Abstract
Background: Acute kidney injury (AKI) is a serious disease that can cause distant organ injuries and is associated with high mortality rates.
Objective: To identify the hemodynamic and respiratory dysfunction triggered by AKI, in an animal model of renal ischemia-reperfusion.
Method: Twelve anesthetized juvenile pigs (11.9 ± 1.0 kg). Six animals underwent ischemia/reperfusion-induced AKI: 45 min of ischemia and 240 minutes of reperfusion, while the remaining six animals were the control group. In basal conditions and after AKI, a conventional hemodynamic monitoring and transpulmonary thermodilution were performed. At the same time, arterial blood gases and lung mechanics were measured.
Results: There was a 29% increase in volumetric preload (221 ± 22 ml/m2 vs 286 ± 16 ml/m2, p = 0.04) and a 58% mean arterial pressure increase (71 ± 6 mmHg vs 112 ± 17 mmHg, p = 0.04) compared to controls, without changes in heart rate, central venous pressure and cardiac output. In addition, an increase of 86% in extravascular lung water (7.6 ± 0.6 ml/kg vs 14.1 ± 1.4 ml/ kg, p = 0.02) was reported, without changes in gas exchange and lung mechanics. Simultaneously, a slight increase in serum creatinine (1.12 ± 0.07 mg/dl vs 1.45 ± 0.10 mg/dl, p = 0.03) was described.
Discussion: An early development of hemodynamic and pulmonary dysfunction was observed in this experimental reperfusion model. An increase in volumetric preload and blood pressure associated with a substantial increase in the extravascular lung water were also reported. It is essential serially monitor the hemodynamic and respiratory functions in AKI, including nonuremic subjects.
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