Evidence map›Paper›PMID 40604496›Full record

ArticleBMC nephrology2025

Evaluation of kidney injury and metabolomic analysis in adulthood in a non-obese hyperglycemic female mouse model after birth with low birthweight.

Shoichi Shimizu, Nobuhiko Nagano, Daichi Katayama, Kengo Matsuda, Wataru Tokunaga, Kimitaka Nakazaki, Ryoji Aoki, Kazumasa Fuwa, Ichiro Morioka

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC nephrology, 2025. 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
–field-weighted citation impact
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.

  1. Developmental origins of hypertension and renal injury: epigenetic memory in renal stem and progenitor cells.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
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

9 authors.

Shoichi ShimizuDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan. shimizu.shoichi@nihon-u.ac.jp.
Nobuhiko NaganoDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Daichi KatayamaDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Kengo MatsudaDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Wataru TokunagaDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Kimitaka NakazakiDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Ryoji AokiDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Kazumasa FuwaDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.
Ichiro MoriokaDepartment of Pediatrics and Child Health, Nihon University School of Medicine, Tokyo, Japan.

Funding

JSPS KAKENHI 19K20194JSPS KAKENHI 21K11582JSPS KAKENHI 22K15446JSPS KAKENHI 22K15908JSPS KAKENHI 22K17839
6 · The paper itself

Abstract

backgroundLow birthweight infants have high risk of developing chronic kidney disease (CKD) in later in life, however, the pathogenesis of this disease remains unclear. This study aimed to investigate the underlying mechanism using a low birthweight-non-obese hyperglycemic adulthood mouse model.

methodsPregnant ICR-strain mice underwent uterine artery ligation at day 16.5 of gestation to induce fetal hypoxia (ischemic group, I). Female newborns were weaned at 4 weeks of age and fed a normal diet until 8 weeks of age (n = 10). The group I was compared to the control group (C) regarding the body weight, tubular injury markers, renal function, pathology, and metabolome analysis.

resultsGroup I were born with a low birth weight (group I: C = 1.4:1.9 g, p < 0.01), which persisted after birth. By 8 weeks of age, there were minimal changes in kidney histopathology between the two groups. However, group I showed an increase in markers for detection of CKD, such as urinary β2-microglobulin levels (group I: C = 116:26 µg/L), albumin levels (group I: C=0.14:0.07 mg/gCr) (both p < 0.01) and serum creatinine levels (group I: C= 0.18:0.12 mg/dL, p < 0.05). Furthermore, kidney metabolomic analysis revealed notable differences between the two groups, particularly in succinic acid, S-adenosylmethionine, and N1-methyl-4-pyridone-5-carboxamide (4PY), which are closely linked to kidney injury.

conclusionThe low birthweight-non-obese hyperglycemic mouse model may develop CKD in adulthood, potentially caused by increased renin activity related to succinic acid and tissue injury related to S-adenosylmethionine and 4PY. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

HyperglycemiaRenal Insufficiency, ChronicAnimalsAnimals, NewbornBirth WeightDisease Models, AnimalFemaleFetal HypoxiaKidneyMetabolomeMetabolomicsMiceMice, Inbred ICRPregnancyChronic kidney disease (CKD)Developmental origins of health and disease (DOHaD)Metabolomic analysisNon-obese-hyperglycemiaSmall-for-gestational-age (SGA)Uterine artery ischemia

Identifiers

PMID40604496
PMCPMC12224424

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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.