Evidence map›Paper›PMID 24658608›Full record

ArticlePloS one2014

MYH9 and APOL1 gene polymorphisms and the risk of CKD in patients with lupus nephritis from an admixture population.

Vinícius Sardão Colares, Silvia Maria de Oliveira Titan, Alexandre da Costa Pereira, Patrícia Malafronte, Mari M Cardena, Sidney Santos, Paulo C Santos, Cíntia Fridman, Rui Toledo Barros, Viktória Woronik

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05515653 (Impact of the Genetic Background as a Risk Factor for Atherosclerotic Cardiovascular Disease in the Brazilian Population), which is not on this map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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.

NCT05515653 unknown statusnot on this mapstarted 2022, after this paper: background citation

Impact of the Genetic Background as a Risk Factor for Atherosclerotic Cardiovascular Disease in the Brazilian Population

TypeobservationalSponsorHospital Alemão Oswaldo CruzRan2022 to 2024Enrolled3,974ConditionsCardiovascular Diseases, Acute MI, Stroke, Peripheral Arterial DiseaseArmsExposure to genetics (polygenic)
3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Progressive glomerular and tubular damage in sickle cell trait and sickle cell anemia mouse models.Translational research : the journal of laboratory and clinical medicine · 2018
    Article
  14. Article
  15. Association between polymorphisms in the APOB gene and hyperlipidemia in the Chinese Yugur population.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    Article
  16. Article
  17. What is damaging the kidney in lupus nephritis?Nature reviews. Rheumatology · 2016
    Review
  18. Lupus Nephritis: A Different Disease in European Patients?Kidney diseases (Basel, Switzerland) · 2015
    Review
  19. Review
  20. Article
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 3 institutions in 1 country.

Vinícius Sardão ColaresNephrology Division, Hospital das Clínicas, Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Silvia Maria de Oliveira TitanNephrology Division, Hospital das Clínicas, Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Alexandre da Costa PereiraMolecular Cardiology Laboratory, Heart Institute (InCor), Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Patrícia MalafronteNephrology Division, Hospital das Clínicas, Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Mari M CardenaDepartment of Legal Medicine, Ethics and Occupational Health, Medical School, University of São Paulo, Sao Paulo, Sao Paulo, Brazil.
Sidney SantosLaboratory of Human Genetics and Medicine, Federal University of Pará, Belém, Pará, Brazil.
Paulo C SantosMolecular Cardiology Laboratory, Heart Institute (InCor), Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Cíntia FridmanDepartment of Legal Medicine, Ethics and Occupational Health, Medical School, University of São Paulo, Sao Paulo, Sao Paulo, Brazil.
Rui Toledo BarrosNephrology Division, Hospital das Clínicas, Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Viktória WoronikNephrology Division, Hospital das Clínicas, Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.
Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo · BRUniversidade de São Paulo · BRUniversidade Federal do Pará · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MYH9 polymorphisms have been described to be associated with the risk of CKD in non-diabetic nephropathy, HIV nephropathy and FSGS. Predominating in black descendants, MHY9 genetic variants could partially explain the excess risk of CKD associated with African ancestry. However, recent data suggests that APOL1 gene co-segregate with MYH9, and could be the gene truly associated with CKD risk. In this study, we evaluated the role of MYH9 and APOL1 gene polymorphisms in the risk of CKD in Brazilian patients with lupus nephritis (LN). A retrospective analysis of 196 LN patients was done. MYH9 rs4821480, rs2032487, rs4821481 and rs3752462, APOL 1rs73885319, rs16996616, rs60910145, rs71785313, and APOL3 rs11089781 gene polymorphisms were determined. Genetic ancestry was ascertained both by autossomal ancestry and mitochondrial haplogroup. Primary outcome was defined as doubling of serum creatinine (DC) or end stage renal disease (ESRD). Sixty-two patients presented the PO. In our population, MYH9 and APOL1 were not in LD. None APOL polymorphism was associated with the PO, whereas rs3752462 MYH9 polymorphism showed a positive association (HR3.72, 95%CI 1.47-9.38, p = 0.005). When we analyzed the MYH9 E1 haplotype, the GCCT carriers (1 or 2 alelles present in 29.7% in the PO group vs. 18.5% in controls) showed a significant association to the risk of PO, even after adjustments for baseline estimated creatinine clearance and autossomal ancestry (HR 2.0, 95%CI 1.2-3.4, p = 0.01). Our results show that in our population MYH9, but not APOL1, gene polymorphisms confer an increased risk of CKD in LN patients, independently of race.

Indexed as

Polymorphism, GeneticAdultApolipoprotein L1ApolipoproteinsBrazilFemaleGenetic Association StudiesGenetic Predisposition to DiseaseHumansLinkage DisequilibriumLipoproteins, HDLLupus NephritisMolecular Motor ProteinsMyosin Heavy ChainsRenal Insufficiency, ChronicAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDLMolecular Motor ProteinsMYH9 protein, humanMyosin Heavy Chains

Identifiers

PMID24658608
PMCPMC3962338
OpenAlexW1974070578

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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.