Evidence map›Paper›PMID 38452919›Full record

ArticleAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2024

Urinary Plasminogen as a Marker of Disease Progression in Human Glomerular Disease.

Marina de Cos, Gohar Mosoyan, Kinsuk Chauhan, Jonathan P Troost, Jenny S Wong, Sean Lefferts, Paul Morgan, Kristin Meliambro, Marc Egerman, Justina Ray and 11 more

Open access · hybridAbstract readMulticenter Study
In one paragraph

Article in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2024. 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
1.0field-weighted citation impact, top 24% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Trial
  2. 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

21 authors at 6 institutions in 1 country.

Marina de CosDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Gohar MosoyanDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Kinsuk ChauhanDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Jonathan P TroostMichigan Institute for Clinical and Health Research, University of Michigan, Ann Arbor, Michigan.
Jenny S WongDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Sean LeffertsDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Paul MorganDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Kristin MeliambroDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Marc EgermanDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Justina RayDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Tom ParkerRogosin Institute, Weill Cornell Medicine, New York, New York.
Daniel LevineRogosin Institute, Weill Cornell Medicine, New York, New York.
Surya SeshanDepartment of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, New York.
Yoni BardashSt. Joseph's University Medical, Paterson, New Jersey.
Benjamin HorowitzRobert Wood Johnson Medical School, Rutgers University, New Brunswick, New Jersey.
Candice A KentSection of Nephrology and Clinical and Translational Research Accelerator, Department of Internal Medicine, School of Medicine, Yale University, New Haven, Connecticut.
Melissa M ShawSection of Nephrology and Clinical and Translational Research Accelerator, Department of Internal Medicine, School of Medicine, Yale University, New Haven, Connecticut.
Alan PerlmanRogosin Institute, Weill Cornell Medicine, New York, New York; Division of Nephrology and Hypertension, Department of Medicine, Weill Cornell Medicine, New York, New York.
Dennis G MoledinaSection of Nephrology and Clinical and Translational Research Accelerator, Department of Internal Medicine, School of Medicine, Yale University, New Haven, Connecticut.
Steven G CocaDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Kirk N CampbellDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: kirk.campbell@mssm.edu.
Icahn School of Medicine at Mount Sinai · USCornell University · USYale University · USRutgers, The State University of New Jersey · USSt. Joseph’s University Medical Center · USUniversity of Michigan · US

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Michigan Institute for Clinical and Health Research (MICHR)UL1TR002240 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, JULIE C, MASHOUR, GEORGE ALEXANDER · 2017 to 2022
$54.9M
Renal Physiology and Phenotyping CoreP30DK079310 · NIDDK · YALE UNIVERSITY · PI SOMLO, STEFAN · 2008 to 2022
$16.8M
CureGNU24DK100845 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CRYSTAL A. GADEGBEKU, Laura H Mariani · 2019 to 2026
$12.1M
CureGN-Penn PCCU01DK100846 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI LAWRENCE B. HOLZMAN · 2019 to 2026
$8.3M
Hippo-YAP in podocyte health and diseaseR01DK122807 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Kirk N Campbell · 2019 to 2026
$4.8M
Plasminogen in glomerular disease progressionR01DK126477 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Kirk N Campbell · 2020 to 2026
$3.8M
Biomarkers for acute interstitial nephritis in humansR01DK128087 · NIDDK · YALE UNIVERSITY · PI MOLEDINA, DENNIS G. · 2021 to 2025
$2.9M
Identification of Non-Invasive Biomarkers and Indices for Diagnosis of Drug-Induced Acute Interstitial NephritisK23DK117065 · NIDDK · YALE UNIVERSITY · PI MOLEDINA, DENNIS G. · 2018 to 2022
$920k
NCATS NIH HHS UL1 TR001863NCATS NIH HHS UL1 TR002240NIDDK NIH HHS K23 DK117065NIDDK NIH HHS P30 DK079310NIDDK NIH HHS R01 DK122807NIDDK NIH HHS R01 DK126477NIDDK NIH HHS R01 DK128087NIDDK NIH HHS U01 DK100846NIDDK NIH HHS U24 DK100845
6 · The paper itself

Abstract

RATIONALE &

objectiveGlomerular disorders have a highly variable clinical course, and biomarkers that reflect the molecular mechanisms underlying their progression are needed. Based on our previous work identifying plasminogen as a direct cause of podocyte injury, we designed this study to test the association between urine plasmin(ogen) (ie, plasmin and its precursor plasminogen) and end-stage kidney disease (ESKD). STUDY

designMulticenter cohort study. SETTING &

participants1,010 patients enrolled in the CureGN Cohort with biopsy-proven glomerular disease (focal segmental glomerulosclerosis, membranous nephropathy, and immunoglobulin A nephropathy). PREDICTORS: The main predictor was urine plasmin(ogen) at baseline. Levels were measured by an electrochemiluminescent immunoassay developed de novo. Traditional clinical and analytical characteristics were used for adjustment. The ratio of urine plasmin(ogen)/expected plasmin(ogen) was evaluated as a predictor in a separate model. OUTCOME: Progression to ESKD. ANALYTICAL APPROACH: Cox regression was used to examine the association between urinary plasmin(ogen) and time to ESKD. Urinary markers were log

resultsAdjusted Log LIMITATIONS: Single plasmin(ogen) determination does not allow for the study of changes over time. The use of a cohort of mostly white patients and the restriction to patients with 3 glomerular disorders limits the external validity of our analysis.

conclusionsUrinary plasmin(ogen) and the ratio of measured/expected plasmin(ogen) are independently associated with ESKD in a cohort of patients with glomerular disease. Taken together with our previous experimental findings, urinary plasmin(ogen) could be a useful biomarker in prognostic decision making and a target for the development of novel therapies in patients with proteinuria and glomerular disease. PLAIN-LANGUAGE SUMMARY: Glomerular diseases are an important cause of morbidity and mortality in patients of all ages. Knowing the individual risk of progression to dialysis or transplantation would help to plan the follow-up and treatment of these patients. Our work studies the usefulness of urinary plasminogen as a marker of progression in this context, since previous studies indicate that plasminogen may be involved in the mechanisms responsible for the progression of these disorders. Our work in a sample of 1,010 patients with glomerular disease demonstrates that urinary plasminogen (as well as the ratio of measured to expected plasminogen) is associated with the risk of progression to end-stage kidney disease. Urine plasminogen exhibited good performance and, if further validated, could enable risk stratification for timely interventions in patients with proteinuria and glomerular disease.

Indexed as

BiomarkersDisease ProgressionKidney Failure, ChronicPlasminogenAdultCohort StudiesFemaleFibrinolysinGlomerulonephritis, IGAGlomerulonephritis, MembranousGlomerulosclerosis, Focal SegmentalHumansMaleMiddle AgedBiomarkersFibrinolysinPlasminogenBiomarkersend-stage kidney diseaseglomerular diseaseurinary plasminogen

Identifiers

PMID38452919
PMCPMC11260534
OpenAlexW4392454615

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Registered trials

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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.