Evidence map›Paper›PMID 27546606›Full record

ReviewKidney international2016

An alternative hypothesis to the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension.

Theodore W Kurtz, Stephen E DiCarlo, Michal Pravenec, Olga Schmidlin, Masae Tanaka, R Curtis Morris

Open access · greenAbstract readReview
In one paragraph

Review in Kidney international, 2016. 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
5.7field-weighted citation impact, top 4% 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, 35 citations in OpenAlex.

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  15. Article
  16. Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017
    Review
  17. Eplerenone-Resistant Salt-Sensitive Hypertension in Nedd4-2 C2 KO Mice.International journal of molecular sciences · 2017
    Article
  18. Understanding the Two Faces of Low-Salt Intake.Current hypertension reports · 2017
    Review
  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

6 authors at 3 institutions in 2 countries.

Theodore W KurtzDepartment of Laboratory Medicine, University of California, San Francisco, California, USA. Electronic address: Ted.Kurtz@ucsf.edu.
Stephen E DiCarloDepartment of Physiology, Wayne State University, Detroit, Michigan, USA.
Michal PravenecInstitute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Olga SchmidlinDepartment of Medicine, University of California, San Francisco, California, USA.
Masae TanakaDepartment of Medicine, University of California, San Francisco, California, USA.
R Curtis MorrisDepartment of Medicine, University of California, San Francisco, California, USA.
University of California, San Francisco · USCzech Academy of Sciences · CZWayne State University · US

Funding

ZD1839 FOR MALIGNANT ASTROCYTOMA OR GLIOBLASTOMA AND MENINGIOMAM01RR000079 · NCRR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KESSLER, DAVID A · 1985 to 2006
$26.0M
SELECTIVE SODIUM-SENSITIVITY IN SALT-SENSITIVE BLACKSR01HL064230 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MORRIS, RALPH CURTIS · 2000 to 2006
$2.1M
NCRR NIH HHS M01 RR000079NHLBI NIH HHS R01 HL064230
6 · The paper itself

Abstract

It is widely held that in response to high salt diets, normal individuals are acutely and chronically resistant to salt-induced hypertension because they rapidly excrete salt and retain little of it so that their blood volume, and therefore blood pressure, does not increase. Conversely, it is also widely held that salt-sensitive individuals develop salt-induced hypertension because of an impaired renal capacity to excrete salt that causes greater salt retention and blood volume expansion than that which occurs in normal salt-resistant individuals. Here we review results of both acute and chronic salt-loading studies that have compared salt-induced changes in sodium retention and blood volume between normal subjects (salt-resistant normotensive control subjects) and salt-sensitive subjects. The results of properly controlled studies strongly support an alternative view: during acute or chronic increases in salt intake, normal salt-resistant subjects undergo substantial salt retention and do not excrete salt more rapidly, retain less sodium, or undergo lesser blood volume expansion than do salt-sensitive subjects. These observations: (i) directly conflict with the widely held view that renal excretion of sodium accounts for resistance to salt-induced hypertension, and (ii) have implications for contemporary understanding of how various genetic, immunologic, and other factors determine acute and chronic blood pressure responses to high salt diets.

Indexed as

Blood VolumeCase-Control StudiesHumansHypertensionSodiumSodium Chloride, DietarySodiumSodium Chloride, Dietaryblood pressurehypertensionkidneysaltsalt-resistancesalt-sensitivitysodiumsodium chloride

Identifiers

PMID27546606
PMCPMC5065753
OpenAlexW2511797717

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.