Evidence map›Paper›PMID 16316596›Full record

ReviewCurrent diabetes reports2005

Lipids and diabetic renal disease.

Mark E Cooper, Karin A M Jandeleit-Dahm

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current diabetes reports, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

  1. Trial
  2. Sodium-Glucose Cotransporter 2 Inhibitors and the Kidney.Diabetes spectrum : a publication of the American Diabetes Association · 2021
    Article
  3. Review
  4. Article
  5. Review
  6. New therapeutic agents in diabetic nephropathy.The Korean journal of internal medicine · 2017
    Review
  7. Article
  8. Article
  9. Diabetes and its comorbidities--where East meets West.Nature reviews. Endocrinology · 2013
    Review
  10. Lipids and diabetic nephropathy.Current diabetes reports · 2006
    Review
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.

Mark E CooperJDRF Danielle Alberti Memorial Centre for Diabetic Complications, Vascular Division - Wynn Domain, Baker Heart Research Institute, 75 Commercial Road, Melbourne, Victoria 3004, Australia. mark.cooper@baker.edu.au
Karin A M Jandeleit-Dahm
The Heart Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is commonly associated with dyslipidemia, but the role of lipids in the progression of this disorder remains unresolved. In particular, the role of lipid-lowering drugs, such as 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors and fibrates, as renoprotective agents is not clarified. Experimental studies have demonstrated that dietary lipids promote renal injury and that statins, independent of their lipid-lowering effects, confer renoprotection via effects on intrarenal hemodynamics and renal cytokine and chemokine expression. Clinical studies have in general been underpowered, but a recent meta-analysis and findings from the Heart Protection Study suggest that statins may be renoprotective. Nevertheless, with the convincing antiatherosclerotic effects of these agents, including in the setting of diabetes, they should be widely administered in the diabetic population with or at risk for nephropathy.

Indexed as

AnimalsDiabetic NephropathiesDyslipidemiasHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLipidsRisk FactorsHydroxymethylglutaryl-CoA Reductase InhibitorsLipids

Identifiers

PMID16316596
OpenAlexW2154247759

What Socratic holds

Texttitle and abstract
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.