Evidence map›Paper›PMID 21782136›Full record

ReviewAdvances in chronic kidney disease2011

Off the beaten renin-angiotensin-aldosterone system pathway: new perspectives on antiproteinuric therapy.

Judit Gordon, Jeffrey B Kopp

Abstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Reno-protective effects of Phosphodiesterase 5 inhibitors.Clinical and experimental nephrology · 2021
    Review
  2. Article
  3. Article
  4. Phosphodiesterase type 5 inhibitors and kidney disease.International urology and nephrology · 2015
    Review
  5. Arrestin(g) podocyte injury with endothelin antagonism.Journal of the American Society of Nephrology : JASN · 2014
    Article
  6. 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 1 institution in 1 country.

Judit GordonDivision of Nephrology, Johns Hopkins Medical Institutions, Baltimore, MD, USA.
Jeffrey B Kopp
National Institutes of Health · US

Funding

Focal segmental glomerulosclerosis: TreatmentZIADK043412 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$7.4M
Focal segmental glomerulosclerosis: TreatmentZ01DK043412 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2007 to 2008
$989k
Intramural NIH HHS Z01 DK043412
6 · The paper itself

Abstract

CKD is a major public health problem in the developed and the developing world. The degree of proteinuria associated with renal failure is a generally well accepted marker of disease severity. Agents with direct antiproteinuric effects are highly desirable therapeutic strategies for slowing, or even halting, progressive loss of kidney function. We review progress on therapies acting further downstream of the renin-angiotensin-aldosterone system pathway (e.g., transforming growth factor-beta antagonism, endothelin antagonism) and on those acting independent of the renin-angiotensin-aldosterone system pathway. In all, we discuss 26 therapeutic targets or compounds and 2 lifestyle changes (dietary modification and weight loss) that have been used clinically for diabetic or nondiabetic kidney disease. These therapies include endogenous molecules (estrogens, isotretinoin), biologic antagonists (monoclonal antibodies, soluble receptors), and small molecules. Where mechanistic data are available, these therapies have been shown to exert favorable effects on glomerular cell phenotype. In some cases, recent work has indicated surprising new molecular pathways for some therapies, such as direct effects on the podocyte by glucocorticoids, rituximab, and erythropoietin. It is hoped that recent advances in the basic science of kidney injury will prompt development of more effective pharmaceutical and biologic therapies for proteinuria.

Indexed as

AnimalsAntibodies, Monoclonal, Murine-DerivedAntihypertensive AgentsCalcineurin InhibitorsEndothelinsErythropoietinFatty Acids, Omega-3Feeding BehaviorGlucocorticoidsHumansKidney DiseasesMiceProteinuriaRatsRenin-Angiotensin SystemRituximabAntibodies, Monoclonal, Murine-DerivedAntihypertensive AgentsCalcineurin InhibitorsEndothelinsErythropoietinFatty Acids, Omega-3GlucocorticoidsRituximabTransforming Growth Factors

Identifiers

PMID21782136
PMCPMC3245863
OpenAlexW2066152102

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.