Evidence map›Paper›PMID 30801542›Full record

ArticleTransplantation2019

Urine Angiotensin II Signature Proteins as Markers of Fibrosis in Kidney Transplant Recipients.

Zahraa Mohammed-Ali, Tomas Tokar, Ihor Batruch, Shelby Reid, Alexandre Tavares-Brum, Paul Yip, Héloïse Cardinal, Marie-Josée Hébert, Yanhong Li, S Joseph Kim and 3 more

Abstract read
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In one paragraph

Article in Transplantation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Review
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  5. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 1 country.

Zahraa Mohammed-AliToronto General Hospital Research Institute, Advanced Diagnostics Division, University Health Network, Toronto, ON, Canada.
Tomas TokarData Science Discovery Centre for Chronic Diseases, Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Ihor BatruchDepartment of Laboratory Medicine and Pathobiology, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, University of Toronto, Toronto, ON, Canada.
Shelby ReidInstitute of Medical Science, University of Toronto, Toronto, ON, Canada.
Alexandre Tavares-BrumDepartment of Medicine, Division of Nephrology, Centre Hospitalier de l'Université de Montréal, Université de Montréal, Montréal, QC, Canada.
Paul YipToronto General Hospital Research Institute, Advanced Diagnostics Division, University Health Network, Toronto, ON, Canada.
Héloïse CardinalDepartment of Medicine, Division of Nephrology, Centre Hospitalier de l'Université de Montréal, Université de Montréal, Montréal, QC, Canada.
Marie-Josée HébertDepartment of Medicine, Division of Nephrology, Centre Hospitalier de l'Université de Montréal, Université de Montréal, Montréal, QC, Canada.
Yanhong LiToronto General Hospital Research Institute, Advanced Diagnostics Division, University Health Network, Toronto, ON, Canada.
S Joseph KimToronto General Hospital Research Institute, Advanced Diagnostics Division, University Health Network, Toronto, ON, Canada.
Igor JurisicaData Science Discovery Centre for Chronic Diseases, Krembil Research Institute, Toronto Western Hospital, University Health Network, Toronto, ON, Canada.
Rohan JohnDepartment of Pathology, Toronto General Hospital, University Health Network, Toronto, ON, Canada.
Ana KonvalinkaToronto General Hospital Research Institute, Advanced Diagnostics Division, University Health Network, Toronto, ON, Canada.
Toronto General Hospital · CAUniversity of Toronto · CAKrembil Research InstituteUniversity Health Network · CA

Funding

CIHR
6 · The paper itself

Abstract

backgroundInterstitial fibrosis/tubular atrophy (IFTA) is an important cause of kidney allograft loss; however, noninvasive markers to identify IFTA or guide antifibrotic therapy are lacking. Using angiotensin II (AngII) as the prototypical inducer of IFTA, we previously identified 83 AngII-regulated proteins in vitro. We developed mass spectrometry-based assays for quantification of 6 AngII signature proteins (bone marrow stromal cell antigen 1, glutamine synthetase [GLNA], laminin subunit beta-2, lysophospholipase I, ras homolog family member B, and thrombospondin-I [TSP1]) and hypothesized that their urine excretion will correlate with IFTA in kidney transplant patients.

methodsUrine excretion of 6 AngII-regulated proteins was quantified using selected reaction monitoring and normalized by urine creatinine. Immunohistochemistry was used to assess protein expression of TSP1 and GLNA in kidney biopsies.

resultsThe urine excretion rates of AngII-regulated proteins were found to be increased in 15 kidney transplant recipients with IFTA compared with 20 matched controls with no IFTA (mean log2[fmol/µmol of creatinine], bone marrow stromal cell antigen 1: 3.8 versus 3.0, P = 0.03; GLNA: 1.2 versus -0.4, P = 0.03; laminin subunit beta-2: 6.1 versus 5.4, P = 0.06; lysophospholipase I: 2.1 versus 0.6, P = 0.002; ras homolog family member B: 1.2 versus -0.1, P = 0.006; TSP1_GGV: 2.5 versus 1.9; P = 0.15; and TSP1_TIV: 2.0 versus 0.6, P = 0.0006). Receiver operating characteristic curve analysis demonstrated an area under the curve = 0.86 for the ability of urine AngII signature proteins to discriminate IFTA from controls. Urine excretion of AngII signature proteins correlated strongly with chronic IFTA and total inflammation. In a separate cohort of 19 kidney transplant recipients, the urine excretion of these 6 proteins was significantly lower following therapy with AngII inhibitors (P < 0.05).

conclusionsAngII-regulated proteins may represent markers of IFTA and guide antifibrotic therapies.

Indexed as

ADP-ribosyl CyclaseAdultAngiotensin IIAntigens, CDBiomarkersCase-Control StudiesFemaleFibrosisGlutamate-Ammonia LigaseGPI-Linked ProteinsHumansKidneyKidney DiseasesKidney TransplantationLamininMaleADP-ribosyl CyclaseADP-ribosyl cyclase 2Angiotensin IIAntigens, CDBiomarkersGlutamate-Ammonia Ligaseglutamine synthetase IGPI-Linked ProteinsLamininlaminin beta2LYPLA1 protein, humanrhoB GTP-Binding ProteinRHOB protein, humanThiolester HydrolasesThrombospondin 1thrombospondin-1, human

Identifiers

PMID30801542
OpenAlexW2920038677

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.