Evidence map›Paper›PMID 25377913›Full record

ReviewAmerican journal of physiology. Renal physiology2015

The discovery of hypertension: evolving views on the role of the kidneys, and current hot topics.

Richard J Johnson, Miguel A Lanaspa, L Gabriela Sánchez-Lozada, Bernardo Rodriguez-Iturbe

Abstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2015. 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
3.7field-weighted citation impact, top 7% 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, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Role of hypertension in progression of pediatric CKD.Pediatric nephrology (Berlin, Germany) · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Uncovering the Complexities of Salt Sensitivity.Function (Oxford, England) · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Gut microbiota in hypertension.Current opinion in nephrology and hypertension · 2015
    Review
  18. Article
  19. Review
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

4 authors at 3 institutions in 3 countries.

Richard J JohnsonDivision of Renal Diseases and Hypertension, University of Colorado, Denver, Colorado; Richard.johnson@ucdenver.edu.
Miguel A LanaspaDivision of Renal Diseases and Hypertension, University of Colorado, Denver, Colorado;
L Gabriela Sánchez-LozadaLaboratory of Renal Physiopathology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico; and.
Bernardo Rodriguez-IturbeHospital Universitario y Universidad del Zulia; and Instituto Venezolano de Investigaciones Científicas (IVIC)-Zulia, Maracaibo, Venezuela.
University of Colorado Denver · USInstituto Nacional de Cardiología · MXUniversity of Zulia · VE

Funding

A novel role for endogenous fructose in ischemic acute kidney injuryK01DK095930 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LANASPA GARCIA, MIGUEL ANGEL · 2012 to 2016
$686k
NIDDK NIH HHS K01 DK095930
6 · The paper itself

Abstract

Primary hypertension is increasingly common and is associated with significant morbidity. Here, we review the history of its discovery and rise during the last century with an emphasis on studies trying to identify its cause. Early studies identified a defect in sodium excretion by the kidney as being central to the pathogenesis. Recent studies have focused on a variety of genetic, congenital (fetal programming), and acquired mechanisms for causing the defect in natriuresis. Certain risk factors are apparent, including genetic polymorphisms that regulate sodium excretion, a congenital reduction in nephron number, obesity and hyperleptinemia, an elevated sympathetic nervous system, diet (salt and fructose), and metabolic (hyperuricemia) mechanisms. The kidney shows evidence for renal arteriolar vasoconstriction, an intrarenal inflammatory response, local oxidative stress, and intrarenal activation of the renin-angiotensin system. Recent studies suggest that intrarenal T cells have an important role in causing hypertension to be persistent, likely due to the induction of a local autoimmune response to neoantigens such as heat shock protein 70 and protein aggregates formed by isoketals resulting from lipid peroxidation. Salt retention due to impairment in pressure-diuresis leads to the release of cardiotonic steroids and central nervous system effects that cause systemic vasoconstriction and a rise in blood pressure. Some recent studies suggest that salt may increase blood pressure not simply by effects on extracellular volume but rather as a consequence of hyperosmolarity. These new insights could lead to new approaches for the prevention and treatment of this important disease.

Indexed as

AnimalsBlood PressureEssential HypertensionHumansHypertensionKidneyObesityRenin-Angiotensin SystemSodium, DietarySodium, Dietaryautoimmunityprimary hypertensionsaltsodium

Identifiers

PMID25377913
PMCPMC6189741
OpenAlexW1986161908

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.