Evidence map›Paper›PMID 40087735›Full record

ArticleJournal of translational medicine2025

Serum Uromodulin as early marker for ischemic acute kidney injury and nephron loss: association with kidney tissue distribution pattern.

Eva Vonbrunn, Nadja Ebert, Nada Cordasic, Kerstin Amann, Anke Büttner, Maike Büttner-Herold, Jürgen E Scherberich, Christoph Daniel

Abstract read
In one paragraph

Article in Journal of translational medicine, 2025. 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

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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.

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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

8 authors.

Eva VonbrunnDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Nadja EbertDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Nada CordasicDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Kerstin AmannDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Anke BüttnerSchool of Psychology, College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK.
Maike Büttner-HeroldDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Krankenhausstr. 8-10, 91054, Erlangen, Germany.
Jürgen E ScherberichKlinikum Munich-Harlaching, Ludwig-Maximilians University, Munich, Germany.
Christoph DanielDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, Universitätsklinikum Erlangen, Krankenhausstr. 8-10, 91054, Erlangen, Germany. Christoph.Daniel@uk-erlangen.de.ORCID 0000-0002-6803-4755

Funding

Deutsche Forschungsgemeinschaft 509149993Deutsche Forschungsgemeinschaft TP C2Deutsche Forschungsgemeinschaft TRR 374
6 · The paper itself

Abstract

backgroundUromodulin (UMOD) is expressed in kidneys and is mainly excreted in the urine, although a smaller amount is also released into the serum. Here, we investigated UMOD in acute kidney injury (AKI), with particular focus on the utility of serum UMOD as marker for nephron loss.

methodsBlood and kidney samples were collected 6 h, 24 h, 3 days and 8 weeks after ischemia/reperfusion (I/R) in a rat model. To investigate the impact of nephron number on UMOD levels, sera and tissue from healthy, uninephrectomized (Unx) and 5/6-nephrectomized (Snx) rats were analyzed. Histological changes, kidney function and cell damage were evaluated and serum UMOD, Umod mRNA expression and distribution of UMOD protein in the kidney were examined.

resultsIn AKI, kidney function was markedly impaired 24 h after I/R, while kidney injury and serum UMOD was increased transiently. Simultaneously, the amount of UMOD-positive kidney cells rapidly decreased 24 h after I/R compared to healthy kidneys, and mRNA expression of Umod was lowest on days 1-3 after I/R. Serum UMOD correlated with nephron number showing the highest levels in healthy rats, which were reduced after Unx and further reduced after Snx.

conclusionIn an AKI model with severe tubular damage, a transient increase in UMOD serum levels in parallel with loss of UMOD-positive cells suggests temporary release of UMOD from destroyed tubular cells into the blood. Serum UMOD appears to be not only a marker of chronic renal failure but also of acute loss of functional and cellular integrity of kidney epithelia in AKI.

Indexed as

Acute Kidney InjuryIschemiaKidneyNephronsUromodulinAnimalsBiomarkersMaleRatsRats, Sprague-DawleyReperfusion InjuryRNA, MessengerBiomarkersRNA, MessengerUromodulinAcute kidney injuryIschemia/reperfusionNephron lossTamm-Horsfall proteinUromodulin

Identifiers

PMID40087735
PMCPMC11907908

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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.