Evidence map›Paper›PMID 25908466›Full record

ReviewAdvances in chronic kidney disease2015

Sodium retention and volume expansion in nephrotic syndrome: implications for hypertension.

Evan C Ray, Helbert Rondon-Berrios, Cary R Boyd, Thomas R Kleyman

Abstract readReview
In one paragraph

Review in Advances in chronic kidney disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Implications of Dysnatremia and Endocrine Disturbances in COVID-19 Patients.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Influence of proteolytic cleavage of ENaC's γ subunit upon NaAmerican journal of physiology. Renal physiology · 2024
    Article
  9. Review
  10. Review
  11. Article
  12. Metabolomic Analysis ofPharmaceuticals (Basel, Switzerland) · 2023
    Article
  13. ENaC activation by proteases.Acta physiologica (Oxford, England) · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. NOX4-dependent regulation of ENaC in hypertension and diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  19. Review
  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

4 authors at 1 institution in 1 country.

Evan C RayRenal Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, PA; and Department of Cell Biology, University of Pittsburgh, Pittsburgh, PA.
Helbert Rondon-BerriosRenal Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, PA; and Department of Cell Biology, University of Pittsburgh, Pittsburgh, PA. Electronic address: rondonberriosh@upmc.edu.
Cary R BoydRenal Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, PA; and Department of Cell Biology, University of Pittsburgh, Pittsburgh, PA.
Thomas R KleymanRenal Electrolyte Division, Department of Medicine, University of Pittsburgh, Pittsburgh, PA; and Department of Cell Biology, University of Pittsburgh, Pittsburgh, PA.
University of Pittsburgh · US

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
Biomechanical Regulation of Renal Ion TransportersR37DK051391 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2006 to 2015
$3.2M
Renal and Epithelial Biology Training ProgramT32DK061296 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2002 to 2022
$3.1M
SODIUM CHANNELS IN THE MAMMALIAN URINARY BLADDERR01DK051391 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R. · 1996 to 2005
$1.5M
NIDDK NIH HHS P30 DK079307NIDDK NIH HHS R01 DK051391NIDDK NIH HHS R37 DK051391NIDDK NIH HHS T32 DK061296
6 · The paper itself

Abstract

Sodium retention is a major clinical feature of nephrotic syndrome. The mechanisms responsible for sodium retention in this setting have been a subject of debate for years. Excessive sodium retention occurs in some individuals with nephrotic syndrome in the absence of activation of the renin-angiotensin-aldosterone system, suggesting an intrinsic defect in sodium excretion by the kidney. Recent studies have provided new insights regarding mechanisms by which sodium transporters are activated by factors present in nephrotic urine. These mechanisms likely have a role in the development of hypertension in nephrotic syndrome, where hypertension may be difficult to control, and provide new therapeutic options for the management of blood pressure and edema in the setting of nephrotic syndrome.

Indexed as

Epithelial Sodium ChannelsHumansHypertensionKidneyNephrotic SyndromeProteinuriaSodiumWater-Electrolyte ImbalanceEpithelial Sodium ChannelsSodiumEpithelial sodium channelNephrotic syndromePotassium sparing diureticsProteinuriaSerine proteases

Identifiers

PMID25908466
PMCPMC4409655
OpenAlexW2100681727

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.