Evidence map›Paper›PMID 31117065›Full record

ArticleAmerican journal of nephrology2019

Effect of a Vasopressin V2 Receptor Antagonist on Polycystic Kidney Disease Development in a Rat Model.

Xiaofang Wang, Megan M Constans, Fouad T Chebib, Vicente E Torres, Lorenzo Pellegrini

Open access · bronzeAbstract read
In one paragraph

Article in American journal of nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
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  3. SAR-Guided Scaffold Innovation of Selective VACS medicinal chemistry letters · 2026
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  12. Pre-clinical evaluation of dual targeting of the GPCRs CaSR and V2R as therapeutic strategy for autosomal dominant polycystic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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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

5 authors at 1 institution in 1 country.

Xiaofang WangDepartment of Nephrology, Mayo Clinic, Rochester, Minnesota, USA.
Megan M ConstansDepartment of Nephrology, Mayo Clinic, Rochester, Minnesota, USA.
Fouad T ChebibDepartment of Nephrology, Mayo Clinic, Rochester, Minnesota, USA.
Vicente E TorresDepartment of Nephrology, Mayo Clinic, Rochester, Minnesota, USA.
Lorenzo PellegriniPalladio Biosciences, Inc., Newtown, Pennsylvania, USA, lpellegrini@palladiobio.com.
Mayo Clinic · US

Funding

Pilot and FeasibilityP30DK090728 · NIDDK · MAYO CLINIC ROCHESTER · PI ROMERO, MICHAEL F. · 2010 to 2019
$11.8M
RENIN ANGIOTENSIN SYSTEM IN THE PATHOGENESIS OF ADPKDR01DK044863 · NIDDK · MAYO CLINIC ROCHESTER · PI TORRES, VICENTE E · 1991 to 2019
$4.5M
Novel treatment for polycystic kidney diseaseR56DK044863 · NIDDK · MAYO CLINIC ROCHESTER · PI TORRES, VICENTE E · 2015 to 2015
$119k
NIDDK NIH HHS P30 DK090728NIDDK NIH HHS R01 DK044863NIDDK NIH HHS R56 DK044863
6 · The paper itself

Abstract

backgroundVasopressin V2 receptor inhibition is a clinically validated mechanism of action in the treatment of autosomal dominant polycystic kidney disease (ADPKD). In this study, the effect of lixivaptan, a potent, selective vasopressin V2 antagonist, was evaluated in PCK rats, a validated animal model of PKD.

methodsFour-week old PCK rats were fed rodent chow with 0.5% lixivaptan (low dose) or 1% lixivaptan (high dose), or chow only (control) for 8 weeks. Urine output was measured at weeks 7 and 10 of age. Animals were killed at 12 weeks of age; kidneys and livers were collected, weighted, and analyzed for cyclic adenosine 3',5'-monophosphate (cAMP) levels and cystic burden and fibrosis; serum creatinine and sodium were measured.

resultsConsistent with the development of a polycystic kidney phenotype, control PCK rats showed enlarged kidneys, extensive cyst formation, and early signs of serum creatinine elevation at 12 weeks of age. Compared to controls, PCK rats treated with low-dose lixivaptan showed a 26% reduction in % kidney weight/body weight (p < 0.01); a 54% reduction in kidney cystic score (p < 0.001), a histomorphometric measure of cystic burden; a 23% reduction in kidney cAMP levels (p < 0.05), a biochemical marker of disease; and a 13% reduction in plasma creatinine (p < 0.001), indicating preserved renal function. These reductions were associated with 3-fold increases in 24-h urine output, demonstrating the potent aquaretic effect of lixivaptan. The fact that the high dose was less efficacious than the low dose is discussed.

conclusionsThese results provide the first evidence of the potential utility of lixivaptan for the treatment of ADPKD.

Indexed as

Administration, OralAnimalsAntidiuretic Hormone Receptor AntagonistsBenzamidesBenzodiazepinesCreatinineCystsDisease Models, AnimalDose-Response Relationship, DrugHumansKidneyLiverLiver DiseasesMutationOrgan SizePolycystic Kidney, Autosomal DominantAntidiuretic Hormone Receptor AntagonistsAvpr2 protein, ratBenzamidesBenzodiazepinesCreatininelixivaptanPKHD1 protein, ratPyrrolesReceptors, Cell SurfaceReceptors, VasopressinLixivaptanPCK rat modelPolycystic kidney diseaseVasopressin V2 receptor antagonist

Identifiers

PMID31117065
PMCPMC6647848
OpenAlexW2946791982

What OpenQuestion holds

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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.