Evidence map›Paper›PMID 33141305›Full record

ArticleClinical and experimental nephrology2021

Effect of tolvaptan on renal involvement in patients with autosomal dominant polycystic kidney disease according to different gene mutations.

Tomofumi Moriyama, Yosuke Nakayama, Mikiko Soejima, Yunosuke Yokota, Kanji Ota, Sakuya Ito, Goh Kodama, Nao Nakamura, Yuka Kurokawa, Junko Yano and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Clinical and experimental nephrology, 2021. 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
0.4field-weighted citation impact, top 31% 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. Article
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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

17 authors at 1 institution in 1 country.

Tomofumi MoriyamaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Yosuke NakayamaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Mikiko SoejimaDepartment of Forensic Medicine, Kurume University School of Medicine, Kurume, Japan.
Yunosuke YokotaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Kanji OtaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Sakuya ItoDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Goh KodamaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Nao NakamuraDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Yuka KurokawaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Junko YanoDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Utako UedaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Yoshimi TakamiyaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Yusuke KaidaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Takuma HazamaDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Ryo ShibataDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan.
Yoshiro KodaDepartment of Forensic Medicine, Kurume University School of Medicine, Kurume, Japan.
Kei FukamiDivision of Nephrology, Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume city, Fukuoka, Japan. fukami@med.kurume-u.ac.jp.
Kurume University · JP

Funding

a Grant-in-Aid for Welfare and Scientific Research (C) 19k08693
6 · The paper itself

Abstract

backgroundAutosomal dominant polycystic kidney disease (ADPKD) is an inherited disorder caused by mutations in the polycystic kidney disease (PKD) gene. Although tolvaptan has benefits for renal involvement, the different effects depending on the gene mutation type are unknown. Thus, we explore the different effects of tolvaptan on the annual changes in total kidney volume (%TKV) and estimated glomerular filtration rate (eGFR) according to the gene mutation type in ADPKD patients.

methodsIn total, 135 ADPKD patients were screened, and 22 patients taking tolvaptan for at least a year were retrospectively studied at the Kurume University Hospital. We examined the decline in renal function and %TKV by computed tomography and analyzed the gene mutation. Patients were classified into the following four groups according to gene mutation type: PKD1-truncated, PKD1-non-truncated, PKD2, and mutation not found. Patients were treated with tolvaptan, and the effects of tolvaptan were analyzed according to the gene mutation type.

resultsPatients (age: 52.3 ± 11.2 years) were administered tolvaptan at a dose of 45 or 60 mg. No variation was observed in the annual changes in eGFR (%eGFR) (before: - 10.5% ± 13.9%, after: - 14.4% ± 8.1%, P = 0.139), whereas %TKV was significantly improved after the tolvaptan treatment (before: 14.9% ± 8.0%, after: - 5.4% ± 7.6%, P < 0.001). Unlike %eGFR, tolvaptan treatment significantly improved %TKV, regardless of the type of gene mutation.

conclusionsA year treatment with tolvaptan significantly improved %TKV in patients with ADPKD, regardless of the gene mutation type.

Indexed as

MutationAdultAgedAntidiuretic Hormone Receptor AntagonistsFemaleGenetic Predisposition to DiseaseGlomerular Filtration RateHumansKidneyMaleMiddle AgedPolycystic Kidney, Autosomal DominantRecovery of FunctionRetrospective StudiesTime FactorsTolvaptanAntidiuretic Hormone Receptor AntagonistsTolvaptanTRPP Cation ChannelsAutosomal dominant polycystic kidney diseasePKD1PKD2Renal functionTolvaptanTotal kidney volume

Identifiers

PMID33141305
PMCPMC7925507
OpenAlexW3096314598

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.