Evidence map›Paper›PMID 25007871›Full record

ReviewAmerican journal of physiology. Renal physiology2014

Infiltrating immune cells in the kidney in salt-sensitive hypertension and renal injury.

David L Mattson

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
10.5field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 145 citations in OpenAlex.

  1. Trial
  2. Article
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  4. Animal models of hypertension and concurrent organs injury.Animal models and experimental medicine · 2025
    Review
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  20. VASCULAR AND RENAL MECHANISMS OF PREECLAMPSIA.Current opinion in physiology · 2023
    Article

51 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

1 author at 1 institution in 1 country.

David L MattsonDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin dmattson@mcw.edu.
Medical College of Wisconsin · US

Funding

Therapeutic Effects of mTOR Inhibition in Salt-Sensitive HypertensionP01HL116264 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W · 2013 to 2021
$18.7M
Role of CD247 in Salt-Sensitive Hypertension and Renal DiseaseR01DK096859 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI MATTSON, DAVID L. · 2012 to 2016
$1.7M
NHLBI NIH HHS HL116264NHLBI NIH HHS P01 HL116264NIDDK NIH HHS DK96859NIDDK NIH HHS R01 DK096859
6 · The paper itself

Abstract

The importance of the immune system in hypertension, vascular disease, and renal disease has been appreciated for over 50 years. Recent experimental advances have led to a greater appreciation of the mechanisms whereby inflammation and immunity participate in cardiovascular disease. In addition to the experimental data, multiple studies in patients have demonstrated a strong correlation between the observations made in animals and humans. Of great interest is the development of salt-sensitive hypertension in humans with the concurrent increase in albumin excretion rate. Experiments in our laboratory have demonstrated that feeding a high-NaCl diet to Dahl salt-sensitive (SS) rats results in a significant infiltration of T lymphocytes into the kidney that is accompanied by the development of hypertension and renal disease. The development of disease in the Dahl SS closely resembles observations made in patients; studies were therefore performed to investigate the pathological role of infiltrating immune cells in the kidney in hypertension and renal disease. Pharmacological and genetic studies indicate that immune cell infiltration into the kidney amplifies the disease process. Further experiments demonstrated that infiltrating T cells may accentuate the Dahl SS phenotype by increasing intrarenal ANG II and oxidative stress. From these and other data, we hypothesize that infiltrating immune cells, which surround the blood vessels and tubules, can serve as a local source of bioactive molecules which mediate vascular constriction, increase tubular sodium reabsorption, and mediate the retention of sodium and water to amplify sodium-sensitive hypertension. Multiple experiments remain to be performed to refine and clarify this hypothesis.

Indexed as

AnimalsBlood PressureCell MovementDisease Models, AnimalHumansHypertensionImmune SystemKidneyKidney DiseasesRatsRats, Inbred DahlSodiumT-LymphocytesVasoconstrictionSodiumhypertensioninfiltrating immune cells

Identifiers

PMID25007871
PMCPMC4154114
OpenAlexW2116261776

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.