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Urinary low-molecular-weight protein excretion in pediatric idiopathic nephrotic syndrome

Chehade, Hassib ; Parvex, Paloma ; Poncet, Antoine ; Werner, Dominique ; Mosig, Dolores ; Cachat, Francois ; Girardin, Eric

In: Pediatric Nephrology, 2013, vol. 28, no. 12, p. 2299-2306

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    Title
    • Urinary low-molecular-weight protein excretion in pediatric idiopathic nephrotic syndrome
    Author
    • Chehade, Hassib. Division of Pediatric Nephrology, Department of Pediatrics, Lausanne University Hospital, Rue Bugnon 46, 1011, Lausanne, Switzerland
    • Parvex, Paloma. Division of Pediatric Nephrology, Department of Pediatrics, Geneva University Hospital, Rue Willy-Donzé 6, 1205, Geneva, Switzerland
    • Poncet, Antoine. CRC & Division of Clinical-Epidemiology, Department of Health and Community Medicine, University of Geneva & University Hospitals of Geneva, Rue Willy-Donzé 6, 1205, Geneva, Switzerland
    • Werner, Dominique. Central Chemistry Laboratory, Lausanne University Hospital, Rue Bugnon 46, 1011, Lausanne, Switzerland
    • Mosig, Dolores. Division of Pediatric Nephrology, Department of Pediatrics, Lausanne University Hospital, Rue Bugnon 46, 1011, Lausanne, Switzerland
    • Cachat, Francois. Division of Pediatric Nephrology, Department of Pediatrics, Lausanne University Hospital, Rue Bugnon 46, 1011, Lausanne, Switzerland
    • Girardin, Eric. Division of Pediatric Nephrology, Department of Pediatrics, Lausanne University Hospital, Rue Bugnon 46, 1011, Lausanne, Switzerland
    Document Type
    • Postprint
    OAI-PMH Identifier
    • oai:doc.rero.ch:321889
    Summary
    Background: Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are the most common causes of idiopathic nephrotic syndrome (INS). We have evaluated the reliability of urinary neutrophil-gelatinase-associated lipocalin (uNGAL), urinary alpha1-microglobulin (uα1M) and urinary N-acetyl-beta-D-glucosaminidase (uβNAG) as markers for differentiating MCD from FSGS. We have also evaluated whether these proteins are associated to INS relapses or to glomerular filtration rate (GFR). Methods: The patient cohort comprised 35 children with MCD and nine with FSGS; 19 healthy age-matched children were included in the study as controls. Of the 35 patients, 28 were in remission (21 MCD, 7 FSGS) and 16 were in relapse (14 MCD, 2 FSGS). The prognostic accuracies of these proteins were assessed by receiver operating characteristic (ROC) curve analyses. Results: The level of uNGAL, indexed or not to urinary creatinine (uCreat), was significantly different between children with INS and healthy children (p = 0.02), between healthy children and those with FSGS (p = 0.007) and between children with MCD and those with FSGS (p = 0.01). It was not significantly correlated to proteinuria or GFR levels. The ROC curve analysis showed that a cut-off value of 17ng/mg for the uNGAL/uCreat ratio could be used to distinguish MCD from FSGS with a sensitivity of 0.77 and specificity of 0.78. uβNAG was not significantly different in patients with MCD and those with FSGS (p = 0.86). Only uα1M, indexed or not to uCreat, was significantly (p < 0.001) higher for patients in relapse compared to those in remission. Conclusions: Our results indicate that in our patient cohort uNGAL was a reliable biomarker for differentiating MCD from FSGS independently of proteinuria or GFR levels