ArticleInternational journal of clinical and experimental medicine2015
Serum galactose-deficient IgA1 levels in children with IgA nephropathy.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Examining the association between serum galactose-deficient IgA1 and primary IgA nephropathy: a systematic review and meta-analysis.Journal of nephrology · 2024Pooled it
- Is Childhood IgA Nephropathy Different From Adult IgA Nephropathy? A Narrative Review.Canadian journal of kidney health and disease · 2025Review
- Relationship between Gd-IgA1 and TNFR1 in IgA nephropathy and IgA vasculitis nephritis in children - multicenter study.Central-European journal of immunology · 2021Article
- Clinical Significance of Serum Galactose-Deficient IgA1 Level in Children with IgA Nephropathy.Journal of immunology research · 2020Article
- Serum GDIgA1 levels in children with IgA nephropathy and Henoch-Schönlein nephritis.Central-European journal of immunology · 2018Article
- Clinical significance of serum and mesangial galactose-deficient IgA1 in patients with IgA nephropathy.PloS one · 2018Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A nephropathy (IgAN) is an immunopathologic diagnosis based on a renal biopsy, it is characterized by deposits of IgA-containing immune complexes in the mesangium. Adults with IgAN have a galactose-deficient IgA1 in the circulation and glomerular deposition. There are few studies on the glycosylation of serum IgA1 in children with IgAN. To measure the serum levels of galactose-deficient IgA1 in pediatric patients with IgAN, 72 biopsy-proven IgAN children were divided into 3 groups based on the clinical features: isolated hematuria group (24 patients), hematuria and proteinuria group (22 patients), and nephritic syndrome group (26 patients). They were also divided into 3 groups according to pathologic grading: grade I + II group (25 patients), grade III group (33 patients) and grade IV + V group (14 patients). 30 healthy children were recruited as a control group. We used vicia villosa lectin binding enzyme-linked immunosorbent assay to measure the serum levels of galactose-deficient IgA1 in all groups and controls. Serum levels of galactose-deficient IgA1 in children with IgAN were higher than controls (P < 0.01). There were no significant differences in serum levels of galactose-deficient IgA1 among the different clinical and pathologic grading groups. The values of the area under the curve for galactose-deficient IgA1 levels were 0.976 (95% CI, 0.953-1.000). The cutoff point for galactose-deficient IgA1 levels was 0.125, with a sensitivity of 87.5% and a specificity of 83.3%, with a positive predictive value of 92.6% and a negative predictive value of 73.5% (P < 0.01). Children with IgAN presented serum galactose-deficient IgA1, which has shown no relationship with the clinical manifestations and pathologic grading of the disease. Detection of serum galactose-deficient IgA1 levels by vicia villosa lectin binding enzyme-linked immunosorbent assay has a certain clinical value in diagnosis of children with IgAN.
Indexed as
Identifiers
26221341PMC4509286W2412405888What OpenQuestion holds
Registered trials
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