Abstract
Acute kidney injury associated with renal hypoperfusion is a frequent and severe complication during sepsis. Fluid resuscitation is the main therapy. However, heart failure is usually lethal for those patients receiving large volumes of fluids. We compared the effects of small-volume resuscitation using four different treatment regimens, involving saline, hypertonic saline (HTS), hydroxyethyl starch (HES), or hypertonic saline hydroxyethyl starch (HSH), on the kidneys of rats treated with lipopolysaccharide (LPS) to induce endotoxemia. LPS injection caused reduced and progressively deteriorated systemic (arterial blood pressure) and renal hemodynamics (renal blood flow and renal vascular resistance index) over time. This deterioration was accompanied by marked renal functional and pathological injury, as well as an oxidative and inflammatory response, manifesting as increased levels of tumor necrosis factor-α, nitric oxide, and malondialdehyde and decreased activity of superoxide dismutase. Small-volume perfusion with saline failed to improve renal and systemic circulation. However, small-volume perfusion with HES and HSH greatly improved the above parameters, while HTS only transiently improved systemic and renal hemodynamics with obvious renal injury. Therefore, single small-volume resuscitation with HES and HSH could be valid therapeutic approaches to ameliorate kidney injury induced by endotoxemia, while HTS transiently delays injury and saline shows no protective effects.
Highlights
Endotoxemia frequently occurs during critical phases of clinical diseases, including trauma and infectious diseases, and inevitably causes shock and organ damage contributing to poor survival rate [1, 2]
Small-volume resuscitation with colloid and hyperoncotic solutions markedly ameliorated the renal injury, showing that local epithelial and mitochondrial edema, cellular necrosis, and abscission were seen in the hypertonic saline (HTS) group, while kidneys in the hydroxyethyl starch (HES) and hydroxyethyl starch (HSH) groups appeared with only slight edema with occasional cellular necrosis and abscission
Reports indicate that endotoxemia-induced renal hypoperfusion contributes to an ischemia-reperfusion insult that potentially leads to the activation of renal inflammation and oxidative stress [10]
Summary
Endotoxemia frequently occurs during critical phases of clinical diseases, including trauma and infectious diseases, and inevitably causes shock and organ damage contributing to poor survival rate [1, 2]. Acute kidney injury (AKI) is a common complication following endotoxic shock and is associated with a high morbidity rate of up to 64% [3]. Resuscitation using crystal or colloid fluids to improve tissue perfusion and inhibit oxidative and inflammatory response may provide a meaningful degree of renal protection [7, 8]. The potential protective effects of small-volume fluid resuscitation on kidney injury induced by endotoxemia are currently unknown. We compared the effects of small-volume resuscitation with saline, 7.5% hypertonic saline (HTS), hydroxyethyl starch 130/0.4 (HES), and hypertonic saline hydroxyethyl starch 40 (HSH) at a dose of 4 mL/kg on acute kidney injury induced by endotoxemia. The potential mechanism of the hypothesized protection was further explored, focusing on renal perfusion and variations of oxidative and inflammatory mediators
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