Evidence map›Paper›PMID 40887581›Full record

ArticleBMC nephrology2025

Kidney transcriptomics signature of prospective rapid diabetic kidney disease progression.

Dianne Acoba, Anna Levin, Anna Witasp, Kerstin Ebefors, Johan Mölne, Peter J Greasley, Jenny Nyström, Annika Wernerson, Anna Reznichenko

Abstract read
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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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.

Dianne AcobaTranslational Science & Experimental Medicine, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Anna LevinDepartment of Clinical Science, Intervention and Technology, Division of Renal Medicine, Karolinska Institutet, Stockholm, Sweden.
Anna WitaspDepartment of Clinical Science, Intervention and Technology, Division of Renal Medicine, Karolinska Institutet, Stockholm, Sweden.
Kerstin EbeforsDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Johan MölneDepartment of Laboratory Medicine, Institute of Biomedicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Peter J GreasleyEarly Clinical Development, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden.
Jenny NyströmDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Annika WernersonDepartment of Clinical Science, Intervention and Technology, Division of Renal Medicine, Karolinska Institutet, Stockholm, Sweden.
Anna ReznichenkoTranslational Science & Experimental Medicine, Research and Early Development, Cardiovascular, Renal and Metabolism, BioPharmaceuticals R&D, AstraZeneca, Gothenburg, Sweden. Anna.Reznichenko@astrazeneca.com.

Funding

Horizon 2020 860977
6 · The paper itself

Abstract

backgroundPrevious cross-sectional transcriptomics studies on diabetic kidney disease (DKD) kidney tissue have shown correlations between gene expression and both disease status and kidney function at the time of biopsy; however, longitudinal data are scarce.

methodsWe utilized clinical follow-up data up to five years post-biopsy, linking the transcriptomes of diagnostic kidney biopsies to progression rates and outcomes in 19 patients with DKD. Patients were stratified into “rapid progressors” and “non-rapid progressors” based on clinical parameters (eGFR slope, CKD stage advancement, degree of albuminuria, composite outcome of kidney failure or 40% eGFR decline). Differential expression and pathway enrichment analyses were performed to identify dysregulated genes and pathways associated with rapid progression.

resultsWe identified 265 genes in the glomeruli and tubulointerstitium that were significantly modulated between rapid and non-rapid DKD progression. Rapid progression-associated genes were enriched for well-established (extracellular matrix organization, inflammation) and novel pathways in the context of DKD (circadian rhythm, cytoskeleton reorganization, NOTCH signaling).

conclusionsThis study illuminates kidney gene expression patterns that may be predictive of rapid progression in DKD and are distinct from those associated with cross-sectional kidney function. CLINICAL TRIAL NUMBER: Not applicable.

Indexed as

Diabetic NephropathiesKidneyTranscriptomeDisease ProgressionFemaleGene Expression ProfilingHumansMaleMiddle AgedProspective StudiesChronic kidney diseaseDiabetic kidney diseaseeGFR slopeLongitudinal studyRapid progressionRNA-seqTranscriptomics

Identifiers

PMID40887581
PMCPMC12399014

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.