Evidence map›Paper›PMID 25037561›Full record

ReviewAmerican journal of kidney diseases : the official journal of the National Kidney Foundation2014

Protein carbamylation in kidney disease: pathogenesis and clinical implications.

Sahir Kalim, S Ananth Karumanchi, Ravi I Thadhani, Anders H Berg

Abstract readCase ReportsReview
In one paragraph

Review in American journal of kidney diseases : the official journal of the National Kidney Foundation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 2 pooled it
6.6field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 2 syntheses or guidelines pooled it, 120 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

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

4 authors at 4 institutions in 1 country.

Sahir KalimDepartment of Medicine, Division of Nephrology, Massachusetts General Hospital, Boston, MA; Harvard Medical School, Boston, MA.
S Ananth KarumanchiHarvard Medical School, Boston, MA; Division of Nephrology, Beth Israel Deaconess Medical Center, Boston, MA; Howard Hughes Medical Institute, Boston, MA.
Ravi I ThadhaniDepartment of Medicine, Division of Nephrology, Massachusetts General Hospital, Boston, MA; Harvard Medical School, Boston, MA.
Anders H BergHarvard Medical School, Boston, MA; Department of Pathology, Division of Clinical Chemistry, Beth Israel Deaconess Medical Center, Boston, MA. Electronic address: ahberg@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USHarvard University · USHoward Hughes Medical Institute · USMassachusetts General Hospital · US

Funding

The role of carbamylation in uremia associated heart diseaseK08HL121801 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI BERG, ANDERS HAYDEN · 2014 to 2017
$588k
Patient Oriented Studies of Vitamin D in Chronic Kidney DiseaseK24DK094872 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI THADHANI, RAVI · 2012 to 2016
$546k
Howard Hughes Medical InstituteNHLBI NIH HHS K08 HL121801NIDDK NIH HHS K24 DK094872
6 · The paper itself

Abstract

Carbamylation describes a nonenzymatic posttranslational protein modification mediated by cyanate, a dissociation product of urea. When kidney function declines and urea accumulates, the burden of carbamylation naturally increases. Free amino acids may protect proteins from carbamylation, and protein carbamylation has been shown to increase in uremic patients with amino acid deficiencies. Carbamylation reactions are capable of altering the structure and functional properties of certain proteins and have been implicated directly in the underlying mechanisms of various disease conditions. A broad range of studies has demonstrated how the irreversible binding of urea-derived cyanate to proteins in the human body causes inappropriate cellular responses leading to adverse outcomes such as accelerated atherosclerosis and inflammation. Given carbamylation's relationship to urea and the evidence that it contributes to disease pathogenesis, measurements of carbamylated proteins may serve as useful quantitative biomarkers of time-averaged urea concentrations while also offering risk assessment in patients with kidney disease. Moreover, the link between carbamylated proteins and disease pathophysiology creates an enticing therapeutic target for reducing the rate of carbamylation. This article reviews the biochemistry of the carbamylation reaction, its role in specific diseases, and the potential diagnostic and therapeutic implications of these findings based on recent advances.

Indexed as

AnimalsBiomarkersCarbamatesHumansKidney Failure, ChronicMaleMiddle AgedProtein Processing, Post-TranslationalUremiaBiomarkersCarbamatescarbamic acidcarbamoylationCarbamylationchronic kidney disease (CKD)cyanateend-stage renal disease (ESRD)inflammationpathophysiologyposttranslational protein modification (PTM)ureauremia

Identifiers

PMID25037561
PMCPMC4209336
OpenAlexW2033513345

What OpenQuestion holds

Textmetadata
LicenceTDM
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.