Evidence map›Paper›PMID 24600241›Full record

ReviewInternational journal of nephrology and renovascular disease2014

Obesity, hypertension, and chronic kidney disease.

Michael E Hall, Jussara M do Carmo, Alexandre A da Silva, Luis A Juncos, Zhen Wang, John E Hall

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of nephrology and renovascular disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 233 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
233citing papers in PubMed, 10 pooled it
20.9field-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

233 citing papers in PubMed, 10 syntheses or guidelines pooled it, 509 citations in OpenAlex.

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  18. Is hyperdynamic circulation a hallmark of obesity?International journal of obesity (2005) · 2026
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173 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

6 authors at 1 institution in 1 country.

Michael E HallDepartment of Medicine, University of Mississippi Medical Center, Jackson, MS, USA ; Department of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA.
Jussara M do CarmoDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA.
Alexandre A da SilvaDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA.
Luis A JuncosDepartment of Medicine, University of Mississippi Medical Center, Jackson, MS, USA ; Department of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA.
Zhen WangDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA.
John E HallDepartment of Physiology and Biophysics, Mississippi Center for Obesity Research, University of Mississippi Medical Center, Jackson, MS, USA.
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HALL, JOHN E · 1993 to 2018
$39.4M
The role of leptin in autoimmune-associated hypertensionP20GM104357 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI TAYLOR, ERIN BASSFORD · 2013 to 2022
$23.4M
NHLBI NIH HHS P01 HL051971NIGMS NIH HHS P20 GM104357
6 · The paper itself

Abstract

Obesity is a major risk factor for essential hypertension, diabetes, and other comorbid conditions that contribute to development of chronic kidney disease. Obesity raises blood pressure by increasing renal tubular sodium reabsorption, impairing pressure natriuresis, and causing volume expansion via activation of the sympathetic nervous system and renin-angiotensin-aldosterone system and by physical compression of the kidneys, especially when there is increased visceral adiposity. Other factors such as inflammation, oxidative stress, and lipotoxicity may also contribute to obesity-mediated hypertension and renal dysfunction. Initially, obesity causes renal vasodilation and glomerular hyperfiltration, which act as compensatory mechanisms to maintain sodium balance despite increased tubular reabsorption. However, these compensations, along with increased arterial pressure and metabolic abnormalities, may ultimately lead to glomerular injury and initiate a slowly developing vicious cycle that exacerbates hypertension and worsens renal injury. Body weight reduction, via caloric restriction and increased physical activity, is an important first step for management of obesity, hypertension, and chronic kidney disease. However, this strategy may not be effective in producing long-term weight loss or in preventing cardiorenal and metabolic consequences in many obese patients. The majority of obese patients require medical therapy for obesity-associated hypertension, metabolic disorders, and renal disease, and morbidly obese patients may require surgical interventions to produce sustained weight loss.

Indexed as

glomerular filtration raterenin–angiotensin–aldosterone systemsodium reabsorptionsympathetic nervous systemtype II diabetesvisceral adiposity

Identifiers

PMID24600241
PMCPMC3933708
OpenAlexW2004830232

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.