ArticleMolecular biology reports2009
Association of polymorphisms at restriction enzyme recognition sites of apolipoprotein B and E gene with dyslipidemia in children undergoing primary nephrotic syndrome.
Article in Molecular biology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
12 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.
- Roles of ApoB-100 gene polymorphisms and the risks of gallstones and gallbladder cancer: a meta-analysis.PloS one · 2013Pooled it
- Association of apoE gene expression and its gene polymorphism with nephrotic syndrome susceptibility: a meta-analysis of experimental and human studies.Molecular biology reports · 2012Pooled it
- Metabolic syndrome, ApoE genotype, and cognitive dysfunction in an elderly population: A single-center, case-control study.World journal of clinical cases · 2021Article
- Relationship between the Apolipoprotein AI, B gene polymorphism and the risk of non-traumatic osteonecrosis.Lipids in health and disease · 2014Article
- Polymorphisms of the MDR1 and MIF genes in children with nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2011Article
- Modulation of vitamin D signaling is a potential therapeutic target to lower cardiovascular risk in chronic kidney disease.Medical science monitor : international medical journal of experimental and clinical research · 2011Review
- Antioxidant activities of recombinant amphioxus (Branchiostoma belcheri) apolipoprotein D.Molecular biology reports · 2011Article
- Microarray analysis of cultured rat hippocampal neurons treated with brain derived neurotrophic factor.Molecular biology reports · 2011Article
- Variable frequencies of apolipoprotein E genotypes and its effect on serum lipids in the Guangxi Zhuang and Han children.International journal of molecular sciences · 2011Article
- Does the geographical gradient of ApoE4 allele exist in China? A systemic comparison among multiple Chinese populations.Molecular biology reports · 2011Article
- Identification of a recurrent insertion mutation in the LDLR gene in a Pakistani family with autosomal dominant hypercholesterolemia.Molecular biology reports · 2010Article
- Genetic variants involved in gallstone formation and capsaicin metabolism, and the risk of gallbladder cancer in Chilean women.World journal of gastroenterology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDyslipidemia, a common complication, is very prevalent in children with primary nephrotic syndrome (PNS). Recent studies have shown that genetic basis may be involved in the onset of HLP secondary to PNS. ApoB and E have been identified as the important candidate genes for lipid abnormalities.
objectiveTo investigate the association of apolipoprotein B (apoB) and E (apoE) genetic polymorphisms (Xba I, EcoR I, Msp I, and Hha I) with parameters describing the serum lipid profiles in children undergoing PNS.
methodsGenomic DNA was extracted from 250 children diagnosed with PNS and 200 healthy controls with neither allergic nor renal disease. ApoB (Xba I, EcoR I, and Msp I) and apoE (Hha I) genotypes were determined by PCR-restriction fragment length polymorphism (RFLP) analysis. The fasting serum lipoprotein (a) [Lp(a)], total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apolipoprotein A1 (apoA1), apoB, and total protein from a 24-h urine sample were measured.
resultsNo significant differences in genotypes and alleles frequencies were observed for the apoB Xba I, EcoR I, Msp I and the apoE Hha I restriction sites in PNS patients as compared to controls (P > 0.05). Patients and controls with X + allele exhibited significantly higher serum levels of Lp(a), TC, nonHDL-C, LDL-C, LDL-C/HDL-C ratio, and apoB than that with X- allele (P < 0.05), whereas for apoA1/B ratio the opposite was found (P < 0.01). E-/E- carriers had significantly higher Lp(a), TC, HDL-C, and apoA1 concentrations than did E+/E- or E+/E+ carriers in control group (P < 0.05). Healthy children carrying the rare EcoR I allele had higher mean Lp(a), TC, and HDL-C levels than homozygotes for E+ (P < 0.05). Higher Lp(a) serum concentrations were observed in patients with E- allele (P < 0.05). No significant differences in lipid parameters were determined for the apoB Msp I and apoE Hha I the polymorphisms study (P > 0.05). When genetic variations were compared with urinary protein excretion, the Xba I X- allele was more frequent in patients with elevated proteinuria (P < 0.01).
conclusionPresence of Xba I X+ allele and/or EcoR I E- at the apoB gene may be risk factors for lipid abnormalities secondary to childhood PNS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.