Tubular Dysfunction in Idiopathic Nephrotic Syndrome
Détails
ID Serval
serval:BIB_7ADBD5CD3C6B
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Sous-type
Abstract (résumé de présentation): article court qui reprend les éléments essentiels présentés à l'occasion d'une conférence scientifique dans un poster ou lors d'une intervention orale.
Collection
Publications
Institution
Titre
Tubular Dysfunction in Idiopathic Nephrotic Syndrome
Titre de la conférence
15th Congress of the International Pediatric Nephrology Association
Adresse
New York, United States, August 29-September 2, 2010
ISBN
0931-041X
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
25
Série
Pediatric Nephrology
Pages
1803
Langue
anglais
Notes
Meeting Abstract
Résumé
Objectives:
To evaluate the degree of tubular involvement in INS at various stage of the disease.
Methods:
19 patients with INS were studied. 13 were steroid responders (group 1). 5 of them had biopsy which showed MCD. 6 patients were non responder to steroid or were steroid dependant with frequent relapses (group 2). Biopsies showed 3 FSGS and 3 MCD. They were treated with prednisone, ciclosporin and/ or mycofenolate mofetil. Protein, microalbumin (ALB), alpha-microglobulin (AMG), N-acetyl-beta-D-glucosaminidase (NAG) and creatinine (cr) were measured in each urine sample. Patients were considered in remission if prot/ cr ratio (g/mol) was < 20 (group 1a and 2a), and in relapse if the ratio was > 200 (group 1c and 2c). Some patients in group 1 had non nephrotic proteinuria (group 1b). Tubular dysfunction was defi ned by NAG/cr ratio (mg/mmol) > 0.86 or by AMG/cr ratio (mg/mmol) > 1.58.
Results:
Prot/cr ALB/cr NAG/cr AMG/cr
Group 1a 10.3 ± 4.1 1.1 ± 1.0 0.19 ± 0.12 1.40 ± 0.97
Group 1b 60.4 ± 63.4 42.8 ± 66.7 0.39 ± 0.21 1.20 ± 0.56
Group 1c 713.3 ± 276.8 799.8 ± 534.9 2.25 ± 1.86* 4.25 ± 2.09*
Group 2a 11.3 ± 6.1 4.7 ± 5.7 0.26 ± 0.19 1.18 ± 0.60
Group 2c 914.9 ± 718.6 682.9 ± 589.3 3.00 ± 2.72* 5.47 ± 4.30*
Results are mean ± SD, p < 0.001 compared to group 1a and 2a
No difference was observed between group 1 and group 2 neither in remission nor in relapse.
Conclusions:
These data indicate that tubular dysfunction occurs in INS but only in patients in relapse. In this population, tubular dysfunction was independent of the severity of the nephrotic syndrome, the treatment protocol and the histopathology.
To evaluate the degree of tubular involvement in INS at various stage of the disease.
Methods:
19 patients with INS were studied. 13 were steroid responders (group 1). 5 of them had biopsy which showed MCD. 6 patients were non responder to steroid or were steroid dependant with frequent relapses (group 2). Biopsies showed 3 FSGS and 3 MCD. They were treated with prednisone, ciclosporin and/ or mycofenolate mofetil. Protein, microalbumin (ALB), alpha-microglobulin (AMG), N-acetyl-beta-D-glucosaminidase (NAG) and creatinine (cr) were measured in each urine sample. Patients were considered in remission if prot/ cr ratio (g/mol) was < 20 (group 1a and 2a), and in relapse if the ratio was > 200 (group 1c and 2c). Some patients in group 1 had non nephrotic proteinuria (group 1b). Tubular dysfunction was defi ned by NAG/cr ratio (mg/mmol) > 0.86 or by AMG/cr ratio (mg/mmol) > 1.58.
Results:
Prot/cr ALB/cr NAG/cr AMG/cr
Group 1a 10.3 ± 4.1 1.1 ± 1.0 0.19 ± 0.12 1.40 ± 0.97
Group 1b 60.4 ± 63.4 42.8 ± 66.7 0.39 ± 0.21 1.20 ± 0.56
Group 1c 713.3 ± 276.8 799.8 ± 534.9 2.25 ± 1.86* 4.25 ± 2.09*
Group 2a 11.3 ± 6.1 4.7 ± 5.7 0.26 ± 0.19 1.18 ± 0.60
Group 2c 914.9 ± 718.6 682.9 ± 589.3 3.00 ± 2.72* 5.47 ± 4.30*
Results are mean ± SD, p < 0.001 compared to group 1a and 2a
No difference was observed between group 1 and group 2 neither in remission nor in relapse.
Conclusions:
These data indicate that tubular dysfunction occurs in INS but only in patients in relapse. In this population, tubular dysfunction was independent of the severity of the nephrotic syndrome, the treatment protocol and the histopathology.
Web of science
Création de la notice
21/10/2010 10:52
Dernière modification de la notice
20/08/2019 14:36