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Hepcidin, in contrast to heparin binding protein, does not portend acute kidney injury in patients with community acquired septic shock

Olinder, Jon LU ; Jovanovic Stjernqvist, Matilda ; Lindén, Albin ; Salomonsson, Evelina Thaphikul LU ; Annborn, Martin LU ; Herwald, Heiko LU orcid and Rydén, Cecilia LU (2024) In PLoS ONE 19(5 MAY).
Abstract

Background Acute kidney injury (AKI) is a common and severe complication in patients treated at an Intensive Care Unit (ICU). The pathogenesis of AKI has been reported to involve hypoperfusion, diminished oxygenation, systemic inflammation, and damage by increased intracellular iron concentration. Hepcidin, a regulator of iron metabolism, has been shown to be associated with sepsis and septic shock, conditions that can result in AKI. Heparin binding protein (HBP) has been reported to be associated with sepsis and AKI. The aim of the present study was to compare serum hepcidin and heparin binding protein (HBP) levels in relation to AKI in patients admitted to the ICU. Methods One hundred and forty patients with community acquired illness... (More)

Background Acute kidney injury (AKI) is a common and severe complication in patients treated at an Intensive Care Unit (ICU). The pathogenesis of AKI has been reported to involve hypoperfusion, diminished oxygenation, systemic inflammation, and damage by increased intracellular iron concentration. Hepcidin, a regulator of iron metabolism, has been shown to be associated with sepsis and septic shock, conditions that can result in AKI. Heparin binding protein (HBP) has been reported to be associated with sepsis and AKI. The aim of the present study was to compare serum hepcidin and heparin binding protein (HBP) levels in relation to AKI in patients admitted to the ICU. Methods One hundred and forty patients with community acquired illness admitted to the ICU within 24 hours after first arrival to the hospital were included in the study. Eighty five of these patients were diagnosed with sepsis and 55 with other severe non-septic conditions. Logistic and linear regression models were created to evaluate possible correlations between circulating hepcidin and heparin-binding protein (HBP), stage 2–3 AKI, peak serum creatinine levels, and the need for renal replacement therapy (RRT). Results During the 7-day study period, 52% of the 85 sepsis and 33% of the 55 non-sepsis patients had been diagnosed with AKI stage 2–3 already at inclusion. The need for RRT was 20% and 15%, respectively, in the groups. Hepcidin levels at admission were significantly higher in the sepsis group compared to the non-sepsis group but these levels did not significantly correlate to the development of stage 2–3 AKI in the sepsis group (p = 0.189) nor in the non-sepsis group (p = 0.910). No significant correlation between hepcidin and peak creatinine levels, nor with the need for RRT was observed. Stage 2–3 AKI correlated, as expected, significantly with HBP levels at admission in both groups (Odds Ratio 1.008 (CI 1.003–1.014, p = 0.005), the need for RRT, as well as with peak creatinine in septic patients. Conclusion Initial serum hepcidin, and HBP levels in patients admitted to the ICU are biomarkers for septic shock but in contrast to HBP, hepcidin does not portend progression of disease into AKI or a later need for RRT. Since hepcidin is a key regulator of iron metabolism our present data do not support a decisive role of initial iron levels in the progression of septic shock into AKI.

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organization
publishing date
type
Contribution to journal
publication status
published
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in
PLoS ONE
volume
19
issue
5 MAY
article number
e0299257
publisher
Public Library of Science (PLoS)
external identifiers
  • pmid:38696394
  • scopus:85192042510
ISSN
1932-6203
DOI
10.1371/journal.pone.0299257
language
English
LU publication?
yes
id
c3867450-4f56-4b1b-9835-610c29c8a125
date added to LUP
2024-05-15 15:25:08
date last changed
2024-05-29 17:17:18
@article{c3867450-4f56-4b1b-9835-610c29c8a125,
  abstract     = {{<p>Background Acute kidney injury (AKI) is a common and severe complication in patients treated at an Intensive Care Unit (ICU). The pathogenesis of AKI has been reported to involve hypoperfusion, diminished oxygenation, systemic inflammation, and damage by increased intracellular iron concentration. Hepcidin, a regulator of iron metabolism, has been shown to be associated with sepsis and septic shock, conditions that can result in AKI. Heparin binding protein (HBP) has been reported to be associated with sepsis and AKI. The aim of the present study was to compare serum hepcidin and heparin binding protein (HBP) levels in relation to AKI in patients admitted to the ICU. Methods One hundred and forty patients with community acquired illness admitted to the ICU within 24 hours after first arrival to the hospital were included in the study. Eighty five of these patients were diagnosed with sepsis and 55 with other severe non-septic conditions. Logistic and linear regression models were created to evaluate possible correlations between circulating hepcidin and heparin-binding protein (HBP), stage 2–3 AKI, peak serum creatinine levels, and the need for renal replacement therapy (RRT). Results During the 7-day study period, 52% of the 85 sepsis and 33% of the 55 non-sepsis patients had been diagnosed with AKI stage 2–3 already at inclusion. The need for RRT was 20% and 15%, respectively, in the groups. Hepcidin levels at admission were significantly higher in the sepsis group compared to the non-sepsis group but these levels did not significantly correlate to the development of stage 2–3 AKI in the sepsis group (p = 0.189) nor in the non-sepsis group (p = 0.910). No significant correlation between hepcidin and peak creatinine levels, nor with the need for RRT was observed. Stage 2–3 AKI correlated, as expected, significantly with HBP levels at admission in both groups (Odds Ratio 1.008 (CI 1.003–1.014, p = 0.005), the need for RRT, as well as with peak creatinine in septic patients. Conclusion Initial serum hepcidin, and HBP levels in patients admitted to the ICU are biomarkers for septic shock but in contrast to HBP, hepcidin does not portend progression of disease into AKI or a later need for RRT. Since hepcidin is a key regulator of iron metabolism our present data do not support a decisive role of initial iron levels in the progression of septic shock into AKI.</p>}},
  author       = {{Olinder, Jon and Jovanovic Stjernqvist, Matilda and Lindén, Albin and Salomonsson, Evelina Thaphikul and Annborn, Martin and Herwald, Heiko and Rydén, Cecilia}},
  issn         = {{1932-6203}},
  language     = {{eng}},
  number       = {{5 MAY}},
  publisher    = {{Public Library of Science (PLoS)}},
  series       = {{PLoS ONE}},
  title        = {{Hepcidin, in contrast to heparin binding protein, does not portend acute kidney injury in patients with community acquired septic shock}},
  url          = {{http://dx.doi.org/10.1371/journal.pone.0299257}},
  doi          = {{10.1371/journal.pone.0299257}},
  volume       = {{19}},
  year         = {{2024}},
}