Evidence map›Paper›PMID 38114999›Full record

ArticleBMC nephrology2023

IL-1β may be an indicator of peritoneal deterioration after healing of peritoneal dialysis-associated peritonitis.

Akira Hirano, Hiroyuki Kadoya, Yu Yamanouchi, Seiji Kishi, Tamaki Sasaki, Naoki Kashihara

Open access · goldAbstract readCase Reports
In one paragraph

Article in BMC nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

6 authors at 1 institution in 1 country.

Akira HiranoDepartment of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, 701-0192, Japan.
Hiroyuki KadoyaDepartment of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, 701-0192, Japan. kadoya-hiro@med.kawasaki-m.ac.jp.
Yu YamanouchiDepartment of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, 701-0192, Japan.
Seiji KishiDepartment of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, 701-0192, Japan.
Tamaki SasakiDepartment of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, 701-0192, Japan.
Naoki KashiharaDepartment of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, 701-0192, Japan.
Kawasaki Medical School · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPeritoneal dialysis (PD) is an essential lifesaving treatment for end-stage renal disease. However, PD therapy is limited by peritoneal inflammation, which leads to peritoneal membrane failure because of progressive peritoneal deterioration. Peritonitis is the most common complication in patients undergoing PD. Thus, elucidating the mechanism of chronic peritoneal inflammation after PD-associated peritonitis is an urgent issue for patients undergoing PD. This first case report suggests that an increased interleukin-1β (IL-1β) expression in the peritoneal dialysate after healing of peritonitis can contribute to peritoneal deterioration. CASE PRESENTATION: A 64-year-old woman was diagnosed with diabetes mellitus 10 years ago and had been started on PD for end-stage renal disease. One day, the patient developed PD-associated acute peritonitis and was admitted to our hospital for treatment. Thus, treatment with antimicrobial agents was initiated for PD-associated peritonitis. Dialysate turbidity gradually disappeared after treatment with antimicrobial agents, and the number of cells in the PD fluid decreased. After 2 weeks of antimicrobial therapy, peritonitis was clinically cured, and the patient was discharged. Thereafter, the patient did not develop peritonitis; however, residual renal function tended to decline, and peritoneal function also decreased in a relatively short period. We evaluated pro-inflammatory cytokine levels before and after PD-associated peritonitis; interestingly, the levels of IL-1β remained high in the PD fluid, even after remission of bacterial peritonitis. In addition, it correlated with decreased peritoneal function.

conclusionsThis case suggests that inflammasome-derived pro-inflammatory cytokines may contribute to chronic inflammation-induced peritoneal deterioration after PD-related peritonitis is cured.

Indexed as

Anti-Infective AgentsKidney Failure, ChronicPeritoneal DialysisPeritonitisCytokinesDialysis SolutionsFemaleHumansInflammationInterleukin-1betaMiddle AgedAnti-Infective AgentsCytokinesDialysis SolutionsInterleukin-1betaChronic inflammationIL-1βInflammasomePeritoneal dialysisPeritonitis

Identifiers

PMID38114999
PMCPMC10731768
OpenAlexW4389976909

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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.