Evidence map›Paper›PMID 31317114›Full record

ArticleKidney international reports2019

APOL1-Associated Kidney Disease in Brazil.

Cristian Riella, Tobias A Siemens, Minxian Wang, Rodrigo P Campos, Thyago P Moraes, Leonardo V Riella, David J Friedman, Miguel C Riella, Martin R Pollak

Abstract read
In one paragraph

Article in Kidney international reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Review
  3. Article
  4. Kidney international reports · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. ADAR regulates APOL1 via A-to-I RNA editing by inhibition of MDA5 activation in a paradoxical biological circuit.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Kidney disease and APOL1.Human molecular genetics · 2021
    Review
  17. Article
  18. Article
  19. Article
  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

9 authors.

Cristian RiellaDivision of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Tobias A SiemensKidney Transplant Division, Cajuru Hospital, Curitiba, Brazil.
Minxian WangProgram in Medical and Population Genetics, Broad Institute of Harvard and MIT, Cambridge, Massachusetts, USA.
Rodrigo P CamposUniversidade Federal de Alagoas Medical School, Alagoas, Brazil.
Thyago P MoraesPontifícia Universidade Católica do Paraná Medical School, Curitiba, Brazil.
Leonardo V RiellaSchuster Transplantation Research Center, Renal Division, Brigham & Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
David J FriedmanDivision of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Miguel C RiellaPontifícia Universidade Católica do Paraná Medical School, Curitiba, Brazil.
Martin R PollakDivision of Nephrology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.

Funding

Harvard Clinical and Translational Science CenterUL1TR001102 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$106.2M
The Harvard Clinical and Translational Science CenterUL1TR002541 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2018 to 2022
$93.0M
APOL1 variants: Understanding the basis of disparities in rates of kidney diseaseR01MD007092 · NIMHD · BETH ISRAEL DEACONESS MEDICAL CENTER · PI FRIEDMAN, DAVID J, POLLAK, MARTIN R. · 2012 to 2021
$4.3M
NCATS NIH HHS UL1 TR001102NCATS NIH HHS UL1 TR002541NIMHD NIH HHS R01 MD007092
6 · The paper itself

Abstract

introductionCoding variants in apolipoprotein L-1 (APOL1) are associated with an increased risk of end-stage kidney disease (ESRD) in African American individuals under a recessive model of inheritance. The effect of the APOL1 risk alleles on kidney disease has been observed in studies in African American and African populations. Despite the 130 million individuals of recent African ancestry in South America, the impact of APOL1 has not been explored.

methodsIn this case-control study, we tested APOL1 genotype in 106 Brazilian HD (hemodialysis) patients with African ancestry and compared risk allele frequency with 106 healthy first-degree relatives. The association of risk alleles and ESRD was calculated with a linear mixed model and was adjusted for relatedness and additional confounders. In a broader survey, the age of dialysis initiation and APOL1 variants were analyzed in 274 HD patients.

resultsTwo APOL1 risk alleles were 10 times more common in patients with ESRD than in controls (9.4% vs. 0.9%; odds ratio [OR]: 10.95, SE = 1.49,

conclusionThe APOL1 risk variants were less frequent in dialysis patients of African ancestry in Brazil than in the United States. Nonetheless, carriers of 2 risk variants had 10-fold higher odds of ESRD. Age of dialysis initiation was markedly lower in 2-risk allele carriers, suggesting a more aggressive disease phenotype. The Brazilian population represents an opportunity to identify different sets of genetic modifiers or environmental triggers that might be present in more extensively studied populations.

Indexed as

age of dialysis initiationAPOL1APOL1-associated kidney diseaseend-stage kidney diseasegeneticsSouth America

Identifiers

PMID31317114
PMCPMC6611925

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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.