Evidence map›Paper›PMID 28845468›Full record

ArticleKidney international reports2017

Evolutionary Nephrology.

Robert L Chevalier

Open access · goldAbstract read
In one paragraph

Article in Kidney international reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Evolution-informed therapy for kidney disease.Evolution, medicine, and public health · 2023
    Article
  7. Article
  8. Review
  9. Neonatal acute kidney injury: a case-based approach.Pediatric nephrology (Berlin, Germany) · 2021
    Review
  10. Nephron number and its determinants: a 2020 update.Pediatric nephrology (Berlin, Germany) · 2021
    Article
  11. Article
  12. Review
  13. Evolution, kidney development, and chronic kidney disease.Seminars in cell & developmental biology · 2019
    Review
  14. Article
  15. Are Current Strategies for Building a Human Kidney Misguided? Speculative Alternatives.Journal of the American Society of Nephrology : JASN · 2018
    Article
  16. Renal fibrosis: Primacy of the proximal tubule.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  17. Evolution and Kidney Development: A Rosetta Stone for Nephrology.Journal of the American Society of Nephrology : JASN · 2018
    Article
  18. Measuring rat kidney glomerular number and size in vivo with MRI.American journal of physiology. Renal physiology · 2018
    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.

Robert L ChevalierDepartment of Pediatrics, The University of Virginia, Charlottesville, VA.
University of Virginia · US

Funding

Single-Cell Epigenomics, Transcriptomics, and Bioinformatics CoreP50DK096373 · NIDDK · UNIVERSITY OF VIRGINIA · PI Silvia Medrano · 2012 to 2026
$13.8M
NIDDK NIH HHS P50 DK096373
6 · The paper itself

Abstract

Progressive kidney disease follows nephron loss, hyperfiltration, and incomplete repair, a process described as "maladaptive." In the past 20 years, a new discipline has emerged that expands research horizons: evolutionary medicine. In contrast to physiologic (homeostatic) adaptation, evolutionary adaptation is the result of reproductive success that reflects natural selection. Evolutionary explanations for physiologically maladaptive responses can emerge from mismatch of the phenotype with environment or evolutionary tradeoffs. Evolutionary adaptation to a terrestrial environment resulted in a vulnerable energy-consuming renal tubule and a hypoxic, hyperosmolar microenvironment. Natural selection favors successful energy investment strategy: energy is allocated to maintenance of nephron integrity through reproductive years, but this declines with increasing senescence after ~40 years of age. Risk factors for chronic kidney disease include restricted fetal growth or preterm birth (life history tradeoff resulting in fewer nephrons), evolutionary selection for APOL1 mutations (that provide resistance to trypanosome infection, a tradeoff), and modern life experience (Western diet mismatch leading to diabetes and hypertension). Current advances in genomics, epigenetics, and developmental biology have revealed proximate causes of kidney disease, but attempts to slow kidney disease remain elusive. Evolutionary medicine provides a complementary approach by addressing ultimate causes of kidney disease. Marked variation in nephron number at birth, nephron heterogeneity, and changing susceptibility to kidney injury throughout life history are the result of evolutionary processes. Combined application of molecular genetics, evolutionary developmental biology (evo-devo), developmental programming and life history theory may yield new strategies for prevention and treatment of chronic kidney disease.

Indexed as

adaptationchronic kidney diseaseenergyevolutionlife historyprogression

Identifiers

PMID28845468
PMCPMC5568830
OpenAlexW4211099190

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.