Evidence map›Paper›PMID 31236335›Full record

ReviewTranslational andrology and urology2019

Biomarkers and the role of mast cells as facilitators of inflammation and fibrosis in chronic kidney disease.

Evan P Owens, David A Vesey, Andrew J Kassianos, Helen Healy, Wendy E Hoy, Glenda C Gobe

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Translational andrology and urology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Role of Mast Cells and Their Mediators in Chronic Kidney Diseases.International journal of molecular sciences · 2025
    Review
  4. Article
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  17. Renal Mast Cell-Specific Proteases in the Pathogenesis of Tubulointerstitial Fibrosis.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
    Article
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

6 authors at 4 institutions in 1 country.

Evan P OwensNHMRC Chronic Kidney Disease Centre of Research Excellence, University of Queensland, Brisbane, Australia.
David A VeseyKidney Disease Research Collaborative, University of Queensland and Princess Alexandra Hospital, Translational Research Institute, Brisbane, Australia.
Andrew J KassianosConjoint Kidney Research Laboratory, Pathology Queensland, Brisbane, Queensland, Australia.
Helen HealyNHMRC Chronic Kidney Disease Centre of Research Excellence, University of Queensland, Brisbane, Australia.
Wendy E HoyNHMRC Chronic Kidney Disease Centre of Research Excellence, University of Queensland, Brisbane, Australia.
Glenda C GobeNHMRC Chronic Kidney Disease Centre of Research Excellence, University of Queensland, Brisbane, Australia.
Princess Alexandra Hospital · AURoyal Brisbane and Women's Hospital · AUNational Health and Medical Research Council · AUTranslational Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic kidney disease (CKD) is a clinical syndrome with many adverse sequelae and is currently a major global health and economic burden. Regardless of aetiology, inflammation and fibrosis are common manifestations of CKD. Unfortunately, the underlying pathophysiological mechanisms are poorly understood, and robust prognostic and early diagnostic biomarkers of CKD are lacking. One immune cell population that has received little attention in the context of CKD is mast cells (MCs). This mini review will examine the role of MCs as facilitators of kidney inflammation and fibrosis, propose a mechanistic structure for MCs in CKD, and give consideration to biomarkers specific for MC activation that can be deployed clinically. MCs are derived from haematopoietic stem cells. They are characterised by electron-dense granules in the cytoplasm, filled with preformed mediators. MCs can synthesise a range of bio-active compounds. Activation of MCs modulates an innate immune and adaptive effector response. Increased MC counts have been observed in animal models of kidney disease and a range of kidney diseases in humans where MC presence has been linked to biomarkers of kidney function and tissue damage. To further implicate MCs in CKD, several chemokines, cytokines and proteases released by MCs have been observed in their own right in various kidney diseases and linked to progressive CKD. One compound released by MCs that is of particular interest is the MC-specific protease tryptase. This protease is capable of activating the G-protein coupled receptor (GPCR) protease activated receptor-2 (PAR-2). PAR-2 is widely expressed throughout the kidney and highly expressed in the tubular epithelial cells where its activation induces robust inflammatory and fibrotic responses. Novel prognostic and diagnostic biomarkers of CKD are needed. MC-specific proteases [tryptase, chymase and carboxypeptidase A3 (CPA3)] are easily detectable in the blood but questionably in the urine. This review aims to promote these as prognostic and diagnostic biomarkers in the context of CKD.

Indexed as

biomarkerschronic kidney disease (CKD)kidney fibrosiskidney inflammationMast cell (MC)

Identifiers

PMID31236335
PMCPMC6559929
OpenAlexW2903039203

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.