Abstract
There are different underlying mechanisms of acute kidney injury (AKI) in various type of shock, but restoration of renal blood flow (RBF) is crucial in prevention of AKI. The first 24-48 hours of shock seem to be critical. Monitoring of global RBF and its intrarenal distribution is not possible in current clinical practice. The only way for optimization of renal blood supply is optimization of macrohemodynamics. In volume-responsive AKI, fluid therapy restores kidney function. Many clinical signs and parameters can be of use in determining the volume status. The accuracy of the assessment may be improved with the help of tools quantifying the clinical parameters (e.g. hypovolemic index – HVI). The basis of intravenous fluid therapy are crystalloids, and their effect is reported to be shorter than 120 min. Every form of hydroxyethyl starch has been shown to be harmful for patients at risk of impaired renal function. In sepsis, the boundary between volume-responsive and volume-unresponsive AKI is blurred. Fluid responsiveness can be lost in the course of AKI as early as on the first day of sepsis. According to the results of the ARDS Network study, the conservative approach in fluid therapy resulted in a shorter time of mechanical ventilation and did not affect the renal function, except for a slight increase of the serum creatinine level. Fluid overload is to be avoided, as renal venous and lymphatic congestion can limit the urine filtration rate, further worsening edema.
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