Evidence map›Paper›PMID 23470819›Full record

ReviewCurrent opinion in nephrology and hypertension2013

Rethinking hypertensive kidney disease: arterionephrosclerosis as a genetic, metabolic, and inflammatory disorder.

Jeffrey B Kopp

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.4field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Heterogeneous afferent arteriolopathy: a key concept for understanding blood pressure-dependent renal damage.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Frontiers in medicine · 2022
    Article
  13. Kidney disease and APOL1.Human molecular genetics · 2021
    Review
  14. Review
  15. Article
  16. Article
  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

1 author at 1 institution in 1 country.

Jeffrey B KoppKidney Disease Section, NIDDK, NIH, Bethesda, Maryland, USA.
National Institutes of Health · US

Funding

Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
Focal segmental glomerulosclerosis: HIV-associated nephropathyZIADK043411 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HEYMANN, JURGEN · 2009 to 2024
$7.3M
FOCAL SEGMENTAL GLOMERULOSCLEROSIS--PATHOGENESIS AND TREATMENTZ01DK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 1997 to 2008
$1.0M
Intramural NIH HHS Z01 DK043308
6 · The paper itself

Abstract

purpose of reviewHypertension is the attributed cause of approximately 30% of end-stage kidney disease cases in the United States, but there has been controversy as to whether benign hypertension is a cause of chronic kidney disease. RECENT

findingsThe histology of chronic kidney disease attributed to nonmalignant hypertension is arterionephrosclerosis, with pathology in the terminal branches of the interlobular arteries, together with global glomerulosclerosis. The identification of coding region variants in APOL1, encoding apolipoprotein L1, has opened a new perspective on this debate. These variants are restricted to populations of recent African descent and are strongly associated with clinically diagnosed arterionephrosclerosis, particularly when there is moderate-grade or high-grade proteinuria or progression to more advanced levels of kidney dysfunction. Nevertheless, not all African Americans with hypertension who progress to end-stage kidney disease have two APOL1 risk variants, and individuals of European and Asian descent also manifest arterionephrosclerosis. Further, we do not understand the mechanisms by which APOL1 initiates pathology in the renal microcirculation. SUMMARY: APOL1 nephropathy comprises a disease spectrum (perhaps with distinct endophenotypes), including focal segmental glomerulosclerosis, collapsing glomerulopathy, and arterionephrosclerosis. The terms hypertensive kidney disease and hypertensive nephrosclerosis have outlived their usefulness. It may be time to use the established, etiologically neutral term, arterionephrosclerosis, to consider whether this is a disease rather than a pathologic description, and to determine the causal role of various clinical correlates including aging, obesity, hyperlipidemia, smoking, chronic inflammation, and oxidative stress.

Indexed as

Energy MetabolismGenetic VariationOxidative StressAnimalsApolipoprotein L1ApolipoproteinsComorbidityDisease ProgressionGenetic Predisposition to DiseaseHumansHypertension, RenalInflammation MediatorsLipoproteins, HDLNephritisPhenotypePrognosisAPOL1 protein, humanApolipoprotein L1ApolipoproteinsInflammation MediatorsLipoproteins, HDL

Identifiers

PMID23470819
PMCPMC4165431
OpenAlexW1980789419

What OpenQuestion holds

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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.