Evidence map›Paper›PMID 28240259›Full record

ArticleScientific reports2017

Circulating cathepsin-S levels correlate with GFR decline and sTNFR1 and sTNFR2 levels in mice and humans.

Dominik Steubl, Santhosh V Kumar, Maia Tato, Shrikant R Mulay, Anders Larsson, Lars Lind, Ulf Risérus, Lutz Renders, Uwe Heemann, Axel C Carlsson and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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, 17 citations in OpenAlex.

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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

12 authors at 5 institutions in 2 countries.

Dominik SteublAbteilung für Nephrologie, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Santhosh V KumarMedizinische Klinik und Poliklinik IV, Renal Division, Klinikum der Universität München, Campus Innenstadt, München, Germany.
Maia TatoMedizinische Klinik und Poliklinik IV, Renal Division, Klinikum der Universität München, Campus Innenstadt, München, Germany.
Shrikant R MulayMedizinische Klinik und Poliklinik IV, Renal Division, Klinikum der Universität München, Campus Innenstadt, München, Germany.
Anders LarssonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Lars LindDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Ulf RisérusDepartments of Public Health and Caring Sciences/Clinical Nutrition, Uppsala University, Uppsala, Sweden.
Lutz RendersAbteilung für Nephrologie, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Uwe HeemannAbteilung für Nephrologie, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Axel C CarlssonDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Johan ÄrnlövDepartment of Medical Sciences, Uppsala University, Uppsala, Sweden.
Hans-Joachim AndersMedizinische Klinik und Poliklinik IV, Renal Division, Klinikum der Universität München, Campus Innenstadt, München, Germany.
LMU Klinikum · DEUppsala University · SETechnical University of Munich · DEDalarna University · SEKlinikum rechts der Isar · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular complications determine morbidity/mortality in chronic kidney disease (CKD). We hypothesized that progressive CKD drives the release of cathepsin-S (Cat-S), a cysteine protease that promotes endothelial dysfunction and cardiovascular complications. Therefore, Cat-S, soluble tumor-necrosis-factor receptor (sTNFR) 1/2 and glomerular filtration rate (GFR) were measured in a CKD mouse model, a German CKD-cohort (MCKD, n = 421) and two Swedish community-based cohorts (ULSAM, n = 764 and PIVUS, n = 804). Association between Cat-S and sTNFR1/2/GFR was assessed using multivariable linear regression. In the mouse model, Cat-S and sTNFR1/2 concentrations were increased following the progressive decline of GFR, showing a strong correlation between Cat-S and GFR (r = -0.746, p < 0.001) and Cat-S and sTNFR1/sTNFR2 (r = 0.837/0.916, p < 0.001, respectively). In the human cohorts, an increase of one standard deviation of estimated GFR was associated with a decrease of 1.008 ng/ml (95%-confidence interval (95%-CI) -1.576-(-0.439), p < 0.001) in Cat-S levels in MCKD; in ULSAM and PIVUS, results were similar. In all three cohorts, Cat-S and sTNFR1/sTNFR2 levels were associated in multivariable linear regression (p < 0.001). In conclusion, as GFR declines Cat-S and markers of inflammation-related endothelial dysfunction increase. The present data indicating that Cat-S activity increases with CKD progression suggest that Cat-S might be a therapeutic target to prevent cardiovascular complications in CKD.

Indexed as

AdultAgedAnimalsBiomarkersCathepsinsDisease Models, AnimalFemaleGermanyGlomerular Filtration RateGuanine Nucleotide Exchange FactorsHumansKidney Function TestsMaleMiceMiddle AgedReceptors, Tumor Necrosis Factor, Type IBiomarkerscathepsin SCathepsinsGuanine Nucleotide Exchange FactorsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type II

Identifiers

PMID28240259
PMCPMC5327444
OpenAlexW2593459708

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.