Evidence map›Paper›PMID 27474473›Full record

ReviewActa physiologica (Oxford, England)2017

Biomarkers in acute kidney injury - pathophysiological basis and clinical performance.

E V Schrezenmeier, J Barasch, K Budde, T Westhoff, K M Schmidt-Ott

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Acta physiologica (Oxford, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04865510 (Citrate Versus Heparin in Continuous Renal Replacement Therapy), which is not on this map. Cited by 216 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 8 pooled it
–field-weighted citation impact
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.

NCT04865510 nacompletednot on this mapstarted 2019, after this paper: background citation

Citrate Versus Heparin in Continuous Renal Replacement Therapy : Effect on Cardiovascular System and Clot Circuit in Critically Ill Patients

TypeinterventionalSponsorBangkok Metropolitan Administration Medical College and Vajira HospitalRan2019 to 2021Enrolled41ConditionsAcute Kidney Injury, Citrate, Cytokines, Hemodynamic ResponsesArmsRegional citrate anticoagulation
3 · Its place in the literature

Who cites it

216 citing papers in PubMed, 8 syntheses or guidelines pooled it.

  1. Pooled it
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  5. Biomarkers of acute kidney injury in pediatric cardiac surgery.Pediatric nephrology (Berlin, Germany) · 2022
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  15. The effect of citrate in cardiovascular system and clot circuit in critically ill patients requiring continuous renal replacement therapy.Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs · 2023
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  19. Water intake mediates cross-sectional associations between urinary kidney injury biomarkers and race in emerging adults.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
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156 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

E V SchrezenmeierDepartment of Nephrology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
J BaraschDivision of Nephrology, Columbia University College of Physicians and Surgeons, New York, NY, USA.
K BuddeDepartment of Nephrology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
T WesthoffMedical Department I, Universitätsklinikum Marien Hospital Herne, Ruhr University of Bochum, Bochum, Germany.
K M Schmidt-OttDepartment of Nephrology, Charité - Universitätsmedizin Berlin, Berlin, Germany.

Funding

IRON LIPOCALIN NGAL IN KIDNEY DISEASER01DK073462 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BARASCH, JONATHAN M. · 2007 to 2015
$3.0M
Analysis of NGAL Metabolism Identifies a Therapy for Iron OverloadR21DK091729 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BARASCH, JONATHAN M. · 2011 to 2012
$437k
NIDDK NIH HHS R01 DK073462NIDDK NIH HHS R21 DK091729
6 · The paper itself

Abstract

Various biomarkers of acute kidney injury (AKI) have been discovered and characterized in the recent past. These molecules can be detected in urine or blood and signify structural damage to the kidney. Clinically, they are proposed as adjunct diagnostics to serum creatinine and urinary output to improve the early detection, differential diagnosis and prognostic assessment of AKI. The most obvious requirements for a biomarker include its reflection of the underlying pathophysiology of the disease. Hence, a biomarker of AKI should derive from the injured kidney and reflect a molecular process intimately connected with tissue injury. Here, we provide an overview of the basic pathophysiology, the cellular sources and the clinical performance of the most important currently proposed biomarkers of AKI: neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid-binding protein (L-FABP), interleukin-18 (IL-18), insulin-like growth factor-binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2) and calprotectin (S100A8/9). We also acknowledge each biomarker's advantages and disadvantages as well as important knowledge gaps and perspectives for future studies.

Indexed as

Acute Kidney InjuryBiomarkersHumansBiomarkersacute kidney injurybiomarkerscalprotectinkidney injury molecule 1 (KIM-1)neutrophil gelatinase-associated lipocalin (NGAL)tissue inhibitor of metalloproteinase-2 (TIMP-2) and IGF-binding protein 7 (IGFBP7)

Identifiers

PMID27474473
PMCPMC5575831

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Registered trials

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.