Evidence map›Paper›PMID 26337134›Full record

ReviewAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2015

Cholesterol Metabolism in CKD.

Allison B Reiss, Iryna Voloshyna, Joshua De Leon, Nobuyuki Miyawaki, Joseph Mattana

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06795698 (The Effect of Prophylactic Anticoagulation on Major Bleeding Events in Hospitalized Chronic Kidney Disease and Lower Limb Fracture Patients. a Phase 2, Randomized, Doble Blind, Control Trial), which is not on this map. Cited by 76 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 3 pooled it
6.5field-weighted citation impact, top 3% 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.

NCT06795698 phase2completednot on this mapstarted 2019, after this paper: background citation

The Effect of Prophylactic Anticoagulation on Major Bleeding Events in Hospitalized Chronic Kidney Disease and Lower Limb Fracture Patients. a Phase 2, Randomized, Doble Blind, Control Trial

TypeinterventionalSponsorHospital Civil de GuadalajaraRan2019 to 2024Enrolled61ConditionsFractures, Bone, CKD Stage 4, CKD Stage 3, CKD Stage 5ArmsEnoxaparin
3 · Its place in the literature

Who cites it

76 citing papers in PubMed, 3 syntheses or guidelines pooled it, 130 citations in OpenAlex.

  1. Pooled it
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  6. Features of Lipid Disorders in Cardiovascular-Kidney-Metabolic Syndrome.International journal of molecular sciences · 2026
    Review
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16 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

5 authors at 1 institution in 1 country.

Allison B ReissDepartment of Medicine and Winthrop Research Institute, Winthrop University Hospital, Mineola, NY. Electronic address: areiss@winthrop.org.
Iryna VoloshynaDepartment of Medicine and Winthrop Research Institute, Winthrop University Hospital, Mineola, NY.
Joshua De LeonDepartment of Medicine and Winthrop Research Institute, Winthrop University Hospital, Mineola, NY.
Nobuyuki MiyawakiDepartment of Medicine and Winthrop Research Institute, Winthrop University Hospital, Mineola, NY.
Joseph MattanaDepartment of Medicine and Winthrop Research Institute, Winthrop University Hospital, Mineola, NY.
Winthrop-University Hospital · US

Funding

Resveratrol as an Innovative Cardiovascular Therapeutic Strategy in LupusR21AT007032 · NCCIH · NYU WINTHROP HOSPITAL · PI REISS, ALLISON B · 2013 to 2014
$353k
NCCIH NIH HHS R21 AT007032NCCIH NIH HHS R21 AT007032-01A1
6 · The paper itself

Abstract

Patients with chronic kidney disease (CKD) have a substantial risk of developing coronary artery disease. Traditional cardiovascular disease (CVD) risk factors such as hypertension and hyperlipidemia do not adequately explain the high prevalence of CVD in CKD. Both CVD and CKD are inflammatory states and inflammation adversely affects lipid balance. Dyslipidemia in CKD is characterized by elevated triglyceride levels and high-density lipoprotein levels that are both decreased and dysfunctional. This dysfunctional high-density lipoprotein becomes proinflammatory and loses its atheroprotective ability to promote cholesterol efflux from cells, including lipid-overloaded macrophages in the arterial wall. Elevated triglyceride levels result primarily from defective clearance. The weak association between low-density lipoprotein cholesterol level and coronary risk in CKD has led to controversy over the usefulness of statin therapy. This review examines disrupted cholesterol transport in CKD, presenting both clinical and preclinical evidence of the effect of the uremic environment on vascular lipid accumulation. Preventative and treatment strategies are explored.

Indexed as

AnimalsBiological TransportCardiovascular DiseasesCholesterol, HDLHumansRenal Insufficiency, ChronicRisk FactorsCholesterol, HDLatherosclerosiscardiovascular disease (CVD)Cholesterol transportchronic kidney disease (CKD)dyslipidemiahigh-density lipoprotein (HDL)inflammationlipid-lowering therapylow-density lipoprotein (LDL)nontraditional risk factorreactive oxygen species (ROS)statin therapyuremic toxins

Identifiers

PMID26337134
PMCPMC4658227
OpenAlexW1273733467

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.