Evidence map›Paper›PMID 37916147›Full record

ArticleFrontiers in endocrinology2023

Relationship between plasma leucine-rich α-2-glycoprotein 1 and urinary albumin excretion in patients with type 2 diabetes.

Jin Ook Chung, Seon-Young Park, Dong Hyeok Cho, Dong Jin Chung, Min Young Chung

Abstract read
In one paragraph

Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  2. Article
  3. 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

5 authors.

Jin Ook ChungDivision of Endocrinology and Metabolism, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Seon-Young ParkDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Dong Hyeok ChoDivision of Endocrinology and Metabolism, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Dong Jin ChungDivision of Endocrinology and Metabolism, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.
Min Young ChungDivision of Endocrinology and Metabolism, Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aims: To explore the relationship between plasma leucine-rich α-2-glycoprotein 1 (LRG1) level and the degree of urinary albumin excretion in patients with type 2 diabetes. Methods: We evaluated 332 patients with type 2 diabetes in a cross-sectional study. Result: The plasma LRG1 level differed significantly according to the quartiles of urinary albumin excretion (Q1 [<7.7 mg/g], 17.1 μg/mL; Q2 [7.7-15.0 mg/g], 17.5 μg/mL; Q3 [15.1-61.4 mg/g], 18.6 μg/mL; Q4 [≥61.5 mg/g], 22.3 μg/mL; Conclusion: Plasma LRG1 level was independently associated with urinary albumin excretion in patients with type 2 diabetes. This study suggests that LRG1 may be associated with increased excretion of urinary albumin in the early stages of diabetic nephropathy.

Indexed as

Diabetes Mellitus, Type 2Diabetic NephropathiesCross-Sectional StudiesGlycoproteinsHumansLeucineGlycoproteinsLeucineLRG1 protein, humanalbuminuriabiomarkersdiabetes mellitusdiabetic nephropathiesLRG1 proteintype 2

Identifiers

PMID37916147
PMCPMC10617030

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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.