Evidence map›Paper›PMID 25762356›Full record

ReviewNephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association2015

Immunity in arterial hypertension: associations or causalities?

Hans-Joachim Anders, Marcus Baumann, Giovanni Tripepi, Francesca Mallamaci

Open access · bronzeAbstract readReview
In one paragraph

Review in Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 28 citations in OpenAlex.

  1. Inflammatory Biomarkers in Hypertension.Current medicinal chemistry · 2025
    Review
  2. Article
  3. Observational
  4. Inflammatory pathways are central to posterior cerebrovascular artery remodelling prior to the onset of congenital hypertension.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  5. Review
  6. Review
  7. Role of Inflammatory Diseases in Hypertension.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2017
    Review
  8. Article
  9. Review
  10. Immune Mechanisms in Arterial Hypertension.Journal of the American Society of Nephrology : JASN · 2016
    Review
  11. 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 2 countries.

Hans-Joachim AndersNephrologisches Zentrum, Medizinische Klinik und Poliklinik IV, Klinikum der Universität München, Munich, Germany.
Marcus BaumannDepartment of Nephrology, Klinikum rechts der Isar der Technischen Universität München, Munich, Germany.
Giovanni TripepiNephrology, Dialysis and Transplantation Unit & CNR-IFC, Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension of Reggio Calabria, Reggio Calabria, Italy.
Francesca MallamaciNephrology, Dialysis and Transplantation Unit & CNR-IFC, Clinical Epidemiology and Physiopathology of Renal Disease and Hypertension of Reggio Calabria, Reggio Calabria, Italy.
Istituto di Fisiologia Clinica · ITLMU Klinikum · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Numerous studies describe associations between markers of inflammation and arterial hypertension (aHT), but does that imply causality? Interventional studies that reduce blood pressure reduced also markers of inflammation, but does immunosuppression improve hypertension? Here, we review the available mechanistic data. Aberrant immunity can trigger endothelial dysfunction but is hardly ever the primary cause of aHT. Innate and adaptive immunity get involved once hypertension has caused vascular wall injury as immunity is a modifier of endothelial dysfunction and vascular wall remodelling. As vascular remodelling progresses, immunity-related mechanisms can become significant cofactors for cardiovascular (CV) disease progression; vice versa, suppressing immunity can improve hypertension and CV outcomes. Innate and adaptive immunity both contribute to vascular wall remodelling. Innate immunity is driven by danger signals that activate Toll-like receptors and other pattern-recognition receptors. Adaptive immunity is based on loss of tolerance against vascular autoantigens and includes autoreactive T-cell immunity as well as non-HLA angiotensin II type 1 receptor-activating autoantibodies. Such processes involve numerous other modulators such as regulatory T cells. Together, immunity is not causal for hypertension but rather an important secondary pathomechanism and a potential therapeutic target in hypertension.

Indexed as

AnimalsCardiovascular DiseasesCausalityHumansHypertensionImmunity, InnateInflammationatherosclerosisblood pressureinfectioninflammasomestenosis

Identifiers

PMID25762356
PMCPMC4832987
OpenAlexW2022071998

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.