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Balanced Hydroxyethylstarch (HES 130/0.4) Impairs Kidney Function In-Vivo without Inflammation
Martin Alexander Schick1, Wolfgang Baar2, Raphael Romano Bruno1
1Institute of Anaesthesia and Critical Care, University Hospital Würzburg, Würzburg, Germany.
Hydroxyethylstarch (HES) fluid resuscitation can cause acute kidney injury (AKI), even without sepsis. This study shows HES alone, not just in sepsis, impairs kidney function and integrity in animal models.
Area of Science:
- Nephrology
- Critical Care Medicine
- Pharmacology
Background:
- Volume therapy is crucial in perioperative care, with ongoing debate on hydroxyethylstarch (HES) benefits.
- HES is contraindicated in sepsis due to increased acute kidney injury (AKI) risk, but its effects in non-septic patients are controversial.
Purpose of the Study:
- To investigate the impact of 6% HES 130/0.4 on kidney integrity in a sepsis model and under healthy conditions.
- To evaluate if HES induces AKI independently of sepsis.
Main Methods:
- Sepsis was induced using standardized Colon Ascendens Stent Peritonitis (sCASP) in rats.
- Groups received either HES (VOL) or no fluid, with or without sCASP, over 6 hours.
- Kidney function assessed via clearance tests, serum markers (urea, creatinine, cystatin C, NGAL), and histopathology. In vitro studies used human proximal tubule cells.
Main Results:
- Sepsis induced severe AKI, with HES potentially altering renal function measurements.
- HES administration alone (without sepsis) significantly deteriorated renal function and caused histopathological damage.
- In vitro, lipopolysaccharide did not exacerbate HES-induced reduction in proximal tubule cell viability.
Conclusions:
- HES 130/0.4 administration can induce AKI and kidney damage even in the absence of sepsis.
- The severity of septic AKI may not be influenced by the type of volume expansion used.
- Findings highlight the nephrotoxic potential of HES independent of septic insult.
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