Intra-renal microcirculatory alterations on non-traumatic hemorrhagic shock induced acute kidney injury in pigs

Bülent Ergin*, Tom van Rooij, Alex Lima, Yasin Ince, Patricia Ac Specht, Bert Mik, Ugur Aksu, Berna Yavuz-Aksu, Klazina Kooiman, Nico de Jong, Can Ince

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

1 Citation (Scopus)
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Acute kidney injury (AKI) is frequently seen in patients with hemorrhagic shock due to hypotension, tissue hypoxia, and inflammation despite adequate resuscitation. There is a lack of information concerning the alteration of renal microcirculation and perfusion during shock and resuscitation. The aim of this study was to investigate the possible role of renal microcirculatory alterations on development of renal dysfunction in a pig model of non-traumatic hemorrhagic shock (HS) induced AKI. Fully instrumented female pigs were divided into the two groups as Control (n = 6) and HS (n = 11). HS was achieved by withdrawing blood until mean arterial pressure (MAP) reached around 50 mmHg. After an hour cessation period, fluid resuscitation with balanced crystalloid was started for the duration of 1 h. The systemic and renal hemodynamics, renal microcirculatory perfusion (contrast-enhanced ultrasound (CEUS)) and the sublingual microcirculation were measured. CEUS peak enhancement was significantly increased in HS during shock, early-, and late resuscitation indicating perfusion defects in the renal cortex (p < 0.05 vs. baseline, BL) despite a stable renal blood flow (RBF) and urine output. Following normalization of systemic hemodynamics, we observed persistent hypoxia (high lactate) and high red blood cell (RBC) velocity just after initiation of resuscitation resulting in further endothelial and renal damage as shown by increased plasma sialic acid (p < 0.05 vs. BL) and NGAL levels. We also showed that total vessel density (TVD) and functional capillary density (FCD) were depleted during resuscitation (p < 0.05). In this study, we showed that the correction of systemic hemodynamic variables may not be accompanied with the improvement of renal cortical perfusion, intra-renal blood volume and renal damage following fluid resuscitation. We suggest that the measurement of renal injury biomarkers, systemic and renal microcirculation can be used for guiding to the optimization of fluid therapies.

Original languageEnglish
Pages (from-to)1193-1205
Number of pages13
JournalJournal of Clinical Monitoring and Computing
Issue number5
Early online date6 Feb 2023
Publication statusPublished - Oct 2023

Bibliographical note

Funding Information:
This study was financially supported by an Innovation Grant of the Dutch Kidney Foundation (14 OI 11) and NanoNextNL, a micro- and nanotechnology consortium of the Government of the Netherlands.

Publisher Copyright:
© 2023, The Author(s).


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