Evidence map›Paper›PMID 23360744›Full record

ReviewEndocrine reviews2013

Nephrogenic diabetes insipidus: essential insights into the molecular background and potential therapies for treatment.

Hanne B Moeller, Søren Rittig, Robert A Fenton

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Endocrine reviews, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02523001 (Urinary AQP2 Excretion in Hypercholesterolemic Patients as a Measure of Effect of Statin Therapy), which is not on this map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
9.4field-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.

NCT02523001 completednot on this map

Urinary AQP2 Excretion in Hypercholesterolemic Patients as a Measure of Effect of Statin Therapy

TypeobservationalSponsorUniversity of BariRan2013 to 2015Enrolled37ConditionsHypercholesterolemia, Diabetes Insipidus
3 · Its place in the literature

Who cites it

96 citing papers in PubMed, 200 citations in OpenAlex.

  1. Article
  2. Transcriptional regulatory factors of the Aqp2 gene.Kidney research and clinical practice · 2026
    Article
  3. Review
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Renal Ghrelin-Family GPR39 Receptor and Urinary Concentrating Ability.Journal of the American Society of Nephrology : JASN · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Aquaporin Modulation by Cations, a Review.Current issues in molecular biology · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

36 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Hanne B MoellerDepartment of Biomedicine, Aarhus University, and Department of Pediatrics, Aarhus University Hospital, Wilhelm Meyers Alle 3, Building 1234, Aarhus 8000, Denmark. hbmo@ana.au.dk
Søren Rittig
Robert A Fenton
Aarhus University Hospital · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The water channel aquaporin-2 (AQP2), expressed in the kidney collecting ducts, plays a pivotal role in maintaining body water balance. The channel is regulated by the peptide hormone arginine vasopressin (AVP), which exerts its effects through the type 2 vasopressin receptor (AVPR2). Disrupted function or regulation of AQP2 or the AVPR2 results in nephrogenic diabetes insipidus (NDI), a common clinical condition of renal origin characterized by polydipsia and polyuria. Over several years, major research efforts have advanced our understanding of NDI at the genetic, cellular, molecular, and biological levels. NDI is commonly characterized as hereditary (congenital) NDI, arising from genetic mutations in the AVPR2 or AQP2; or acquired NDI, due to for exmple medical treatment or electrolyte disturbances. In this article, we provide a comprehensive overview of the genetic, cell biological, and pathophysiological causes of NDI, with emphasis on the congenital forms and the acquired forms arising from lithium and other drug therapies, acute and chronic renal failure, and disturbed levels of calcium and potassium. Additionally, we provide an overview of the exciting new treatment strategies that have been recently proposed for alleviating the symptoms of some forms of the disease and for bypassing G protein-coupled receptor signaling.

Indexed as

AnimalsAquaporin 2Arginine VasopressinDiabetes Insipidus, NephrogenicDisease Models, AnimalHumansMutationRatsReceptors, VasopressinAquaporin 2Arginine VasopressinReceptors, Vasopressin

Identifiers

PMID23360744
PMCPMC3610677
OpenAlexW2158265710

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.