ArticlePediatric nephrology (Berlin, Germany)2008
Association of the macrophage migration inhibitory factor -173*C allele with childhood nephrotic syndrome.
Article in Pediatric nephrology (Berlin, Germany), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Association Between Macrophage Migration Inhibitory Factor -173 G>C Gene Polymorphism and Childhood Idiopathic Nephrotic Syndrome: A Meta-Analysis.Frontiers in pediatrics · 2021Pooled it
- Association ofInternational journal of clinical and experimental pathology · 2021Article
- Correlations ofThe Journal of international medical research · 2020Article
- MIF plasma level as a possible tool to predict steroid responsiveness in children with idiopathic nephrotic syndrome.European journal of clinical pharmacology · 2019Article
- Pharmacology and pharmacogenetics of prednisone and prednisolone in patients with nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2019Review
- A Macrophage Migration Inhibitory Factor Polymorphism Is Associated with Autoimmune Hepatitis Severity in US and Japanese Patients.Digestive diseases and sciences · 2016Article
- Single Nucleotide Polymorphisms in Pediatric Idiopathic Nephrotic Syndrome.International journal of nephrology · 2016Article
- Macrophage Migration Inhibitory Factor in Clinical Kidney Disease.Frontiers in immunology · 2016Review
- Influence of MIF, CD40, and CD226 polymorphisms on risk of rheumatoid arthritis.Molecular biology reports · 2012Article
- Polymorphisms of the MDR1 and MIF genes in children with nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage migration inflammatory factor (MIF) is a proinflammatory cytokine with a unique role as the physiologic counterregulator of the immunosuppressive effects of glucocorticoids. MIF has been implicated in the pathogenesis of glomerular inflammation. The MIF promoter contains a G/C polymorphism that is functionally relevant, with the C allele being associated with higher MIF production and linked to susceptibility to inflammatory diseases. We genotyped the MIF -173 polymorphism in 257 children with idiopathic nephrotic syndrome (INS) and 355 controls. Frequency of carriers of the high-producer MIF -173*C allele was higher in patients with INS (31.7%) than in controls (22.0%) [odds ratio (OR) 1.67, p = 0.006] The MIF -173 C allele was more frequent in steroid-resistant patients (43.5%) compared with steroid responders (22.8%) (OR 2.61, p = 0.0005). This difference was particularly evident in focal segmental glomerulosclerosis patients (OR 14.0, p = 0.002). No association with response to cyclosporin A was found. Carriers of the MIF -173*C allele had a significantly higher probability of end-stage renal disease (ESRD) compared with G/G homozygous patients within 5 years from onset (log rank 5.11 p = 0.024). These results underscore the role of MIF in INS disease progression and in the response to glucocorticoid treatment and suggest that screening of MIF genotype at disease onset may identify patients requiring a more aggressive therapeutic approach.
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