Evidence map›Paper›PMID 36192385›Full record

ArticleNature communications2022

Macromolecular crowding and supersaturation protect hemodialysis patients from the onset of dialysis-related amyloidosis.

Kichitaro Nakajima, Keiichi Yamaguchi, Masahiro Noji, César Aguirre, Kensuke Ikenaka, Hideki Mochizuki, Lianjie Zhou, Hirotsugu Ogi, Toru Ito, Ichiei Narita and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

9 citing papers in PubMed, 26 citations in OpenAlex.

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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

14 authors at 7 institutions in 1 country.

Kichitaro Nakajima *Global Center for Medical Engineering and Informatics, Osaka University, Suita, Osaka, 565-0871, Japan.
Keiichi Yamaguchi *Global Center for Medical Engineering and Informatics, Osaka University, Suita, Osaka, 565-0871, Japan.
Masahiro Noji *Graduate School of Human and Environmental Studies, Kyoto University, Yoshidahonmatsu-cho, Sakyo-ku, Kyoto, 606-8316, Japan.
César AguirreDepartment of Neurology, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.
Kensuke IkenakaDepartment of Neurology, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID 0000-0002-5559-1966
Hideki MochizukiDepartment of Neurology, Graduate School of Medicine, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID 0000-0002-0874-7542
Lianjie ZhouGraduate School of Engineering, Osaka University, Suita, Osaka, 565-0871, Japan.ORCID 0000-0002-9285-2176
Hirotsugu OgiGraduate School of Engineering, Osaka University, Suita, Osaka, 565-0871, Japan.
Toru ItoDivision of Clinical Nephrology and Rheumatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Ichiei NaritaDivision of Clinical Nephrology and Rheumatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.
Fumitake GejyoNiigata University of Pharmacy and Applied Life Sciences, Niigata, 956-8603, Japan.
Hironobu NaikiFaculty of Medical Sciences, University of Fukui, Fukui, 910-1193, Japan.
Suguru YamamotoDivision of Clinical Nephrology and Rheumatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan. yamamots@med.niigata.ac.jp.ORCID 0000-0002-8279-2966
Yuji GotoGlobal Center for Medical Engineering and Informatics, Osaka University, Suita, Osaka, 565-0871, Japan. gtyj8126@protein.osaka-u.ac.jp.ORCID 0000-0003-1221-1270
The University of Osaka · JPNiigata University · JPKyoto University · JPNiigata University Medical and Dental Hospital · JPNiigata University of Pharmacy and Medical and Life Sciences · JPOsaka Gakuin University · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dialysis-related amyloidosis (DRA), a serious complication among long-term hemodialysis patients, is caused by amyloid fibrils of β2-microglobulin (β2m). Although high serum β2m levels and a long dialysis vintage are the primary and secondary risk factors for the onset of DRA, respectively, patients with these do not always develop DRA, indicating that there are additional risk factors. To clarify these unknown factors, we investigate the effects of human sera on β2m amyloid fibril formation, revealing that sera markedly inhibit amyloid fibril formation. Results from over 100 sera indicate that, although the inhibitory effects of sera deteriorate in long-term dialysis patients, they are ameliorated by maintenance dialysis treatments in the short term. Serum albumin prevents amyloid fibril formation based on macromolecular crowding effects, and decreased serum albumin concentration in dialysis patients is a tertiary risk factor for the onset of DRA. We construct a theoretical model assuming cumulative effects of the three risk factors, suggesting the importance of monitoring temporary and accumulated risks to prevent the development of amyloidosis, which occurs based on supersaturation-limited amyloid fibril formation in a crowded milieu.

Indexed as

AmyloidosisRenal DialysisAmyloidbeta 2-MicroglobulinHumansSerum AlbuminAmyloidbeta 2-MicroglobulinSerum Albumin

Identifiers

PMID36192385
PMCPMC9530240
OpenAlexW4300961948

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.