Evidence map›Paper›PMID 40307866›Full record

ArticleCritical care (London, England)2025

Procalcitonin levels in septic and nonseptic subjects with AKI and ESKD prior to and during continuous kidney replacement therapy (CKRT).

North Foulon, Sarah M Haeger, Kayo Okamura, Zhibin He, Bryan D Park, Isadore M Budnick, David Madison, Matthew Kennis, Rachel Blaine, Makoto Miyazaki and 5 more

Abstract read
In one paragraph

Article in Critical care (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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.

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

3 citing papers in PubMed.

  1. Observational
  2. Article
  3. Review
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

15 authors.

North FoulonDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Sarah M HaegerDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Kayo OkamuraDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Zhibin HeDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Bryan D ParkDepartment of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Isadore M BudnickDepartment of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
David MadisonDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Matthew KennisDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Rachel BlaineDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Makoto MiyazakiDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA.
Diana I JalalDepartment of Medicine, Division of Nephrology, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Benjamin R GriffinDepartment of Medicine, Division of Nephrology, University of Iowa Carver College of Medicine, Iowa City, IA, USA.
Muhammad AftabDepartment of Surgery, Division of Cardiothoracic Surgery, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
James F ColbertDepartment of Medicine, Division of Infectious Diseases, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Sarah FaubelDepartment of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Anschutz Medical Campus, 12700 East 19th Ave, Box C281, Aurora, CO, 80045, USA. Sarah.Faubel@cuanschutz.edu.

Funding

MULTIDISCIPLINARY RESPIRATORY DISEASES RESEARCH TRAININGT32HL007085 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ELLEN L BURNHAM, LISA A MAIER · 1985 to 2026
$21.6M
The role of MLKL in the regulation of vascular calcification in CKDR01HL132318 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MIYAZAKI, MAKOTO · 2016 to 2025
$3.8M
The transcriptional control of vascular calcification in diseaseR01HL157064 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI Makoto Miyazaki · 2023 to 2026
$2.5M
A Novel Driver of Hyperphosphatemia and Vascular Calcification in CKDR01DK124901 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI BLAINE, JUDITH T.,, MIYAZAKI, MAKOTO · 2021 to 2024
$1.9M
NHLBI NIH HHS R01 HL132318NHLBI NIH HHS R01 HL157064NHLBI NIH HHS T32 HL007085NIDDK NIH HHS R01 DK124901
6 · The paper itself

Abstract

backgroundProcalcitonin is a 14.5 kDa protein used clinically as a marker of sepsis and therapeutic response to antibiotic therapy. However, its utility in critically ill patients with either acute kidney injury (AKI) or end-stage kidney disease (ESKD) who require continuous kidney replacement therapy (CKRT) is unknown. The aim of this study was to determine if plasma levels of procalcitonin could reliably distinguish septic from nonseptic status in patients with AKI or ESKD prior to or during CKRT.

methodsProcalcitonin concentrations were measured in plasma of 41 critically ill septic or non-septic subjects with AKI or ESKD prior to CKRT (pre-CKRT) and on days 1, 2, and 3 of CKRT in this retrospective cohort study (n = 111 total plasma measurements). Continuous venovenous hemodialysis was the modality of CKRT in these patients. Sepsis status was stringently defined based on culture results. Effluent procalcitonin levels were ascertained on days 1, 2, and 3 of CKRT to assess the clearance of procalcitonin and effects on plasma levels.

results92% (66/72) of the plasma procalcitonin measurements among nonseptic patients with either AKI or ESKD were ≥ 0.5 ng/mL (the diagnostic threshold beyond which bacterial infection is very likely). Prior to CKRT initiation, procalcitonin levels were (median (IQR), ng/mL) 5.6 (1.5-18.9) in nonseptic AKI and 58.1 (6.9-195.5) in septic AKI (P = 0.03) and were 3.3 (1.2-8.3) in nonseptic ESKD and 3.7 (1.4-209.8) in septic ESKD (P = 0.79). However, despite being significantly elevated in septic patients with AKI, substantial overlap among procalcitonin levels was present and ROC curve analysis found no cut point that could reliably separate septic from nonseptic patients. Effluent procalcitonin levels were consistently ~ 20% of plasma levels throughout the course of CKRT (i.e., sieving coefficient was 0.2) suggesting that clearance occurs during therapy. However, plasma procalcitonin levels did not significantly decline during CKRT in either AKI or ESKD.

conclusionProcalcitonin levels are markedly elevated in nonseptic critically ill patients with either AKI or ESKD and do not effectively distinguish sepsis from nonseptic status prior to or during CKRT. We conclude that procalcitonin testing should be avoided in critically ill patients with kidney failure since results are nonspecific in this population.

Indexed as

Acute Kidney InjuryContinuous Renal Replacement TherapyKidney Failure, ChronicProcalcitoninSepsisAgedBiomarkersCohort StudiesFemaleHumansMaleMiddle AgedRetrospective StudiesBiomarkersProcalcitoninAKICKRTESKDProcalcitoninSepsis

Identifiers

PMID40307866
PMCPMC12044748

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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.