Evidence map›Paper›PMID 32300065›Full record

ArticleJournal of the American Society of Nephrology : JASN2020

Nephron-Specific Disruption of Polycystin-1 Induces Cyclooxygenase-2-Mediated Blood Pressure Reduction Independent of Cystogenesis.

Jayalakshmi Lakshmipathi, Yang Gao, Chunyan Hu, Deborah Stuart, Jonathan Genzen, Nirupama Ramkumar, Donald E Kohan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. 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

7 authors at 1 institution in 1 country.

Jayalakshmi LakshmipathiDivision of Nephrology, University of Utah Health Center, Salt Lake City, Utah.
Yang GaoDivision of Nephrology, University of Utah Health Center, Salt Lake City, Utah.
Chunyan HuDivision of Nephrology, University of Utah Health Center, Salt Lake City, Utah.
Deborah StuartDivision of Nephrology, University of Utah Health Center, Salt Lake City, Utah.
Jonathan GenzenDepartment of Pathology, University of Utah Health Center, Salt Lake City, Utah.
Nirupama RamkumarDivision of Nephrology, University of Utah Health Center, Salt Lake City, Utah.
Donald E KohanDivision of Nephrology, University of Utah Health Center, Salt Lake City, Utah donald.kohan@hsc.utah.edu.
University of Utah · US

Funding

Research Supplement to Promote DiversityP01HL136267 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, DAVID M · 2017 to 2021
$11.9M
NHLBI NIH HHS P01 HL136267
6 · The paper itself

Abstract

backgroundHypertension often occurs before renal function deteriorates in autosomal dominant polycystic kidney disease (ADPKD). It is unknown whether the

methodsWe induced nephron-specific disruption of the

resultsKidneys from the Pkd1 knockout mice showed no apparent renal cysts, tubule dilation, or increased cell proliferation. Compared with control mice, Pkd1 knockout mice exhibited reduced arterial pressure during high salt intake; this associated with an increased natriuretic, diuretic, and kaliuretic response during the first 2-3 days of salt loading. The lower arterial pressure and enhanced natriuresis during high salt loading in Pkd1 knockout mice were associated with lower urinary nitrite/nitrate excretion and markedly increased urinary PGE

conclusionsThese studies suggest that nephron polycystin-1 deficiency does not itself contribute to ADPKD hypertension and that it may, in fact, exert a relative salt-wasting effect. The work seems to comprise the first

Indexed as

AnimalsBlood PressureCyclooxygenase 2DinoprostoneGlomerular Filtration RateMiceMice, KnockoutNephronsPolycystic Kidney, Autosomal DominantSolute Carrier Family 12, Member 1TRPP Cation ChannelsCyclooxygenase 2DinoprostoneSlc12a1 protein, mouseSolute Carrier Family 12, Member 1TRPP Cation Channelsblood pressureepithelial sodium transportnephronpolycystic kidney disease

Identifiers

PMID32300065
PMCPMC7269346
OpenAlexW3017293821

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.