Evidence map›Paper›PMID 19430335›Full record

ReviewCurrent opinion in nephrology and hypertension2009

Angiogenesis in the kidney: a new therapeutic target?

Lilach O Lerman, Alejandro R Chade

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. From AKI to CKD: Maladaptive Repair and the Underlying Mechanisms.International journal of molecular sciences · 2022
    Review
  5. Endostatin in Renal and Cardiovascular Diseases.Kidney diseases (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Vascular endothelium in diabetes.American journal of physiology. Renal physiology · 2017
    Review
  10. Renal Arterial Disease and Hypertension.The Medical clinics of North America · 2017
    Review
  11. Article
  12. Review
  13. Obesity and renovascular disease.American journal of physiology. Renal physiology · 2015
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 2 institutions in 1 country.

Lilach O LermanDepartment of Internal Medicine, Divisions of Nephrology and Hypertension and Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota, USA.
Alejandro R Chade
Mayo Clinic · USState Street (United States) · US

Funding

Tissue Oxygenation in Human Renovascular HypertensionP01HL085307 · NHLBI · MAYO CLINIC ROCHESTER · PI ROMERO, JUAN C · 2007 to 2011
$10.4M
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
CT Evaluation of the Myocardial Effects of Risk FactorsR01HL077131 · NHLBI · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2004 to 2013
$2.8M
Autologous Progenitor Cells Delivery in Renovascular DiseaseR21DK077013 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2008 to 2009
$416k
NHLBI NIH HHS HL-77131NHLBI NIH HHS P01 HL085307NHLBI NIH HHS P01HL085307NHLBI NIH HHS R01 HL077131NIDDK NIH HHS DK-73608NIDDK NIH HHS DK77013NIDDK NIH HHS R01 DK073608NIDDK NIH HHS R21 DK077013
6 · The paper itself

Abstract

purpose of reviewThe prevalence of chronic kidney disease has been growing consistently for the past decades. Renal failure is often associated with defective angiogenesis, and recognition of the contribution of the renal microcirculation to the progression of chronic renal disease may aid in the development of therapeutic interventions. RECENT

findingsIntra-renal proliferation, remodeling, and/or rarefaction of microvessels in response to injury can all aggravate nephron damage, and experimental evidence suggests that they may constitute the early steps in the complex pathways involved in progressive renal injury. Recent studies showed the benefits of targeted interventions deemed to promote neovascularization (e.g. progenitor cells, growth factors) on the ischemic myocardium and brain and in a few models of renal disease. SUMMARY: Evidence of aberrant renal microvascular architecture in various forms of renal disease provides the impetus to attempt modulating the renal microcirculation to interfere with the disease process. Targeted interventions to preserve the renal microcirculation may not only decrease the evolving injury in renal vascular disease but also potentially constitute a coadjuvant intervention to become part of a comprehensive management plan to improve the success of parallel strategies to preserve renal function, such as revascularization.

Indexed as

AnimalsCell ProliferationHumansKidneyMicrocirculationNeovascularization, Physiologic

Identifiers

PMID19430335
PMCPMC2796055
OpenAlexW2037520995

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.