Evidence map›Paper›PMID 30451737›Full record

ReviewCurrent opinion in nephrology and hypertension2019

Genes and environment in chronic kidney disease hotspots.

David J Friedman

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

19 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Personalized Antifibrotic Therapy in CKD Progression.Journal of personalized medicine · 2024
    Review
  9. Genetic risk factors for Mesoamerican nephropathy.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Chronic kidney disease of non-traditional origin in Mesoamerica: a disease primarily driven by occupational heat stress.Revista panamericana de salud publica = Pan American journal of public health · 2020
    Article
  19. 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

1 author at 1 institution in 1 country.

David J FriedmanBeth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, USA.
Harvard University · US

Funding

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
Role of Genetic Susceptibility in the Central American Kidney Disease EpidemicR01DK116021 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BROOKS, DANIEL R, FRIEDMAN, DAVID J · 2018 to 2022
$3.7M
NIDDK NIH HHS R01 DK116021NIMHD NIH HHS R01 MD007092
6 · The paper itself

Abstract

purpose of reviewChronic kidney disease (CKD) can cluster in geographic locations or in people of particular genetic ancestries. We explore APOL1 nephropathy and Balkan nephropathy as examples of CKD clustering that illustrate genetics and environment conspiring to cause high rates of kidney disease. Unexplained hotspots of kidney disease in Asia and Central America are then considered from the perspective of potential gene × environment interactions. RECENT

findingsWe report on evidence supporting both genes and environment in these CKD hotspots. Differing genetic susceptibility between populations and within populations may explain why causal environmental risk factors have been so hard to identify conclusively. Similarly, one cannot explain why these epidemics of kidney disease are happening now without invoking environmental changes. SUMMARY: Approaches to these CKD hotspots are of necessity becoming more holistic. Genetic studies may help us identify the environmental triggers by teaching us about disease biology and may empower environmental risk factor studies by allowing for stratification of study participants by genetic susceptibility.

Indexed as

Apolipoprotein L1Balkan NephropathyEnvironmentGenetic Predisposition to DiseaseHumansRenal Insufficiency, ChronicRisk FactorsAPOL1 protein, humanApolipoprotein L1

Identifiers

PMID30451737
PMCPMC6763202
OpenAlexW2900626841

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.