Evidence map›Paper›PMID 30211028›Full record

ArticleWorld journal of nephrology2018

A small molecule fibrokinase inhibitor in a model of fibropolycystic hepatorenal disease.

Prani Paka, Brian Huang, Bin Duan, Jing-Song Li, Ping Zhou, Latha Paka, Michael A Yamin, Scott L Friedman, Itzhak D Goldberg, Prakash Narayan

Open access · bronzeAbstract read
In one paragraph

Article in World journal of nephrology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 30% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

10 authors at 2 institutions in 1 country.

Prani PakaDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Brian HuangDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Bin DuanDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Jing-Song LiDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Ping ZhouDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Latha PakaDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Michael A YaminDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Scott L FriedmanIcahn School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029, United States.
Itzhak D GoldbergDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States.
Prakash NarayanDepartment of Research and Development, Angion Biomedica Corp., Uniondale, NY 11553, United States. pnarayan@angion.com.
Angion (United States) · USIcahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo evaluate the novel platelet-derived growth factor receptor and vascular endothelial growth factor receptor dual kinase inhibitor ANG3070 in a polycystic kidney disease-congenital hepatic fibrosis model.

methodsAt 6 wk of age, PCK rats were randomized to vehicle or ANG3070 for 4 wk. At 10 wk, 24 h urine and left kidneys were collected and rats were continued on treatment for 4 wk. At 14 wk, 24 h urine was collected, rats were sacrificed, and liver and right kidneys were collected for histological evaluation. For Western blot studies, PCK rats were treated with vehicle or ANG3070 for 7 d and sacrificed approximately 30 min after the last treatments.

resultsCompared to the wild-type cohort, the PCK kidney (Vehicle cohort) exhibited a marked increase in kidney and liver mass, hepato-renal cystic volume, hepato-renal fibrosis and hepato-renal injury biomarkers. Intervention with ANG3070 in PCK rats decreased kidney weight, reduced renal cystic volume and reduced total kidney hydroxyproline, indicating significantly reduced rental interstitial fibrosis compared to the PCK-Vehicle cohort. ANG3070 treatment also mitigated several markers of kidney injury, including urinary neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, cystatin C and interleukin-18 levels. In addition, this treatment attenuated key indices of renal dysfunction, including proteinuria, albuminuria and serum blood urea nitrogen and creatinine, and significantly improved renal function compared to the PCK-Vehicle cohort. ANG3070 treatment also significantly decreased liver enlargement, hepatic lesions, and liver fibrosis, and mitigated liver dysfunction compared to the PCK-Vehicle cohort.

conclusionThese results suggest that ANG3070 has the potential to slow disease, and may serve as a bridge toward hepato-renal transplantation in patients with fibropolycystic disease.

Indexed as

Autosomal recessive polycystic kidney diseaseCongenital hepatic fibrosisCystFibrosisKidneyLiverTherapy

Identifiers

PMID30211028
PMCPMC6134267
OpenAlexW2889871001

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.