Introduction
The rate of acute kidney injury (AKI) after open heart surgery is between 3.1% and
42%. Nephrotoxins, ischemia and reperfusion, venous congestion, inflammation, oxidative
stress and genetics have been implicated in the development of AKI. ¹
The primary aim of this study was to investigate the effect of goal-directed fluid
therapy in the perioperative period on the development of AKI in the early period
in patients undergoing cardiac surgery. The secondary aim was to determine the independent
risk factors for the development of AKI.
Methods
Coronary artery by-pass greft (CABG) and valvuler heart disease patients undergoing
open heart surgery were randomly divided into two groups according to their perioperative
fluid management: Group Control (Group C, n=30): Fluid management was performed with
the traditional monitoring method. Group Study (Group S, n=30): Applied with transesophageal
doppler and transthoracic doppler fluid management. It was aimed to keep the hemodynamics
of the patients at normal values.²
Clinical and haemodynamic data were recorded at preoperative baseline (t1), postoperative
4th hour (t2), 24th hour (t3) and 48th hour (t4). Serum creatinine, GFR, Cystatin-C
and KIM-1 values obtained at the same time intervals as indicators of AKI. Akut kidney
injury was defined by KDIGO clasifications.
Two independent groups were compared statistically with appropriate parametric and
non-parametric tests. The development of postoperative AKI was investigated by “Forward
Stepwise Binary Logistic Regression” analysis.
Results
Postoperative fluid requirement was significantly lower in the study group (p=0.002).
Postoperative total balance was significantly more negative in the study group than
in the control group (p<0.0001). ERT requirement was significantly lower in the study
group compared to the control group (intraoperative, p=0.02; postoperative, p=0.002).
Cystatin-C was significantly lower in the study group at the postoperative 24th and
48th hours. (respectively, p<0.04, p<0.02) (Fig.1). AKI development rates were similar
between the groups (p>0.05). In the study group, only age (r=0.60, p=0.02) and only
intraoperative urine output in the control group (r=1.1;p=0.02) were determined as
independent risk factors for the development of AKI. When all cases were evaluated,
the Cystatin-C level at the postoperative 4th hour (r=0.03; p=0.02), intraoperative
noradrenalin requirement (r=0.74; p=0.04) and Euroscore (r=0.61, p=0.04) parameters
were independent risk factors.
Discussion
The incidence of AKI development after cardiac surgery was not different between groups.
Cystatin-C in Group S patients were significantly lower at the postoperative 24th
and 48th hours. Cystatin-C clearence was affected more earlier than creatinine clearence
in patients with AKI. Fluid and ERT requirements were less in Group S than Group C
and the hospital stay was significantly shorter than the control group.
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© 2021 Published by Elsevier Inc.
