Evidence map›Paper›PMID 27871254›Full record

ArticleBMC nephrology2016

Familial aggregation of albuminuria and arterial hypertension in an Aboriginal Australian community and the contribution of variants in ACE and TP53.

David L Duffy, Stephen P McDonald, Beverley Hayhurst, Sianna Panagiotopoulos, Trudy J Smith, Xing L Wang, David E Wilcken, Natalia L Duarte, John Mathews, Wendy E Hoy

Open access · goldAbstract read
In one paragraph

Article in BMC nephrology, 2016. 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.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
15.0field-weighted citation impact, top 1% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 7 institutions in 2 countries.

David L DuffyGenetic Epidemiology Laboratory, QIMR Berghofer Institute of Medical Research, 300 Herston Rd, Brisbane, 4006, Australia.
Stephen P McDonaldThe Queen Elizabeth Hospital, Adelaide, Australia.
Beverley HayhurstCradle Coast Authority, Tasmania, Formerly Menzies School of Health Research, Darwin, Australia.
Sianna PanagiotopoulosDepartment of Medicine, University of Melbourne, Melbourne, Australia.
Trudy J SmithMenzies School of Health Research, Darwin, Australia.
Xing L WangDepartment of Genetics, Southwest Foundation for Biomedical Research, San Antonio, Texas, Australia.
David E WilckenCardiovascular Genetics Department, Prince of Wales Hospital, Sydney, Australia.
Natalia L DuarteCardiovascular Genetics Department, Prince of Wales Hospital, Sydney, Australia.
John MathewsMelbourne School of Population and Global Health, University of Melbourne, Melbourne, Australia.
Wendy E HoyCentre for Chronic Disease, The University of Queensland School of Medicine, Brisbane, Australia.
Menzies School of Health Research · AUPrince of Wales Hospital · AUUniversity of Melbourne · AUQIMR Berghofer Medical Research Institute · AUQueen Elizabeth Hospital · AUTexas Biomedical Research Institute · USUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAboriginal Australians are at high risk of cardiovascular, metabolic and renal diseases, resulting in a marked reduction in life expectancy when compared to the rest of the Australian population. This is partly due to recognized environmental and lifestyle risk factors, but a contribution of genetic susceptibility is also likely.

methodsUsing results from a comprehensive survey of one community (N = 1350 examined individuals), we have tested for familial aggregation of plasma glucose, arterial blood pressure, albuminuria (measured as urinary albumin to creatinine ratio, UACR) and estimated glomerular filtration rate (eGFR), and quantified the contribution of variation at four candidate genes (ACE; TP53; ENOS3; MTHFR).

resultsIn the subsample of 357 individuals with complete genotype and phenotype data we showed that both UACR (h

conclusionsWhile the effects of the ACE insertion-deletion on risk of renal disease (especially in the setting of diabetes) are well recognized, this is only the second study to implicate p53 genotype as a risk factor for albuminuria - the other being an earlier study we performed in a different Aboriginal community (McDonald et al., J Am Soc Nephrol 13: 677-83, 2002). We conclude that there are significant genetic contributions to the high prevalence of chronic diseases observed in this population.

Indexed as

Genes, p53AdolescentAdultAgedAlbuminuriaArterial PressureBlood GlucoseCreatinineFemaleGenotypeGlomerular Filtration RateHumansHypertensionINDEL MutationMaleMethylenetetrahydrofolate Reductase (NADPH2)Blood GlucoseCreatinineMethylenetetrahydrofolate Reductase (NADPH2)MTHFR protein, humanNitric Oxide Synthase Type IIIPeptidyl-Dipeptidase AAlbuminuriaEpidemiologyGeneticsHeritability

Identifiers

PMID27871254
PMCPMC5117595
OpenAlexW2552034501

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Registered trials

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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.