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Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease.
J Am Soc Nephrol. 1999 Feb; 10(2):323-31.JA

Abstract

It has been shown that children with nephrotic syndrome due to minimal change disease (MCD) can present with avid salt retention and stimulated vasoactive hormones, as well as with stable edema. The present study examines these conditions in children with nephrotic syndrome not due to MCD (non-MCD). In six children with hypovolemic symptoms (congenital nephrotic syndrome in four), strong sodium retention (fractional sodium excretion, FE(Na), 0.2 +/- 0.2%) was found. Lithium clearance (FE(Li)) and maximal water excretion (Vmax) were suppressed, suggesting avid sodium reabsorption throughout the nephron. Aldosterone, renin, and norepinephrine were elevated. Sixteen other children with non-MCD had stable edema. FE(Na) was 1.8 +/- 1.1%, whereas FE(Li), Vmax, and hormones were normal, and not different from data in 35 nonproteinuric children. In children with MCD, 12 presented with hypovolemic symptoms and strong sodium retention (FE(Na) 0.3 +/- 0.3%), whereas 15 were stable (FE(Na) 1.1 +/- 0.7%). Regarding tubular sodium handling and hormones, the same distinction could be made as for the children with non-MCD. However, hypoproteinemia differed. In the children with non-MCD lesions, plasma colloid osmotic pressure was significantly lower in the hypovolemic types (4.2 +/- 0.4 mmHg) than in those with stable edema (13.0 +/- 3.8 mmHg; P < 0.05); in MCD, no such difference existed (respectively, 8.1 +/- 3.0 and 9.9 +/- 2.2 mmHg). In summary, children with nephrotic syndrome may present with pathophysiologic pictures of decreased effective circulating volume or of stable edema, regardless of whether they have non-MCD or MCD. The pathogenesis of the hypovolemic picture seems to be different, since it is associated with extreme hypoproteinemia only in the children with non-MCD.

Authors+Show Affiliations

Department of Pediatric Nephrology in Wilhelmina's Children Hospital Utrecht, The Netherlands.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10215332

Citation

Vande Walle, J G., et al. "Pathophysiology of Edema Formation in Children With Nephrotic Syndrome Not Due to Minimal Change Disease." Journal of the American Society of Nephrology : JASN, vol. 10, no. 2, 1999, pp. 323-31.
Vande Walle JG, Donckerwolcke RA, Koomans HA. Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. J Am Soc Nephrol. 1999;10(2):323-31.
Vande Walle, J. G., Donckerwolcke, R. A., & Koomans, H. A. (1999). Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. Journal of the American Society of Nephrology : JASN, 10(2), 323-31.
Vande Walle JG, Donckerwolcke RA, Koomans HA. Pathophysiology of Edema Formation in Children With Nephrotic Syndrome Not Due to Minimal Change Disease. J Am Soc Nephrol. 1999;10(2):323-31. PubMed PMID: 10215332.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Pathophysiology of edema formation in children with nephrotic syndrome not due to minimal change disease. AU - Vande Walle,J G, AU - Donckerwolcke,R A, AU - Koomans,H A, PY - 1999/4/24/pubmed PY - 1999/4/24/medline PY - 1999/4/24/entrez SP - 323 EP - 31 JF - Journal of the American Society of Nephrology : JASN JO - J. Am. Soc. Nephrol. VL - 10 IS - 2 N2 - It has been shown that children with nephrotic syndrome due to minimal change disease (MCD) can present with avid salt retention and stimulated vasoactive hormones, as well as with stable edema. The present study examines these conditions in children with nephrotic syndrome not due to MCD (non-MCD). In six children with hypovolemic symptoms (congenital nephrotic syndrome in four), strong sodium retention (fractional sodium excretion, FE(Na), 0.2 +/- 0.2%) was found. Lithium clearance (FE(Li)) and maximal water excretion (Vmax) were suppressed, suggesting avid sodium reabsorption throughout the nephron. Aldosterone, renin, and norepinephrine were elevated. Sixteen other children with non-MCD had stable edema. FE(Na) was 1.8 +/- 1.1%, whereas FE(Li), Vmax, and hormones were normal, and not different from data in 35 nonproteinuric children. In children with MCD, 12 presented with hypovolemic symptoms and strong sodium retention (FE(Na) 0.3 +/- 0.3%), whereas 15 were stable (FE(Na) 1.1 +/- 0.7%). Regarding tubular sodium handling and hormones, the same distinction could be made as for the children with non-MCD. However, hypoproteinemia differed. In the children with non-MCD lesions, plasma colloid osmotic pressure was significantly lower in the hypovolemic types (4.2 +/- 0.4 mmHg) than in those with stable edema (13.0 +/- 3.8 mmHg; P < 0.05); in MCD, no such difference existed (respectively, 8.1 +/- 3.0 and 9.9 +/- 2.2 mmHg). In summary, children with nephrotic syndrome may present with pathophysiologic pictures of decreased effective circulating volume or of stable edema, regardless of whether they have non-MCD or MCD. The pathogenesis of the hypovolemic picture seems to be different, since it is associated with extreme hypoproteinemia only in the children with non-MCD. SN - 1046-6673 UR - https://www.unboundmedicine.com/medline/citation/10215332/Pathophysiology_of_edema_formation_in_children_with_nephrotic_syndrome_not_due_to_minimal_change_disease_ L2 - http://jasn.asnjournals.org/cgi/pmidlookup?view=long&amp;pmid=10215332 DB - PRIME DP - Unbound Medicine ER -