ArticleRenal failure2017
Does copy number variation of APOL1 gene affect the susceptibility to focal segmental glomerulosclerosis?
Article in Renal failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- A novelRenal failure · 2025Article
- Apolipoprotein L1 nephropathies: 2017 in review.Current opinion in nephrology and hypertension · 2018Review
- Copy Number Variation of Immune-Related Genes and Their Association with Iodine in Adults with Autoimmune Thyroid Diseases.International journal of endocrinology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAPOL1 risk variants (G1 and G2) are associated with increased susceptibility to focal segmental glomerulosclerosis (FSGS) in African population. However, the two risk mutations were not found in Chinese FSGS patients. In this study, we explored the association between the copy number variation (CNV) of APOL1 gene and FSGS.
methodsAPOL1 copy number variations were detected by quantitative real-time PCR with TaqMan probes and compared between 133 FSGS patients and 123 controls. The association between CNV of APOL1 gene and clinical parameters was also investigated.
resultsThe distribution of APOL1 CNV did not show significant difference between FSGS patients and controls. The creatinine and proteinuria in the high copy number group (CN ≥ 3) were higher than the other two groups, but the difference was not significant (p > .05). The FSGS pathological types were different among the three groups.
conclusionThere was no significant difference in the distribution of APOL1 gene copy variants between FSGS patients and normal controls, and there was no significant correlation between the APOL1 gene CNV and the FSGS patients' clinical manifestations. APOL1 CNVs may be not associated with susceptibility to FSGS.
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