Abstract
Wepreviously found increased acute kidney injury (AKI) following orthopedictrauma in obese (OZ) as compared to lean Zucker rats (LZ), in agreement with results reported in lean and obese trauma patients. Impaired renal oxygenation due to elevated oxygen consumption (VO2) and/or decreased oxygen delivery(DO2) has been shown to be an important mechanism of AKI in in many critical illnesses, but few studies have investigated the mechanisms of AKI following orthopedic trauma, particularly in obesity. We hypothesized that the increased AKI in OZ following orthopedic trauma is associated with impaired renal oxygenation. Soft tissue injury, fibula fracture, and bone component injection were performed in both hind limbs in male LZ and OZ (~12wk old) to induce orthopedictrauma. A day later, food intake, circulating aldosterone, renal blood flow (RBF), GFR, and renal medullary glycogen levels were measured. Renal DO2 and VO2 were calculated from renal arterial and venous blood gases. Sodium (Na+) reabsorption was calculated based on GFR, plasma and urine [Na+], and urine output. Following trauma, RBF, GFR, Na+ filtration, renal DO2, and medullary glycogen levels were decreased in OZ but not in LZ. Food intake was markedly decreased in both LZ and OZ, which was associated with significantly increased Na+ reabsorption and aldosterone levels. However, compared to LZ, OZ exhibited lower Na+ uptake but higher aldosterone levels, renal VO2, and oxygen extraction ratio (VO2/DO2). These results suggest that trauma‐induced AKI in OZ is associated with impairments in renal oxygenation and the efficient oxygen utilization.Support or Funding InformationGrants: AHA‐12SDG12050525, National Institutes of HealthP20GM104357, HL‐51971, HL‐89581, and T32 HL‐105324.DoD Disclaimer: The opinions orassertions contained herin are the private views of the author and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
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