Abstract
The use of hydroxyethyl starch (HES) in sepsis has been shown to increase mortality and acute kidney injury. However, the knowledge of the exact mechanism by which several fluids, especially starch preparations may impair end-organ function particularly in the kidney, is still missing. The aim of this study was to measure the influence of different crystalloid and colloid fluid compositions on the inflammatory response in the kidney, the liver and the lung using a rodent model of acute endotoxemia. Rats were anesthetized and mechanically ventilated. Lipopolysaccharide (5 mg/kg) was administered intravenously. After one hour crystalloids [lactate-buffered (RLac) or acetate-buffered (RAc)] were infused i.v. (30 ml/kg) in all groups. At 2 hours rats either received different crystalloids (75 ml/kg of RLac or RAc) or colloids (25 ml/kg of HES in saline or HES in RAc or gelatin in saline). Expression of messenger RNA for cytokine-induced neutrophil chemoattractant-1 (CINC-1), monocyte chemotactic protein-1 (MCP-1), necrosis factor α (TNFα) and intercellular adhesion molecule 1 (ICAM-1) was assessed in kidney, liver and lung tissue by real-time PCR after 4 hours. The use of acetate-buffered solutions was associated with a significantly higher expression of CINC-1 and TNFα mRNA in the liver, in the kidney and in the lung. Only marginal effects of gelatin and hydroxyethyl starch on mRNA expression of inflammatory mediators were observed. The study provides evidence that the type of buffering agent of different colloidal and crystalloid solutions might be a crucial factor determining the extent of early end-organ inflammatory response in sepsis.
Highlights
Acute kidney injury (AKI) is a common complication in sepsis
Independent of the buffering agent, hydroxyethyl starch (HES) as solution ingredient was not found to have a significant influence on CINC-1, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor a (TNFa) and intercellular adhesion molecule 1 (ICAM-1) mRNA expression
The key finding of the study is that acetate-buffered solutions induce a significant higher inflammatory response in the kidney, the liver and the lung as measured by expression of CINC-1 and TNFa in rats suffering from acute endotoxemia
Summary
Acute kidney injury (AKI) is a common complication in sepsis. It has a prevalence of 25% in severe sepsis and up to 50% in septic shock [1]. According to the work from Schortgen et al 6% HES 200/0.60–0.66 is an independent risk factor for AKI in patients with severe sepsis or septic shock [7]. In the VISEP study (Volume Substitution and Insulin Therapy in Severe Sepsis) the use of 10% HES 200/0.5 was associated with a higher incidence of AKI and renal replacement therapy compared to Ringer’s Lactate [9]. The CRYSTMAS study recently demonstrated no differences in mortality, coagulation and the occurrence of AKI between 6% HES 130 and normal saline in patient with a severe sepsis [10]. The 6S-Trial showed increased risk of death at day 90 and a higher incidence for renal replacement therapy in patients with severe sepsis treated with 6% HES 130/0.42 in acetate (HES-RAc) compared to Ringer’s Acetate (RAc) [11]. The clinical relevance of hyperchloremic acidosis is currently unclear [14]
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