Evidence map›Paper›PMID 20169462›Full record

ReviewClinical and experimental nephrology2010

Renal infiltration of immunocompetent cells: cause and effect of sodium-sensitive hypertension.

Bernardo Rodriguez-Iturbe

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical and experimental nephrology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  9. Review
  10. Article
  11. Review
  12. Renal inflammation, autoimmunity and salt-sensitive hypertension.Clinical and experimental pharmacology & physiology · 2012
    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

1 author at 1 institution in 1 country.

Bernardo Rodriguez-IturbeRenal Service, Instituto Venezolano de Investigaciones Científicas (IVIC)-Zulia, Hospital Universitario, Universidad del Zulia, Maracaibo, Venezuela. bernardori@telcel.net.ve
University of Zulia · VE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This review examines the participation of immunocompetent cells that accumulate in tubulointerstitial areas of the kidney in the pathogenesis of sodium-sensitive hypertension. Tubulointerstitial inflammation is a universal feature in experimental models of sodium-sensitive hypertension, and the suppression of inflammation and its constant companions, oxidative stress and renal angiotensin II activity, ameliorates or prevents hypertension. Human studies also support the association between renal inflammation and hypertension. The proinflammatory effects of a high sodium diet and the mechanisms by which renal inflammation induces sodium retention are discussed. It is suggested that autoimmune reactivity may play a role in the development and maintenance of renal inflammation in hypertensive states.

Indexed as

AdultAngiotensin IIAnimalsAutoimmunityDisease Models, AnimalHeat-Shock ProteinsHumansHypertensionImmunocompetenceInflammationKidneyMiddle AgedNephritisOxidative StressRatsSodiumAngiotensin IIHeat-Shock ProteinsSodiumSodium, Dietary

Identifiers

PMID20169462
OpenAlexW2058175966

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.