Evidence map›Paper›PMID 28767097›Full record

ReviewInternational journal of molecular sciences2017

Sympathetic Overactivity in Chronic Kidney Disease: Consequences and Mechanisms.

Jasdeep Kaur, Benjamin E Young, Paul J Fadel

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
7.5field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 153 citations in OpenAlex.

  1. Review
  2. Sex-specific association between obesity and sympathetic nerve activity in HFpEF.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  3. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  4. Article
  5. Observational
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  7. Article
  8. Article
  9. Review
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  16. Review
  17. Future perspective on chronic kidney disease management.Journal of anesthesia and translational medicine · 2025
    Review
  18. Review
  19. Review
  20. Article

27 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

3 authors at 1 institution in 1 country.

Jasdeep KaurDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX 76019, USA. jasdeep.kaur@uta.edu.
Benjamin E YoungDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX 76019, USA. Ben.young@mavs.uta.edu.
Paul J FadelDepartment of Kinesiology, University of Texas at Arlington, Arlington, TX 76019, USA. paul.fadel@uta.edu.
The University of Texas at Arlington · US

Funding

Targeting Sympathetic Overactivity in CKD patients: Mechanisms & Novel TherapiesR01HL127071 · NHLBI · UNIVERSITY OF TEXAS ARLINGTON · PI FADEL, PAUL J · 2016 to 2019
$1.7M
NHLBI NIH HHS R01 HL127071
6 · The paper itself

Abstract

The incidence of chronic kidney disease (CKD) is increasing worldwide, with more than 26 million people suffering from CKD in the United States alone. More patients with CKD die of cardiovascular complications than progress to dialysis. Over 80% of CKD patients have hypertension, which is associated with increased risk of cardiovascular morbidity and mortality. Another common, perhaps underappreciated, feature of CKD is an overactive sympathetic nervous system. This elevation in sympathetic nerve activity (SNA) not only contributes to hypertension but also plays a detrimental role in the progression of CKD independent of any increase in blood pressure. Indeed, high SNA is associated with poor prognosis and increased cardiovascular morbidity and mortality independent of its effect on blood pressure. This brief review will discuss some of the consequences of sympathetic overactivity and highlight some of the potential pathways contributing to chronically elevated SNA in CKD. Mechanisms leading to chronic sympathoexcitation in CKD are complex, multifactorial and to date, not completely understood. Identification of the mechanisms and/or signals leading to sympathetic overactivity in CKD are crucial for development of effective therapeutic targets to reduce the increased cardiovascular risk in this patient group.

Indexed as

AnimalsHumansHypertension, RenalRenal Insufficiency, ChronicSympathetic Nervous Systemangiotensin IIasymmetric dimethylarginineblood pressurecardiovascular diseasehypertensionmuscle sympathetic nerve activitynitric oxideoxidative stresssympathetic outflow

Identifiers

PMID28767097
PMCPMC5578072
OpenAlexW2741868536

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.