Evidence map›Paper›PMID 26553514›Full record

ReviewNature reviews. Nephrology2016

Hypertension-attributed nephropathy: what's in a name?

Barry I Freedman, Arthur H Cohen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing 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

61 citing papers in PubMed, 96 citations in OpenAlex.

  1. Review
  2. Article
  3. Pathophysiology and Clinical Relevance of Microvascular Remodeling in Arterial Hypertension.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Molecular Mechanisms of APOL1-Associated Kidney Disease.International journal of molecular sciences · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. Evaluation for genetic disease in kidney transplant candidates: A practice resource.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2025
    Review
  13. Review
  14. Chronic kidney disease.Nature reviews. Disease primers · 2025
    Review
  15. 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
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Barry I FreedmanDepartment of Internal Medicine, Section on Nephrology, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1053, USA.
Arthur H CohenDepartment of Pathology, Wake Forest School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1053, USA.
Wake Forest University · US

Funding

Genetic Analysis of African American Hypertensive End-Stage Renal DiseaseR01DK070941 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FREEDMAN, BARRY IRA · 2006 to 2015
$4.7M
Natural History of MYH9-Associated NephropathyR01DK084149 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FREEDMAN, BARRY IRA · 2009 to 2012
$2.3M
GENETIC ANALYSIS OF HUMAN HYPERTENSIVE ESRDR01HL056266 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI FREEDMAN, BARRY IRA · 1997 to 2001
$466k
NHLBI NIH HHS R01 HL56266NIDDK NIH HHS R01 DK070941NIDDK NIH HHS R01 DK084149
6 · The paper itself

Abstract

Unrelated disease processes commonly occur in non-diabetic individuals with mild-to-moderate hypertension and low level or absent proteinuria who present with chronic kidney disease: primary glomerulosclerosis in those with recent African ancestry, and arteriolar nephrosclerosis with resultant glomerular ischaemia potentially related to hypertension and vascular disease risk factors in other cases. Unfortunately, nephrologists often indiscriminately apply a diagnosis of 'hypertensive nephrosclerosis' to patients in either scenario, which implies that the hypertension is causative of their renal disease. Although nephropathies that are associated with variants in the apolipoprotein L1 gene (APOL1) often cause secondarily elevated blood pressure, they belong to the spectrum of focal segmental glomerulosclerosis and are not initiated by systemic hypertension. Because genetic testing for APOL1 variants and other glomerulosclerosis-associated gene variants is available and can provide a precise definition of disease pathogenesis, we believe that the term 'hypertensive nephrosclerosis' should now be abandoned and replaced with either gene-based (for example, APOL1-associated) glomerulosclerosis or arteriolar nephrosclerosis. Precision medicine will be key to improving diagnostic accuracy in this field. Discrimination of these disparate disorders has the potential to eradicate primary forms of glomerulosclerosis that are associated with APOL1 renal-risk variants.

Indexed as

Hypertension, RenalNephritisHumansRegistriesTerminology as Topic

Identifiers

PMID26553514
OpenAlexW2194441340

What OpenQuestion holds

Textmetadata
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.