Evidence map›Paper›PMID 30363702›Full record

ArticleCritical care research and practice2018

Creatinine- and Cystatin C-Based Incidence of Chronic Kidney Disease and Acute Kidney Disease in AKI Survivors.

Claire Rimes-Stigare, Bo Ravn, Akil Awad, Klara Torlén, Claes-Roland Martling, Matteo Bottai, Johan Mårtensson, Max Bell

Open access · goldAbstract read
In one paragraph

Article in Critical care research and practice, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Observational
  5. Article
  6. Article
  7. Article
  8. Review
  9. Observational
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

8 authors at 3 institutions in 1 country.

Claire Rimes-StigareSection of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.ORCID 0000-0003-1125-421X
Bo RavnSection of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Akil AwadDepartment of Cardiology, Södersjukhuset, Stockholm, Sweden.
Klara TorlénDepartment of Clinical Science and Education, Södersjukhuset, Karolinska Institute, Stockholm, Sweden.
Claes-Roland MartlingSection of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Matteo BottaiDivision of Biostatistics, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden.
Johan MårtenssonSection of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Max BellSection of Anaesthesia and Intensive Care Medicine, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Karolinska University Hospital · SEKarolinska Institutet · SEStockholm South General Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal dysfunction after acute kidney injury (AKI) is common, potentially modifiable, but poorly understood. Acute kidney disease (AKD) describes renal dysfunction 7 to 90 days after AKI and is determined by percentage change in creatinine from baseline. Chronic kidney disease (CKD) is defined as the estimated glomerular filtration rate (eGFR) less than 60 ml/min/1.73 m

methodsA prospective cohort study was conducted in a Swedish intensive care unit (ICU) between 2008 and 2010. We included AKI patients alive at 90 days. We excluded patients <18 and >100 years, death before follow-up, CKD prior to admission, and follow-up before 60 days or beyond 270 days. Creatinine and cystatin C were measured at 90 days and converted to eGFR (mL/min/1.73 m

resultsWe included 274 patients. At 90-day follow-up, the median creatinine eGFR (MDRD) was 81.6 (IQR 58.6-106.8) and median cystatin C eGFR was 51.5 (IQR 35.8-70.7). The incidence of CKD (eGFR < 60) was 25.8% based on creatinine but 63.7% using cystatin C estimates. AKD was present in 47 patients (18.9%). Age, discharge cystatin C, creatinine at discharge, and female gender predicted creatinine-defined CKD at follow-up. Age, discharge cystatin C, CRRT on ICU, and diabetes were associated with cystatin C-based CKD.

conclusionsIn AKI survivors followed up at 3 months, CKD criteria were met in a quarter of patients using creatinine and in two-thirds using cystatin C eGFR. Less than one-fifth of patients fulfilled AKD criteria. The application of AKD criteria may underestimate renal dysfunction in AKI survivors.

Identifiers

PMID30363702
PMCPMC6180984
OpenAlexW2893909320

What OpenQuestion holds

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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.