Evidence map›Paper›PMID 29600408›Full record

ReviewClinical and experimental nephrology2018

Independent regulation of renin-angiotensin-aldosterone system in the kidney.

Akira Nishiyama, Hiroyuki Kobori

Open access · hybridAbstract readReview
In one paragraph

Review in Clinical and experimental nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
9.1field-weighted citation impact, top 1% 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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Network pharmacology andArchives of medical science : AMS · 2026
    Article
  7. Article
  8. Observational
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Elucidating the complex interplay between chronic kidney disease and hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
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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.

Akira NishiyamaDepartment of Pharmacology, Faculty of Medicine, Kagawa University, 1750-1 Miki-cho, Kita-gun, Kagawa, 761-0793, Japan. akira@med.kagawa-u.ac.jp.ORCID http://orcid.org/0000-0001-5971-820X
Hiroyuki KoboriDepartments of Pharmacology and Nephrology, Faculty of Medicine, International University of Health and Welfare, Narita, Japan.
International University of Health and Welfare · JPKagawa University · JP

Funding

Intrarenal Augmentation of Angiotensinogen by Ang IIR01DK072408 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2006 to 2010
$1.2M
Japan Society for the Promotion of Science (JSPS) Grants-in-Aid for Scientific Research (KAKENHI) 26460343NIDDK NIH HHS R01 DK072408This study was supported in part by the Japan Society for the Promotion of Science (JSPS) Grants-in-Aid for Scientific Research 15K08237
6 · The paper itself

Abstract

Renin-angiotensin-aldosterone system (RAAS) plays important roles in regulating renal hemodynamics and functions, as well as in the pathophysiology of hypertension and renal disease. In the kidney, angiotensin II (Ang II) production is controlled by independent multiple mechanisms. Ang II is compartmentalized in the renal interstitial fluid with much higher concentrations than those existing in the circulation. Inappropriate activation of the intrarenal RAAS is an important contributor to the pathogenesis of hypertension and renal injury. It has been revealed that intrarenal Ang II levels are predominantly regulated by angiotensinogen and therefore, urinary angiotensinogen could be a biomarker for intrarenal Ang II generation. In addition, recent studies have demonstrated that aldosterone contributes to the progression of renal injury via direct actions on glomerular podocytes, mesangial cells, proximal tubular cells and tubulo-interstitial fibroblasts through the activation of locally expressed mineralocorticoid receptor. Thus, it now appears that intrarenal RAAS is independently regulated and its inappropriate activation contributes to the pathogenesis of the development of hypertension and renal disease. This short review article will focus on the independent regulation of the intrarenal RAAS with an emphasis on the specific role of angiotensinogen.

Indexed as

Angiotensin IIAngiotensinogenEnzyme-Linked Immunosorbent AssayHumansHypertensionKidneyKidney DiseasesReninRenin-Angiotensin SystemAngiotensin IIAngiotensinogenReninAngiotensin II (Ang II)AngiotensinogenKidneyRenin–angiotensin–aldosterone system (RAAS)

Identifiers

PMID29600408
PMCPMC6163102
OpenAlexW2794502608

What Socratic 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 Socratic graph.