistance to atrial natriuretic peptide.5
Hypoalbuminaemia and changes in transcapillary pressures, as well as volume regulating hormones and sodium retention, are mechanisms that do have a role in nephrotic, oedematous patients. Whether sodium retention is the dominant mechanism for the development of oedema remains uncertain. For clinicians it is not the oedema but the assessment of intravascular volume status (using clinical and laboratory data) in children with the nephrotic syndrome that remains an inexact science.
a Competing interests None declared.