Evidence map›Paper›PMID 16924469›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2006

Blunted DOCA/high salt induced albuminuria and renal tubulointerstitial damage in gene-targeted mice lacking SGK1.

Ferruh Artunc, Kerstin Amann, Omaima Nasir, Björn Friedrich, Diana Sandulache, Nermina Jahovic, Teut Risler, Volker Vallon, Peer Wulff, Dietmar Kuhl and 1 more

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis.International journal of molecular sciences · 2016
    Review
  8. Article
  9. What level of sodium intake worsens renal outcomes?American journal of hypertension · 2014
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Aldosterone-induced fibrosis in the kidney: questions and controversies.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2011
    Review
  15. Review
  16. The physiological impact of the serum and glucocorticoid-inducible kinase SGK1.Current opinion in nephrology and hypertension · 2009
    Review
  17. Aldosterone activates NF-kappaB in the collecting duct.Journal of the American Society of Nephrology : JASN · 2009
    Article
  18. Article
  19. Aldosterone and glomerular podocyte injury.Clinical and experimental nephrology · 2008
    Review
  20. Aldosterone-stimulated SGK1 activity mediates profibrotic signaling in the mesangium.Journal of the American Society of Nephrology : JASN · 2008
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Ferruh ArtuncDepartment of Physiology, University of Tübingen, Gmelinstr. 5, 72076, Tübingen, Germany.
Kerstin Amann
Omaima Nasir
Björn Friedrich
Diana Sandulache
Nermina Jahovic
Teut Risler
Volker Vallon
Peer Wulff
Dietmar Kuhl
Florian Lang
University of Tübingen · DEFreie Universität Berlin · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEHeidelberg University · DEUniversity of California, San Diego · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mineralocorticoids stimulate renal tubular Na(+) reabsorption, enhance salt appetite, increase blood pressure, and favor the development of renal fibrosis. The effects of mineralocorticoids on renal tubular Na(+) reabsorption and salt appetite involve the serum- and glucocorticoid-inducible kinase 1 (SGK1). The kinase is highly expressed in fibrosing tissue. The present experiments thus explored the involvement of SGK1 in renal fibrosis. To this end, SGK1-knockout mice (sgk1 (-/-)) and their wild-type littermates (sgk1 (+/+)) were implanted with desoxycorticosterone acetate (DOCA)-release pellets and offered 1% saline as drinking water for 12 weeks. The treatment led to significant increases in fluid and Na(+) intake and urinary output of fluid and Na(+) in sgk1 (+/+) mice, effects blunted in sgk1 (-/-) mice. Blood pressure increased within the first 7 weeks to a similar extent in both genotypes, but within the next 5 weeks, it increased further only in sgk1 (+/+) mice. Creatinine clearance did not change significantly but albuminuria increased dramatically in sgk1 (+/+) mice, an effect significantly blunted in sgk1 (-/-) mice. Histology after 12 weeks treatment revealed marked glomerular sclerosis and tubulointerstitial damage with interstitial fibrosis and inflammation in kidneys from sgk1 (+/+) mice, but not from sgk1 (-/-) mice. In conclusion, a lack of SGK1 protects against DOCA/high-salt-induced albuminuria and renal fibrosis.

Indexed as

Gene TargetingAlbuminuriaAnimalsBlood PressureBody WeightCalciumCreatinineDesoxycorticosteroneFeeding BehaviorHematocritImmediate-Early ProteinsKidney GlomerulusKidney TubulesMiceNephritis, InterstitialOrgan SizeCalciumCreatinineDesoxycorticosteroneImmediate-Early ProteinsPotassiumProtein Serine-Threonine KinasesSerum-Glucocorticoid Regulated KinasesSodiumSodium Chloride, Dietary

Identifiers

PMID16924469
OpenAlexW2155300221

What OpenQuestion holds

Textmetadata
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.