Evidence map›Paper›PMID 38723612›Full record

ArticleNephron2024

Indirect Markers of Intestinal Damage in IgA Nephropathy.

Jussi Pohjonen, Katri Kaukinen, Heini Huhtala, Ilkka Pörsti, Katri Lindfors, Jukka Mustonen, Satu Mäkelä

Abstract read
In one paragraph

Article in Nephron, 2024. 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

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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. Review
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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

7 authors.

Jussi PohjonenCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Katri KaukinenCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Heini HuhtalaFaculty of Social Sciences, Tampere University, Tampere, Finland.
Ilkka PörstiDepartment of Internal Medicine, Tampere University Hospital, Tampere, Finland.
Katri LindforsCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Jukka MustonenDepartment of Internal Medicine, Tampere University Hospital, Tampere, Finland.
Satu MäkeläDepartment of Internal Medicine, Tampere University Hospital, Tampere, Finland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionPresence of subclinical intestinal inflammation has repeatedly been shown in IgA nephropathy (IgAN) and the degree of histological inflammation has correlated with abnormal urinary findings. There is lack of noninvasive biomarkers evaluating the presence of subclinical intestinal damage in IgAN. We conducted this study hypothesizing that selected biomarkers regarded as indirect markers of intestinal damage could be elevated in IgAN.

methodsEighty-five primary IgAN patients (median age 55 years, 54% men) participated in this single-center study in Tampere, Finland. None had end-stage kidney disease or previously diagnosed enteropathies. Celiac disease was excluded with serum transglutaminase 2 antibody (TG2Ab) and endomysial antibody tests and inflammatory bowel disease with fecal calprotectin. Intestinal damage was evaluated from sera with analyses of intestinal fatty-acid binding protein (I-FABP), soluble cluster of differentiation molecule 14 (sCD14), and lipopolysaccharide binding protein. Fourteen people suffering from dyspepsia and 15 healthy people served as controls.

resultsI-FABP levels among IgAN patients were higher than in the healthy controls (median 830 pg/mL vs. 289 pg/mL, p < 0.001). Also, sCD14 was increased in IgAN patients compared to dyspepsia controls. Although TG2Ab levels were within the normal range among IgAN patients, they were higher than in the healthy controls (median 1.3 U/mL vs. 0.6 U/mL, p < 0.001).

conclusionsElevated serum levels of I-FABP were present in primary IgAN patients without known enteropathies. Serum I-FABP may indicate the presence of subclinical intestinal damage. These findings encourage further investigation into the role of the intestine in the pathophysiology of IgAN.

Indexed as

BiomarkersFatty Acid-Binding ProteinsGlomerulonephritis, IGAAcute-Phase ProteinsAdultAgedCarrier ProteinsFemaleGTP-Binding ProteinsHumansIntestinesLipopolysaccharide-Binding ProteinLipopolysaccharide ReceptorsMaleMembrane GlycoproteinsMiddle AgedAcute-Phase ProteinsBiomarkersCarrier ProteinsFatty Acid-Binding ProteinsGTP-Binding ProteinsLipopolysaccharide-Binding ProteinLipopolysaccharide ReceptorsMembrane GlycoproteinsProtein Glutamine gamma Glutamyltransferase 2TransglutaminasesDyspepsiaIgA nephropathyIntestinal fatty-acid binding proteinLipopolysaccharide binding proteinSoluble cluster of differentiation molecule 14

Identifiers

PMID38723612
PMCPMC11460831

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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.