Evidence map›Paper›PMID 30019932›Full record

ReviewAmerican journal of physiology. Renal physiology2018

Soluble (pro)renin receptor as a potential therapy for diabetes insipidus.

Kevin T Yang, Tianxin Yang, J David Symons

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.6field-weighted citation impact, top 27% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. 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

3 authors at 2 institutions in 2 countries.

Kevin T YangDepartment of Internal Medicine, University of Utah , Salt Lake City, Utah.
Tianxin YangDepartment of Internal Medicine, University of Utah , Salt Lake City, Utah.
J David SymonsDepartment of Internal Medicine, University of Utah , Salt Lake City, Utah.
University of Utah · USVeterans Health Administration · US

Funding

Interaction of PGE2 and intrarenal RAS in AngII-induced hypertensionR01DK104072 · NIDDK · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2015 to 2025
$3.7M
Role of (pro)renin receptor in aldosterone signaling in the kidneyR01HL139689 · NHLBI · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2018 to 2021
$2.3M
Autophagy maintains vascular function through a novel glycolysis-linked pathway regulating eNOS.R01HL141540 · NHLBI · UNIVERSITY OF UTAH · PI SYMONS, JOHN DAVID · 2018 to 2021
$1.7M
Control of collecting duct function by lipid-derived factors in obesityR01DK094956 · NIDDK · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2013 to 2017
$1.6M
Characterizing the phenotype of young and old mice with disrupted vascular autophagyR03AG052848 · NIA · UNIVERSITY OF UTAH · PI SYMONS, JOHN DAVID · 2017 to 2018
$152k
Role of renal (pro)renin receptor in hypertension and kidney injuryI01BX002817 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI YANG, TIANXIN · 2017 to 2020
–
BLRD VA I01 BX002817NHLBI NIH HHS R01 HL139689NHLBI NIH HHS R01 HL141540NIA NIH HHS R03 AG052848NIDDK NIH HHS R01 DK094956NIDDK NIH HHS R01 DK104072
6 · The paper itself

Abstract

The antidiuretic hormone vasopressin (VP) is produced by the hypothalamus and is stored and secreted from the posterior pituitary. VP acts via VP type 2 receptors (V2Rs) on the basolateral membrane of principal cells of the collecting duct (CD) to regulate fluid permeability. The VP-evoked endocrine pathway is essential in determining urine concentrating capability. For example, a defect in any component of the VP signaling pathway can result in polyuria, polydipsia, and hypotonic urine, collectively termed diabetes insipidus (DI). A lack of VP production precipitates central diabetes insipidus (CDI), which can be managed effectively by VP supplementation. A majority of cases of nephrogenic diabetes insipidus (NDI) result from V2R mutations that impair receptor sensitivity. No specific therapy is currently available for management of NDI. Evidence is evolving that (pro)renin receptor (PRR), a newly identified member of the renin-angiotensin system, is capable of regulating VP production and action. As such, PRR should be considered strongly as a therapeutic target for treating CDI and NDI. The current review will summarize recent advances in understanding the physiology of renal and central PRR as it relates to the two types of DI.

Indexed as

AnimalsAntidiuretic AgentsDiabetes InsipidusDiuresisGenetic Predisposition to DiseaseHumansKidneyMutationPhenotypeProrenin ReceptorReceptors, Cell SurfaceReceptors, VasopressinRenin-Angiotensin SystemVasopressinsAntidiuretic AgentsAVPR2 protein, humanProrenin ReceptorReceptors, Cell SurfaceReceptors, VasopressinVasopressinsaquaporin-2collecting ductrenin-angiotensin systemsite-1 proteasesoluble (pro)renin receptor

Identifiers

PMID30019932
PMCPMC6293289
OpenAlexW2883743220

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.