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Shock (Augusta, Ga.). 2022 May 26. doi: 10.1097/SHK.0000000000001942. pii: 00024382-990000000-00006

Subclinical Kidney Injury is Caused By a Moderate Single Inflammatory Event.

Heinzl MW¹, Resl M², Klammer C³, Fellinger P⁴, Schinagl L⁵, Obendorf F⁶, Feldbauer R⁷, Pohlhammer J⁸, Wagner T⁹, Egger M¹⁰, Dieplinger B¹¹, Clodi M¹²

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¹Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
²Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
³Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
⁴Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Austria.
⁵Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
⁶Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
⁷Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
⁸Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
⁹Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.
¹⁰Department of Laboratory Medicine.
¹¹Department of Laboratory Medicine.
¹²Konventhospital Barmherzige Brueder Linz (St. John of God Hospital Linz), Austria, Department of Internal Medicine.

Abstract

BACKGROUND: Current means of diagnosis of acute kidney injury (AKI) based on serum creatinine have poor sensitivity and may miss possible therapeutic windows in subclinical kidney injury, especially in septic AKI. Kidney injury molecule-1 (KIM-1) may be a valuable biomarker to improve diagnostic algorithms for AKI. The understanding of septic AKI is still insufficient, knowledge about KIM-1 kinetics in inflammation is scarce. The aim of this study was to investigate the possible effect of lipopolysaccharide (LPS) on KIM-1 as a marker of structural kidney injury in healthy volunteers.

METHODS: A single-blinded, placebo-controlled cross-over study using the Human Endotoxin Model (LPS administration) was performed in ten healthy men. KIM-1 and serum creatinine were measured repetitively over 48 hours.

RESULTS: We observed a significant elevation of serum KIM-1 levels following the administration of LPS (p < 0.001). Furthermore, LPS caused a significant elevation of serum creatinine at an early timepoint (p = 0.013) as compared with placebo.

CONCLUSIONS: Even a relatively small inflammatory stimulus is sufficient to cause subclinical structural kidney injury with elevated KIM-1 and serum creatinine in healthy volunteers. This outlines the insufficiency of the current diagnostic approach regarding acute kidney injury and the urgency to develop novel diagnostic algorithms including markers of kidney injury.Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT03392701 (08/01/2018).

Publikations ID: 35616594
Quelle: öffnen

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