Evidence map›Paper›PMID 28025032›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2017

The metabolic syndrome and chronic kidney disease.

Xin Zhang, Lilach O Lerman

Abstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed, 4 pooled it
5.5field-weighted citation impact, top 4% 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

96 citing papers in PubMed, 4 syntheses or guidelines pooled it, 172 citations in OpenAlex.

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36 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

2 authors at 1 institution in 1 country.

Xin ZhangDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minn.
Lilach O LermanDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minn. Electronic address: lerman.lilach@mayo.edu.
Mayo Clinic · US

Funding

CT imaging for the assessment of kidney injury distal to renal artery stenosisR01DK073608 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2006 to 2015
$3.1M
Ultrasound Shockwave Therapy for Post-Stenotic Microvascular RemodelingR01HL123160 · NHLBI · MAYO CLINIC ROCHESTER · PI LERMAN, AMIR, LERMAN, LILACH O · 2015 to 2018
$3.0M
Hypoxia and inflammatory injury in human renovascular hypertensionR01DK100081 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O, TEXTOR, STEPHEN C · 2014 to 2018
$2.8M
MSC-derived microvesicles in metabolic syndrome and renovascular diseaseR01DK102325 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2015 to 2018
$2.8M
Noninvasive assessment of renal fibrosis using magnetization transfer MRIU01DK104273 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2014 to 2018
$1.8M
NHLBI NIH HHS R01 HL123160NIDDK NIH HHS R01 DK073608NIDDK NIH HHS R01 DK100081NIDDK NIH HHS R01 DK102325NIDDK NIH HHS U01 DK104273
6 · The paper itself

Abstract

The metabolic syndrome (MetS) is a cluster of cardiovascular risk factors including insulin resistance (IR), dyslipidemia, and hypertension, which may also foster development of chronic kidney disease. The mechanisms of MetS-induced kidney disease are not fully understood. The purpose of this review is to summarize recent discoveries regarding the impact of MetS on the kidney, particularly on the renal microvasculature and cellular mitochondria. Fundamental manifestations of MetS include IR and adipose tissue expansion, the latter promoting chronic inflammation and oxidative stress that exacerbate IR. Those in turn can elicit various kidney injurious events through endothelial dysfunction, activation of the renin-angiotensin-aldosterone system, and adipokine imbalance. Inflammation and IR are also major contributors to microvascular remodeling and podocyte injury. Hence, these events may result in hypertension, albuminuria, and parenchymal damage. In addition, dyslipidemia and excessive nutrient availability may impair mitochondrial function and thereby promote progression of kidney cell damage. Elucidation of the link between MetS and kidney injury may help develop preventative measures and possibly novel therapeutic targets to alleviate and avert development of renal manifestations.

Indexed as

HumansInflammationInsulin ResistanceMetabolic SyndromeRenal Insufficiency, ChronicRisk Factors

Identifiers

PMID28025032
PMCPMC5393937
OpenAlexW2559913810

What OpenQuestion holds

Textmetadata
LicenceTDM
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.