Evidence map›Paper›PMID 20441574›Full record

ArticleFibrogenesis & tissue repair2010

The role of renin angiotensin system inhibition in kidney repair.

Irene M van der Meer, Paolo Cravedi, Giuseppe Remuzzi

Open access · bronzeAbstract read
In one paragraph

Article in Fibrogenesis & tissue repair, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Non-immunosuppressive treatment for IgA nephropathy.The Cochrane database of systematic reviews · 2024
    Pooled it
  2. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2023
    Pooled it
  3. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2017
    Pooled it
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?Canadian journal of physiology and pharmacology · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Interventions for chronic kidney disease in people with sickle cell disease.The Cochrane database of systematic reviews · 2016
    Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Kidney aging--inevitable or preventable?Nature reviews. Nephrology · 2011
    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

3 authors at 2 institutions in 1 country.

Irene M van der MeerMario Negri Institute for Pharmacological Research, Bergamo, Italy. imvandermeer23@hotmail.com.
Paolo Cravedi
Giuseppe Remuzzi
Mario Negri Institute for Pharmacological Research · ITAzienda Ospedaliero Universitaria Ospedali Riuniti · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney diseases share common pathogenic mechanisms that, independently from the initial injury, lead to glomerular hyperfiltration, proteinuria, and progressive renal scarring and function loss. Inhibition of the renin angiotensin system (RAS) has been consistently found to reduce or halt the progressive deterioration of renal function through reduction of blood pressure and proteinuria, the two main determinants of renal function decline. In few instances, RAS inhibition may even promote amelioration of the glomerular filtration rate. Animal data suggest that chronic therapy with angiotensin-converting enzyme inhibitors or angiotensin II receptor type I blockers promotes regression of glomerulosclerosis, even in later phases of the disease. In humans, studies investigating the effect of angiotensin II inhibition on renal structural changes have shown inconsistent results, possibly due to small numbers and/or short duration of follow-up. Whether regression of glomerulosclerosis relies on a direct regenerative effect of RAS inhibition or on spontaneous kidney self-repair after the injury has been removed is still unknown. Improved understanding of mechanisms that promote renal regeneration may help in designing specific therapies to prevent the development of end-stage renal disease. This is a desirable goal, considering the economic burden of chronic kidney diseases and their effect on morbidity and mortality.

Identifiers

PMID20441574
PMCPMC2888753
OpenAlexW2123515893

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.