Evidence map›Paper›PMID 26752746›Full record

ReviewLaboratory investigation; a journal of technical methods and pathology2016

Links between coagulation, inflammation, regeneration, and fibrosis in kidney pathology.

Beatriz Suárez-Álvarez, Helen Liapis, Hans-Joachim Anders

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Laboratory investigation; a journal of technical methods and pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.9field-weighted citation impact, top 7% of its field
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

34 citing papers in PubMed, 56 citations in OpenAlex.

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  11. Immunology of SARS-CoV-2 infection and vaccination.Clinica chimica acta; international journal of clinical chemistry · 2023
    Review
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  19. Mast Cell Chymase and Kidney Disease.International journal of molecular sciences · 2020
    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

3 authors at 3 institutions in 3 countries.

Beatriz Suárez-ÁlvarezNephrologisches Zentrum, Medizinische Klinik und Poliklinik IV der Ludwig-Maximilians Universität, Munich, Germany.
Helen LiapisDepartment of Pathology and Immunology and Internal Medicine, Washington University, School of Medicine, St Louis, MO, USA.
Hans-Joachim AndersNephrologisches Zentrum, Medizinische Klinik und Poliklinik IV der Ludwig-Maximilians Universität, Munich, Germany.
Hospital Universitario Fundación Jiménez Díaz · ESLudwig-Maximilians-Universität München · DEWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute kidney injury (AKI) involves nephron injury leading to irreversible nephron loss, ie, chronic kidney disease (CKD). Both AKI and CKD are associated with distinct histological patterns of tissue injury, but kidney atrophy in CKD involves tissue remodeling with interstitial inflammation and scarring. No doubt, nephron atrophy, inflammation, fibrosis, and renal dysfunction are associated with each other, but their hierarchical relationships remain speculative. To better understand the pathophysiology, we provide an overview of the fundamental danger response programs that assure host survival upon traumatic injury from as early as the first multicellular organisms, ie, bleeding control by coagulation, infection control by inflammation, epithelial barrier restoration by re-epithelialization, and tissue stabilization by mesenchymal repair. Although these processes assure survival in the majority of the populations, their dysregulation causes kidney disease in a minority. We discuss how, in genetically heterogeneous population, genetic variants shift balances and modulate danger responses toward kidney disease. We further discuss how classic kidney disease entities develop from an insufficient or overshooting activation of these danger response programs. Finally, we discuss molecular pathways linking, for example, inflammation and regeneration or inflammation and fibrosis. Understanding the causative and hierarchical relationships and the molecular links between the danger response programs should help to identify molecular targets to modulate kidney injury and to improve outcomes for kidney disease patients.

Indexed as

Acute Kidney InjuryBlood CoagulationEpitheliumFibrosisHumansInflammationKidneyModels, BiologicalRegenerationRenal Insufficiency, Chronic

Identifiers

PMID26752746
OpenAlexW2239926509

What OpenQuestion holds

Textmetadata
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.