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Reactive oxygen species and acute kidney injury after trauma in obese rats (859.2)
Author(s) -
Mittwede Peter,
Xiang Lusha,
Lu Silu,
Clemmer John,
Hester Robert
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.859.2
Subject(s) - renal function , apocynin , medicine , endocrinology , acute kidney injury , context (archaeology) , excretion , kidney , nadph oxidase , oxidative stress , biology , paleontology
Acute kidney injury (AKI) occurs more often in obese than in lean patients after blunt trauma, with similar results observed in obese rats. While studies have suggested that reactive oxygen species (ROS) are involved in the pathogenesis of organ failure after trauma, their role in the context of obesity is not known. We hypothesized that antioxidant treatment would prevent the development of AKI in obese rats. Trauma was induced in obese (OZ) and lean (LZ) Zucker rats (12‐13 wks old) by soft tissue injury, fibula fracture, and bone component injection in both hindlimbs. In OZ and LZ without trauma, glomerular filtration rate (GFR)(1.7±0.1 vs 1.5±0.1 mL/min/g), renal plasma flow (RPF)(5.8±0.1 vs 5.5±0.2 mL/min/g), and urine albumin excretion (0.63±0.3 vs 0.27±0.1 mg/24hrs) were not different (p=ns; n=6). One day after trauma, OZ had increased urine albumin excretion as compared to LZ (6.6±1.2 vs .22±0.1 mg/24hrs; p<.05; n=6), and decreased GFR (0.9±0.1 vs 1.4±0.2 mL/min/g; p<.05; n=6) and RPF (2.5±0.2 vs 5.2±0.3 mL/min/g; p<.05; n=6). Treatment directly after trauma with a NADPH oxidase inhibitor, Apocynin (50mg/kg i.p.), led to an average GFR of 1.6±0.3 mL/min/g, RPF of 5.1±1.1 mL/min/g, and urine albumin excretion of 2.5±1.0 mg/24hrs in OZ (n=3). These data suggest that ROS may be responsible for the increased incidence of AKI after trauma in obesity, and thus may be a potential therapeutic target in this demographic. Grant Funding Source : Supported by NIH HL‐51971, HL‐89581, AHA‐12SDG12050525