Title of article :
Volume regulation in children with early relapse of minimal-change nephrosis with or without hypovolaemic symptoms
Author/Authors :
J. G. Vande Walle، نويسنده , , R. A. M. G. Donckerwolcke، نويسنده , , J. W. van Isselt، نويسنده , , J. A. Joles، نويسنده , , H. A. Koomans، نويسنده , , F. H. M. Derkx، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1995
Pages :
5
From page :
148
To page :
152
Abstract :
The cause of sodium retention in nephrotic syndrome is unclear. Hypovolaemia has traditionally been labelled as the cause but there is evidence in adults of a renal disturbance as the main cause. We aimed to find out whether children with early nephrosis can be classified as hypovolaemic by objective measures. We measured blood volume, kidney function, and hormone concentrations in children with early relapse of minimal-change nephrosis. Three presentations could be defined. The first was patients with incipient proteinuria and normal plasma protein, characterised by sodium retention, increased renal plasma flow, and slightly increased aldosterone, but normal noradrenaline. The second was patients with severe proteinuria, hypoproteinaemia, and hypovolaemic symptoms, who had oedema, sodium retention, and high concentrations of plasma renin, aldosterone, and noradrenaline, low atrial natriuretic peptide, and low glomerular filtration rate. The third was patients with equally severe proteinuria and hypoproteinaemia, but without hypovolaemic symptoms; they had oedema, but no active sodium retention, and normal plasma hormones and glomerular filtration. Neither blood pressure nor blood volume discriminated patients with or without hypovolaemic symptoms. These findings show that children with early full-blown nephrosis can present both with and without hypovolaemic symptoms and laboratory signs, despite equally severe hypoproteinaemia, and also that sodium retention precedes the reduction in serum protein.
Journal title :
The Lancet
Serial Year :
1995
Journal title :
The Lancet
Record number :
562466
Link To Document :
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