Evidence map›Paper›PMID 19859071›Full record

ReviewNature reviews. Nephrology2009

An update on the lipid nephrotoxicity hypothesis.

Xiong Z Ruan, Zac Varghese, John F Moorhead

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 6 pooled it
3.9field-weighted citation impact, top 6% 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

194 citing papers in PubMed, 6 syntheses or guidelines pooled it, 346 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Lipid homeostasis in diabetic kidney disease.International journal of biological sciences · 2024
    Pooled it
  4. Pooled it
  5. Pooled it
  6. Pooled it
  7. Trial
  8. Trial
  9. Trial
  10. Features of Lipid Disorders in Cardiovascular-Kidney-Metabolic Syndrome.International journal of molecular sciences · 2026
    Review
  11. Article
  12. Review
  13. The roles of free-fatty acid receptors in the pathophysiology of renal disorders.The Journal of pharmacology and experimental therapeutics · 2026
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Protective Role ofAdvanced biomedical research · 2026
    Article

134 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.

Xiong Z RuanCentre for Nephrology, University College London Medical School, Royal Free Campus, London, UK. x.ruan@medsch.ucl.ac.uk
Zac Varghese
John F Moorhead
The Royal Free Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

When the 'lipid nephrotoxicity hypothesis' was proposed in 1982, it brought together several disparate experimental findings in hyperlipidemia and renal disease to suggest that concomitant hyperlipidemia and proteinuria would cause self-perpetuating renal disease once the initial glomerular insult was no longer present. This process would be analogous to atherosclerosis. Since 1982, increasing evidence has supported the hypothesis that lipid abnormalities contribute to both atherosclerosis and glomerulosclerosis. In this Review, we discuss research developments that are relevant to the lipid nephrotoxicity hypothesis. We describe how inflammatory stress accompanying chronic kidney disease modifies lipid homeostasis by increasing cholesterol uptake mediated by lipoprotein receptors, inhibiting cholesterol efflux mediated by the ATP-binding cassette transporter 1 and impairing cholesterol synthesis in peripheral cells. As a result of these events, cholesterol relocates to and accumulates in renal, vascular, hepatic and possibly other tissues. The combination of increased cellular cholesterol influx and reduced efflux causes injury in some tissues and lowers the plasma cholesterol level. In addition, inflammatory stress causes a degree of statin resistance via unknown mechanisms. These phenomena alter traditional understanding of the pathogenesis of lipid-mediated renal and vascular injury and could influence the clinical evaluation of renal and cardiovascular risk and the role of lipid-lowering treatment in affected patients.

Indexed as

AtherosclerosisHumansHyperlipidemiasLipidsProteinuriaRenal Insufficiency, ChronicLipids

Identifiers

PMID19859071
OpenAlexW2054395645

What OpenQuestion holds

Textmetadata
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.