Evidence map›Paper›PMID 26009251›Full record

ReviewArchives of medical research2015

Residual Cardiovascular Risk in Chronic Kidney Disease: Role of High-density Lipoprotein.

Valentina Kon, Haichun Yang, Sergio Fazio

Open access · greenAbstract readReview
In one paragraph

Review in Archives of medical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
5.6field-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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Lifestyles, metabolome and diabetic kidney disease: a cohort study.QJM : monthly journal of the Association of Physicians · 2026
    Article
  3. Article
  4. Lipoprotein(a): structural basis, bidirectional risk, and therapeutic frontiers.Journal of clinical biochemistry and nutrition · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.International journal of environmental research and public health · 2023
    Review
  12. HDL and chronic kidney disease.Atherosclerosis plus · 2023
    Article
  13. Article
  14. Review
  15. Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Valentina KonDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Electronic address: valentina.kon@vanderbilt.edu.
Haichun YangPathology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Sergio FazioCenter for Preventive Cardiology, Knight Cardiovascular Institute, Oregon Health and Science University, Portland, Oregon, USA.
Vanderbilt University Medical Center · USOregon Health & Science University · US

Funding

Non-coding RNA & Bioinformatics CoreP01HL116263 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LINTON, MACRAE F · 2014 to 2025
$24.7M
Role of Macrophage-Specific AT1R in Atherosclerosis of Chronic Kidney DysfunctionR01HL087061 · NHLBI · VANDERBILT UNIVERSITY · PI KON, VALENTINA · 2008 to 2012
$1.9M
NHLBI NIH HHS P01 HL116263NHLBI NIH HHS R01 HL087061
6 · The paper itself

Abstract

Although reducing low-density lipoprotein-cholesterol (LDL-C) levels with lipid-lowering agents (statins) decreases cardiovascular disease (CVD) risk, a substantial residual risk (up to 70% of baseline) remains after treatment in most patient populations. High-density lipoprotein (HDL) is a potential contributor to residual risk, and low HDL-cholesterol (HDL-C) is an established risk factor for CVD. However, in contrast to conventional lipid-lowering therapies, recent studies show that pharmacologic increases in HDL-C levels do not bring about clinical benefits. These observations have given rise to the concept of dysfunctional HDL where increases in serum HDL-C may not be beneficial because HDL loss of function is not corrected by or even intensified by the therapy. Chronic kidney disease (CKD) increases CVD risk, and patients whose CKD progresses to end-stage renal disease (ESRD) requiring dialysis are at the highest CVD risk of any patient type studied. The ESRD population is also unique in its lack of significant benefit from standard lipid-lowering interventions. Recent studies indicate that HDL-C levels do not predict CVD in the CKD population. Moreover, CKD profoundly alters metabolism and composition of HDL particles and impairs their protective effects on functions such as cellular cholesterol efflux, endothelial protection, and control of inflammation and oxidation. Thus, CKD-induced perturbations in HDL may contribute to the excess CVD in CKD patients. Understanding the mechanisms of vascular protection in renal disease can present new therapeutic targets for intervention in this population.

Indexed as

ApolipoproteinsCardiovascular DiseasesDyslipidemiasHumansHypolipidemic AgentsLipoproteins, HDLMaleMiddle AgedRenal Insufficiency, ChronicRisk FactorsApolipoproteinsHypolipidemic AgentsLipoproteins, HDLCardiovascular diseaseCholesterol effluxChronic kidney diseaseHDLResidual cardiovascular riskStatins

Identifiers

PMID26009251
PMCPMC4805367
OpenAlexW1571704165

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.